How Is Hpv Transmitted

  1. There isn’t a test for high-risk HPV in the vulva, penis, anus, or throat, and the HPV itself doesn’t have any symptoms. If it becomes cancer, then there may be some symptoms. Penile cancer — cancer of the penis — might show symptoms like changes in color or thickness of the skin of your penis, or a painful sore might show up on your penis.
  2. HPV is a sexually transmitted disease that is most commonly passed between people during vaginal or anal intercourse. But it can also be transmitted through genital-to-genital, or hand-to-genital.
  3. An HPV infection is caused by human papillomavirus, a DNA virus from the papillomavirus family, of which over 170 types are known. More than 40 types are transmitted through sexual contact and infect the anus and genitals.
  1. How Is Hpv Transmitted If Not Sexually
  2. How Is Hpv Transmitted Treatment

HPV stands for human papillomavirus. It’s the most common sexually transmitted infection. HPV is usually harmless and goes away by itself, but some types can lead to cancer or genital warts. The Centers for Disease Control and Prevention says that male 'condom use may reduce the risk for genital human papillomavirus (HPV) infection' but provides a lesser degree of protection compared with other sexual transmitted diseases 'because HPV also may be transmitted by exposure to areas (e.g., infected skin or mucosal surfaces) that are.

(Redirected from Human papillomavirus)
Human papillomavirus infection
Other namesHuman papillomavirus
Electron micrograph of human papillomavirus from a wart
SpecialtyInfectious disease, gynecology
SymptomsNone, warts[1][2]
ComplicationsCancer of the cervix, vulva, vagina, penis, anus, mouth or throat[1][2]
CausesHuman papillomavirus spread by direct contact[3][4]
PreventionHPV vaccines, condoms[3][5]
FrequencyMost people are infected at some point in time[3]

Human papillomavirus infection (HPV infection) is an infection by human papillomavirus (HPV).[4] Most HPV infections cause no symptoms and resolve spontaneously.[1] In some people, an HPV infection persists and results in warts or precancerous lesions.[2] The precancerous lesions increase the risk of cancer of the cervix, vulva, vagina, penis, anus, mouth, or throat.[1][2] Nearly all cervical cancer is due to HPV; with two types, HPV16 and HPV18, accounting for 70% of cases.[1][6] Between 60% and 90% of the other cancers mentioned above are also linked to HPV.[6] HPV6 and HPV11 are common causes of genital warts and laryngeal papillomatosis.[1]

An HPV infection is caused by human papillomavirus, a DNA virus from the papillomavirus family, of which over 170 types are known.[7] More than 40 types are transmitted through sexual contact and infect the anus and genitals.[3] Risk factors for persistent infection by sexually transmitted types include early age of first sexual intercourse, multiple partners, smoking, and poor immune function.[1] These types are typically spread by sustained direct skin-to-skin contact, with vaginal and anal sex being the most common methods.[3] Occasionally, HPV infection can spread from a mother to baby during pregnancy.[8] HPV does not appear to spread via common items like toilet seats.[8] However, the types that cause warts may spread via surfaces such as floors.[9] People can become infected with more than one type of HPV.[8] HPV affects only humans.[4][10]

HPV vaccines can prevent the most common types of infection.[3] To be most effective, they should be used before the onset of sexual activity and are therefore recommended between the ages of nine and 13.[1]Cervical cancer screening, such as with the Papanicolaou test (pap) or looking at the cervix after using acetic acid, can detect early cancer or abnormal cells that may develop into cancer.[1] Screening allows for early treatment which results in better outcomes.[1] Screening has reduced both the number of cases and the number of deaths from cervical cancer.[11] Warts can be removed by freezing.[4]

HPV is the most common sexually transmitted infection globally.[4] Most people are infected at some point in their lives.[3] In 2018, an estimated 569,000 new cases and 311,000 deaths occurred from cervical cancer worldwide.[12] Around 85% of these occurred in low- and middle-income countries.[1] In the United States, about 30,700 cases of cancer due to HPV occur each year.[13] About 1% of sexually active adults have genital warts.[8] While cases of warts have been described since the time of ancient Greece, their viral nature was not discovered until 1907.[14]

  • 1Signs and symptoms
    • 1.1Warts
    • 1.2Cancer
    • 1.3Penile cancer
  • 2Cause
    • 2.1Transmission
    • 2.2Virology
  • 3Diagnosis
  • 4Prevention
  • 6Epidemiology

Signs and symptoms[edit]

Notable HPV[15] types and associated diseases

Over 170 types of HPV have been identified, and they are designated by numbers.[7][16]

Some HPV types, such as HPV-5, may establish infections that persist for the lifetime of the individual without ever manifesting any clinical symptoms. HPV types 1 and 2 can cause common warts in some infected individuals.[citation needed] HPV types 6 and 11 can cause genital warts and laryngeal papillomatosis.[1]Many HPV types are carcinogenic.[17] The table below lists common symptoms of HPV infection and the associated strains of HPV.

DiseaseHPV type
Common warts2, 7, 22
Plantar warts1, 2, 4, 63
Flat warts3, 10, 28
Anogenital warts6, 11, 42, 44 and others[18]
Anal dysplasia (lesions)6, 16, 18, 31, 53, 58[19]
Genital cancers
  • Highest risk:[18] 16, 18, 31, 45
  • Other high-risk:[18][20] 33, 35, 39, 51, 52, 56, 58, 59
  • Probably high-risk:[20] 26, 53, 66, 68, 73, 82
Epidermodysplasia verruciformismore than 15 types
Focal epithelial hyperplasia (mouth)13, 32
Mouth papillomas6, 7, 11, 16, 32
Oropharyngeal cancer16
Verrucous cyst60
Laryngeal papillomatosis6, 11


A sample DNA test report for HPV Genotype from a laboratory

Skin infection ('cutaneous' infection) with HPV is very widespread.[21]Skin infections with HPV can cause noncancerous skin growths called warts (verrucae). Warts are caused by a rapid growth of cells on the outer layer of the skin.[22]While cases of warts have been described since the time of ancient Greece, their viral cause was not known until 1907.[14]

Skin warts are most common in childhood and typically appear and regress spontaneously over the course of weeks to months. Recurring skin warts are common.[23] All HPVs are believed to be capable of establishing long-term 'latent' infections in small numbers of stem cells present in the skin. Although these latent infections may never be fully eradicated, immunological control is thought to block the appearance of symptoms such as warts. Immunological control is HPV type-specific, meaning an individual may become resistant to one HPV type while remaining susceptible to other types. In one study, infection by HPV types 2, 27, and 57 was found in people with warts, while infection by HPV types 1, 2, 63, and 27 was found in people with clinically normal skin.[24]

Types of warts include:

  • Common warts are usually found on the hands and feet, but can also occur in other areas, such as the elbows or knees. Common warts have a characteristic cauliflower-like surface and are typically slightly raised above the surrounding skin. Cutaneous HPV types can cause genital warts but are not associated with the development of cancer.
  • Plantar warts are found on the soles of the feet; they grow inward, generally causing pain when walking.
  • Subungual or periungual warts form under the fingernail (subungual), around the fingernail, or on the cuticle (periungual). They are more difficult to treat than warts in other locations.[25]
  • Flat warts are most commonly found on the arms, face, or forehead. Like common warts, flat warts occur most frequently in children and teens. In people with normal immune function, flat warts are not associated with the development of cancer.[26]

Genital warts are quite contagious, while common, flat, and plantar warts are much less likely to spread from person to person.

Genital warts[edit]

HPV infection of the skin in the genital area is the most common sexually transmitted infection worldwide.[27] Such infections are associated with genital or anal warts (medically known as condylomata acuminata or venereal warts), and these warts are the most easily recognized sign of genital HPV infection.

The strains of HPV that can cause genital warts are usually different from those that cause warts on other parts of the body, such as the hands or feet, or even the inner thighs. A wide variety of HPV types can cause genital warts, but types 6 and 11 together account for about 90% of all cases.[28][29] However, in total more than 40 types of HPV are transmitted through sexual contact and can infect the skin of the anus and genitals.[3] Such infections may cause genital warts, although they may also remain asymptomatic.

The great majority of genital HPV infections never cause any overt symptoms and are cleared by the immune system in a matter of months. Moreover, people may transmit the virus to others even if they do not display overt symptoms of infection. Most people acquire genital HPV infections at some point in their lives, and about 10% of women are currently infected.[27] A large increase in the incidence of genital HPV infection occurs at the age when individuals begin to engage in sexual activity. As with cutaneous HPVs, immunity to genital HPV is believed to be specific to a specific strain of HPV.

Laryngeal papillomatosis[edit]

In addition to genital warts, infection by HPV types 6 and 11 can cause a rare condition known as recurrent laryngeal papillomatosis, in which warts form on the larynx[30] or other areas of the respiratory tract.[31][32]These warts can recur frequently, may interfere with breathing, and in extremely rare cases can progress to cancer. For these reasons, repeated surgery to remove the warts may be advisable.[31][33]


HPV-induced cancers[34]

About a dozen HPV types (including types 16, 18, 31, and 45) are called 'high-risk' types because persistent infection has been linked to cancers such as cancer of the oropharynx, larynx, vulva, vagina, cervix, penis, and anus.[35][36] These cancers all involve sexually transmitted infection of HPV to the stratified epithelial tissue.[1][2][34] Individuals infected with both HPV and HIV have an increased risk of developing cervical or anal cancer.[35] HPV type 16 is the strain most likely to cause cancer and is present in about 47% of all cervical cancers,[37][38] and in many vaginal and vulvar cancers,[39] penile cancers, anal cancers, and cancers of the head and neck.[40]

An estimated 561,200 new cancer cases worldwide (5.2% of all new cancers) were attributable to HPV in 2002, making HPV one of the most important infectious causes of cancer.[34] HPV-associated cancers make up over 5% of total diagnosed cancer cases worldwide, and this incidence is higher in developing countries where it is estimated to cause almost half a million cases each year.[34]

In the United States, about 30,700 cases of cancer due to HPV occur each year.[13]

The number of HPV-associated cancers in the period of 2008-2012 in the US.[13]
Cancer areaAverage annual number of casesHPV attributable (estimated)HPV 16/18 attributable (estimated)
Oropharynx (men)12,6389,1008,000
Oropharynx (women)3,1002,0001,600
Anus (women)3,2603,0002,600
Anus (men)1,7501,6001,400
Rectal (women)513500400
Rectal (men)237200200
Genome organization of human papillomavirus type 16, one of the subtypes known to cause cervical cancer (E1-E7 early genes, L1-L2 late genes: capsid)

In some infected individuals, their immune systems may fail to control HPV. Lingering infection with high-risk HPV types, such as types 16, 18, 31, and 45, can favor the development of cancer.[41]Co-factors such as cigarette smoke can also enhance the risk of such HPV-related cancers.[42][43]

HPV is believed to cause cancer both by integrating into DNA and in non-integrated episomes.[44] Some of the 'early genes' carried by the HPV virus, such as genes E6 and E7, act as oncogenes that promote tumor growth and malignant transformation. Furthermore, HPV can induce a tumorigenic process through integration into a host genome which is associated with alterations in DNA copy number.[45]

E6 produces a protein (also called E6) that binds to and inactivates a protein in the host cell called p53. Normally, p53 acts to prevent cell growth, and promotes cell death in the presence of DNA damage. p53 also upregulates the p21 protein, which blocks the formation of the cyclin D/Cdk4 complex, thereby preventing the phosphorylation of RB, and in turn, halting cell cycle progression by preventing the activation of E2F. In short, p53 is a tumor-suppressor protein that arrests the cell cycle and prevents cell growth and survival when DNA damage occurs. Thus, inactivation of p53 by E6 can promote unregulated cell division, cell growth, and cell survival, characteristics of cancer.

E6 also has a close relationship with the cellular protein E6-associated protein (E6-AP), which is involved in the ubiquitin ligase pathway, a system that acts to degrade proteins. E6-AP binds ubiquitin to the p53 protein, thereby flagging it for proteosomal degradation.

Studies have also shown a link between a wide range of HPV types and squamous cell carcinoma of the skin. In such cases, in vitro studies suggest that the E6 protein of the HPV virus may inhibit apoptosis induced by ultraviolet light.[46]

Cervical cancer[edit]

Artist's impression of cervical cancer caused by HPV.

Nearly all cases of cervical cancer are associated with HPV infection, with two types, HPV16 and HPV18, present in 70% of cases.[1][6][37][47][48][49] HPV is necessary for cervical cancer to occur.[50] Persistent HPV infection increases the risk for developing cervical carcinoma. Individuals who have an increased incidence of these types of infection are women with HIV/AIDS, who are at a 22-fold increased risk of cervical cancer.[51][52]

In 2012, about 528,000 new cases and 266,000 deaths from cervical cancer occurred worldwide.[27] Around 85% of these occurred in the developing world.[1]

Most HPV infections of the cervix are cleared rapidly by the immune system and do not progress to cervical cancer (see below the Clearance subsection in Virology). Because the process of transforming normal cervical cells into cancerous ones is slow, cancer occurs in people having been infected with HPV for a long time, usually over a decade or more (persistent infection).[31][53]

Non-European (NE) HPV16 variants are significantly more carcinogenic than European (E) HPV16 variants.[54]

Anal cancer[edit]

Studies show a link between HPV infection and anal cancers. Sexually transmitted HPVs are found in a large percentage of anal cancers.[34] Moreover, the risk for anal cancer is 17 to 31 times higher among HIV-positive individuals who were coinfected with high-risk HPV, and 80 times higher for particularly HIV-positive men who have sex with men.[55]

Anal Pap smear screening for anal cancer might benefit some subpopulations of men or women engaging in anal sex.[56] No consensus exists, though, that such screening is beneficial, or who should get an anal Pap smear.[57][58]

Penile cancer[edit]

HPV is associated with approximately 50% of penile cancers. In the United States, penile cancer accounts for about 0.5% of all cancer cases in men. HPV16 is the most commonly associated type detected. The risk of penile cancer increases 2- to 3-fold for individuals who are infected with HIV as well as HPV.[55]

Cancers of the head and neck[edit]

Oral infection with high-risk carcinogenic HPV types (most commonly HPV 16)[13] is associated with an increasing number of head and neck cancers.[59][48][60][61] This association is independent of tobacco and alcohol use.[61][62][63]

Sexually transmitted forms of HPV account for about 25% of cancers of the mouth and upper throat (the oropharynx) worldwide,[34] but the local percentage varies widely, from 70% in the United States[64] to 4% in Brazil.[65] Engaging in anal or oral sex with an HPV-infected partner may increase the risk of developing these types of cancers.[60]

In the United States, the number of newly diagnosed, HPV-associated head and neck cancers has surpassed that of cervical cancer cases.[59] The rate of such cancers has increased from an estimated 0.8 cases per 100,000 people in 1988[66] to 4.5 per 100,000 in 2012,[13] and, as of 2015, the rate has continued to increase.[59] Researchers explain these recent data by an increase in oral sex. This type of cancer is more common in men than in women.[67]

The mutational profile of HPV-positive and HPV-negative head and neck cancer has been reported, further demonstrating that they are fundamentally distinct diseases.[68]

Lung cancer[edit]

Some evidence links HPV to benign and malignant tumors of the upper respiratory tract. The International Agency for Research on Cancer has found that people with lung cancer were significantly more likely to have several high-risk forms of HPV antibodies compared to those who did not have lung cancer.[69] Researchers looking for HPV among 1,633 lung cancer patients and 2,729 people without the lung disease found that people with lung cancer had more types of HPV than noncancer patients did, and among lung cancer patients, the chances of having eight types of serious HPV were significantly increased.[70] In addition, expression of HPV structural proteins by immunohistochemistry and in vitro studies suggest HPV presence in bronchial cancer and its precursor lesions.[71] Another study detected HPV in the EBC, bronchial brushing and neoplastic lung tissue of cases, and found a presence of an HPV infection in 16.4% of the subjects affected by nonsmall cell lung cancer, but in none of the controls.[72] The reported average frequencies of HPV in lung cancers were 17% and 15% in Europe and the Americas, respectively, and the mean number of HPV in Asian lung cancer samples was 35.7%, with a considerable heterogeneity between certain countries and regions.[73]

Immunocompromised individuals[edit]

In very rare cases, HPV may cause epidermodysplasia verruciformis (EV) in individuals with a weakened immune system. The virus, unchecked by the immune system, causes the overproduction of keratin by skin cells, resulting in lesions resembling warts or cutaneous horns which can ultimately transform into skin cancer, but the development is not well understood .[74][75] The specific types of HPV that are associated with EV are HPV5, HPV8, and HPV14.[75]


Sexually transmitted HPV is divided into 2 categories: low-risk and high-risk. Low-risk HPVs cause warts on or around the genitals. Type 6 and 11 cause 90% of all genital warts and recurrent respiratory papillomatosis that causes benign tumors in the air passages. High-risk HPVs cause cancer and consist of about a dozen identified types. Type 16 and 18 are two that are responsible for causing most of HPV-caused cancers. These high-risk HPVs cause 5% of the cancers in the world. In the United States, high-risk HPVs cause 3% of all cancer cases in women and 2% in men.[76]


Risk factors for persistent genital HPV infections, which increases the risk for developing cancer, include early age of first sexual intercourse, multiple partners, smoking, and immunosuppression.[1] Genital HPV is typically spread by sustained direct skin-to-skin contact, with vaginal and anal sex being the most common method though transmission from oral sex can occur.[3][35] Occasionally it can spread from a mother to her baby during pregnancy. HPV is difficult to remove via standard hospital disinfection techniques, and may be transmitted in a healthcare setting on re-usable gynecological equipment, such as vaginal ultrasound transducers.[77] The period of communicability is still unknown, but probably at least as long as visible HPV lesions persist. HPV may still be transmitted even after lesions are treated and no longer visible or present.[78]


Although genital HPV types can be transmitted from mother to child during birth, the appearance of genital HPV-related diseases in newborns is rare. However, the lack of appearance does not rule out asymptomatic latent infection, as the virus has proven to be capable of hiding for decades. Perinatal transmission of HPV types 6 and 11 can result in the development of juvenile-onset recurrent respiratory papillomatosis (JORRP). JORRP is very rare, with rates of about 2 cases per 100,000 children in the United States.[31] Although JORRP rates are substantially higher if a woman presents with genital warts at the time of giving birth, the risk of JORRP in such cases is still less than 1%.

Genital infections[edit]

Since cervical and female genital infection by specific HPV types is highly associated with cervical cancer, those types of HPV infection have received most of the attention from scientific studies.

HPV infections in that area are transmitted primarily via sexual activity.[79]

Of the 120 known human papilloma viruses, 51 species and three subtypes infect the genital mucosa.[80] 15 are classified as high-risk types (16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68, 73, and 82), three as probable high-risk (26, 53, and 66), and 12 as low-risk (6, 11, 40, 42, 43, 44, 54, 61, 70, 72, 81, and CP6108).[81]

If a woman has at least one different partner per year for four years, the probability that she will leave college with an HPV infection is greater than 85%.[82] Condoms do not completely protect from the virus because the areas around the genitals including the inner thigh area are not covered, thus exposing these areas to the infected person’s skin.[82]

Among women who were HPV positive in either the vulva/vagina or the cervix, 90% were positive in the vulvovaginal region, 46% in the cervix.[83]


Studies have shown HPV transmission between hands and genitals of the same person and sexual partners. Hernandez tested the genitals and dominant hand of each person in 25 heterosexual couples every other month for an average of seven months. She found two couples where the man's genitals infected the woman's hand with high-risk HPV, two where her hand infected his genitals, one where her genitals infected his hand, two each where he infected his own hand, and she infected her own hand.[84][85] Hands were not the main source of transmission in these 25 couples, but they were significant.

Partridge reports men's fingertips became positive for high risk HPV at more than half the rate (26% per 2 years) as their genitals (48%).[86] Winer reports 14% of fingertip samples from sexually active women were positive.[87]

Non-sexual hand contact seems to have little or no role in HPV transmission. Winer found all 14 fingertip samples from virgin women negative at the start of her fingertip study.[87] In a separate report on genital HPV infection, 1% of virgin women (1 of 76) with no sexual contact tested positive for HPV, while 10% of virgin women reporting non-penetrative sexual contact were positive (7 of 72).[83]

Shared objects[edit]

Sharing of possibly contaminated objects, for example, razors,[78] may transmit HPV.[88][89][90] Although possible, transmission by routes other than sexual intercourse is less common for female genital HPV infection.[79] Fingers-genital contact is a possible way of transmission but unlikely to be a significant source.[87][91]


Though it has traditionally been assumed that HPV is not transmissible via blood—as it is thought to only infect cutaneous and mucosal tissues—recent studies have called this notion into question. Historically, HPV DNA has been detected in the blood of cervical cancer patients.[92] In 2005, a group reported that, in frozen blood samples of 57 sexually naive pediatric patients who had vertical or transfusion-acquired HIV infection, 8 (14.0%) of these samples also tested positive for HPV-16.[93] This seems to indicate that it may be possible for HPV to be transmitted via blood transfusion. However, as non-sexual transmission of HPV by other means is not uncommon, this could not be definitively proven. In 2009, a group tested Australian Red Cross blood samples from 180 healthy male donors for HPV, and subsequently found DNA of one or more strains of the virus in 15 (8.3%) of the samples.[94] However, it is important to note that detecting the presence of HPV DNA in blood is not the same as detecting the virus itself in blood, and whether or not the virus itself can or does reside in blood in infected individuals is still unknown. As such, it remains to be determined whether HPV can or cannot be transmitted via blood.[92] This is of concern, as blood donations are not currently screened for HPV, and at least some organizations such as the American Red Cross and other Red Cross societies do not presently appear to disallow HPV-positive individuals from donating blood.[95]


Hospital transmission of HPV, especially to surgical staff, has been documented. Surgeons, including urologists and/or anyone in the room, is subject to HPV infection by inhalation of noxious viral particles during electrocautery or laser ablation of a condyloma (wart).[96] There has been a case report of a laser surgeon who developed extensive laryngeal papillomatosis after providing laser ablation to patients with anogenital condylomata.[96]


Cryo-electron microscopy structure of the HPV type 16 viral capsid protein. Rendered from PDB: 5KEQ​.[97]

HPV infection is limited to the basal cells of stratified epithelium, the only tissue in which they replicate.[98] The virus cannot bind to live tissue; instead, it infects epithelial tissues through micro-abrasions or other epithelial trauma that exposes segments of the basement membrane.[98] The infectious process is slow, taking 12–24 hours for initiation of transcription. It is believed that involved antibodies play a major neutralizing role while the virions still reside on the basement membrane and cell surfaces.[98]

HPV lesions are thought to arise from the proliferation of infected basal keratinocytes. Infection typically occurs when basal cells in the host are exposed to the infectious virus through a disturbed epithelial barrier as would occur during sexual intercourse or after minor skin abrasions. HPV infections have not been shown to be cytolytic; rather, viral particles are released as a result of degeneration of desquamating cells. HPV can survive for many months and at low temperatures without a host; therefore, an individual with plantar warts can spread the virus by walking barefoot.[29]

How Is Hpv Transmitted If Not Sexually

HPV is a small double-stranded circular DNA virus with a genome of approximately 8000 base pairs.[35][99] The HPV life cycle strictly follows the differentiation program of the host keratinocyte. It is thought that the HPV virion infects epithelial tissues through micro-abrasions, whereby the virion associates with putative receptors such as alpha integrins, laminins, and annexin A2[100] leading to entry of the virions into basal epithelial cells through clathrin-mediated endocytosis and/or caveolin-mediated endocytosis depending on the type of HPV.[101] At this point, the viral genome is transported to the nucleus by unknown mechanisms and establishes itself at a copy number of 10-200 viral genomes per cell. A sophisticated transcriptional cascade then occurs as the host keratinocyte begins to divide and become increasingly differentiated in the upper layers of the epithelium.

The phylogeny of the various strains of HPV generally reflects the migration patterns of Homo sapiens and suggests that HPV may have diversified along with the human population. Studies suggest that HPV evolved along five major branches that reflect the ethnicity of human hosts, and diversified along with the human population.[102] Researchers have identified two major variants of HPV16, European (HPV16-E), and Non-European (HPV16-NE).[103]

E6/E7 proteins[edit]

X-ray crystallography structure of the HPV type 16 oncoprotein E6 (purple) shown bound to the LxxLL peptide motif of the human protein ubiquitin ligase E6P (cyan). Rendered from PDB: 4GIZ​.[104]

The two primary oncoproteins of high risk HPV types are E6 and E7. The “E” designation indicates that these two proteins are expressed early in the HPV life cycle, while the 'L' designation indicates late expression.[48] The HPV genome is composed of six early (E1, E2, E4, E5, E6, and E7) open-reading frames (ORF), two late (L1 and L2) ORFs, and a non-coding long control region (LCR).[105] After the host cell is infected viral early promoter is activated and a polycistronic primary RNA containing all six early ORFs is transcribed. This polycistronic RNA then undergoes active RNA splicing to generate multiple isoforms of mRNAs.[106] One of the spliced isoform RNAs, E6*I, serves as an E7 mRNA to translate E7 protein.[107] However, viral early transcription subjects to viral E2 regulation and high E2 levels repress the transcription. HPV genomes integrate into host genome by disruption of E2 ORF, preventing E2 repression on E6 and E7. Thus, viral genome integration into host DNA genome increases E6 and E7 expression to promote cellular proliferation and the chance of malignancy. The degree to which E6 and E7 are expressed is correlated with the type of cervical lesion that can ultimately develop.[99]

Role in cancer

The E6/E7 proteins inactivate two tumor suppressor proteins, p53 (inactivated by E6) and pRb (inactivated by E7).[16]The viral oncogenes E6 and E7[108] are thought to modify the cell cycle so as to retain the differentiating host keratinocyte in a state that is favourable to the amplification of viral genome replication and consequent late gene expression. E6 in association with host E6-associated protein, which has ubiquitin ligase activity, acts to ubiquitinate p53, leading to its proteosomal degradation. E7 (in oncogenic HPVs) acts as the primary transforming protein. E7 competes for retinoblastoma protein (pRb) binding, freeing the transcription factor E2F to transactivate its targets, thus pushing the cell cycle forward. All HPV can induce transient proliferation, but only strains 16 and 18 can immortalize cell lines in vitro. It has also been shown that HPV 16 and 18 cannot immortalize primary rat cells alone; there needs to be activation of the ras oncogene. In the upper layers of the host epithelium, the late genes L1 and L2 are transcribed/translated and serve as structural proteins that encapsidate the amplified viral genomes. Once the genome is encapsidated, the capsid appears to undergo a redox-dependent assembly/maturation event, which is tied to a natural redox gradient that spans both suprabasal and cornified epithelial tissue layers. This assembly/maturation event stabilizes virions, and increases their specific infectivity.[109] Virions can then be sloughed off in the dead squames of the host epithelium and the viral lifecycle continues.[110] A 2010 study has found that E6 and E7 are involved in beta-catenin nuclear accumulation and activation of Wnt signaling in HPV-induced cancers.[111]

Latency period[edit]

Once an HPV virion invades a cell, an active infection occurs, and the virus can be transmitted. Several months to years may elapse before squamous intraepithelial lesions (SIL) develop and can be clinically detected. The time from active infection to clinically detectable disease may make it difficult for epidemiologists to establish which partner was the source of infection.[96]


Most HPV infections are cleared up by most people without medical action or consequences. The table provides data for high-risk types (i.e. the types found in cancers).

Clearance rates of high risk types of HPV[112]
Months after initial positive test8 months12 months18 months
% of men tested negative70%80%100%

Clearing an infection does not always create immunity if there is a new or continuing source of infection. Hernandez' 2005-6 study of 25 couples reports 'A number of instances indicated apparent reinfection [from partner] after viral clearance.'[84]


There are multiple types of HPV, sometimes called 'low-risk' and 'high-risk' types. Low-risk types cause warts and high-risk types can cause lesions or cancer.[113][114]

Cervical testing[edit]

Guidelines from the American Cancer Society recommend screening for cervical cancer based on age, screening history, risk factors and choice of tests available. Because of the link between HPV and cervical cancer, the ACS currently recommends early detection of cervical cancer in average-risk asymptomatic adults primarily with cervical cytology by Pap smear, regardless of HPV vaccination status. Women aged 30-65 should preferably be tested every 5 years with both the HPV test and the Pap test. In other age groups, a Pap test alone can suffice unless they have been diagnosed with atypical squamous cells of undetermined significance (ASC-US).[115] Co-testing with a Pap test and HPV test is recommended because it decreases the rate of false-negatives. According to the National Cancer Institute, 'The most common test detects DNA from several high-risk HPV types, but it cannot identify the types that are present. Another test is specific for DNA from HPV types 16 and 18, the two types that cause most HPV-associated cancers. A third test can detect DNA from several high-risk HPV types and can indicate whether HPV-16 or HPV-18 is present. A fourth test detects RNA from the most common high-risk HPV types. These tests can detect HPV infections before cell abnormalities are evident.

'Theoretically, the HPV DNA and RNA tests could be used to identify HPV infections in cells taken from any part of the body. However, the tests are approved by the FDA for only two indications: for follow-up testing of women who seem to have abnormal Pap test results and for cervical cancer screening in combination with a Pap test among women over age 30.'[116]

Mouth testing[edit]

Guidelines for oropharyngeal cancer screening by the Preventive Services Task Force and American Dental Association in the U.S. suggest conventional visual examination, but because some parts of the oropharynx are hard to see, this cancer is often only detected in later stages.[55]

The diagnosis of oropharyngeal cancer occurs by biopsy of exfoliated cells or tissues. The National Comprehensive Cancer Network and College of American Pathologists recommend testing for HPV in oropharyngeal cancer.[55] However, while testing is recommended, there is no specific type of test used to detect HPV from oral tumors that is currently recommended by the FDA in the United States. Because HPV type 16 is the most common type found in oropharyngeal cancer, p16 immunohisochemistry is one test option used to determine if HPV is present,[117] which can help determine course of treatment since tumors that are negative for p16 have better outcomes. Another option that has emerged as a reliable option is HPV DNA in situ hybridization (ISH) which allows for visualization of the HPV.[55]

Studies have found heightened HPV in mouth cell samples from people with squamous cell carcinoma of the mouth. Studies have not found significant HPV in mouth cells after sampling with toothbrushes (5 of 2,619 samples)[83] and cytobrushes (no oral transmission found).[84]

Testing men[edit]

There isn't a wide range of tests available even though HPV is common; most studies of HPV used tools and custom analysis not available to the general public.[118][needs update] Clinicians often depend on the vaccine among young people and high clearance rates (see Clearance subsection in Virology) to create a low risk of disease and mortality, and treat the cancers when they appear. Others believe that reducing HPV infection in more men and women, even when it has no symptoms, is important (herd immunity) to prevent more cancers rather than just treating them.[119][120][needs update] Where tests are used, negative test results show safety from transmission, and positive test results show where shielding (condoms, gloves) is needed to prevent transmission until the infection clears.[121]

Studies have tested for and found HPV in men, including high-risk types (i.e. the types found in cancers), on fingers, mouth, saliva, anus, urethra, urine, semen, blood, scrotum and penis.[118]

The Qiagen/Digene kit mentioned in the previous section was used successfully off label to test the penis, scrotum and anus[122] of men in long-term relationships with women who were positive for high-risk HPV. 60% of them were found to carry the virus, primarily on the penis.[122][needs update] Other studies used cytobrushes and custom analysis.[123][124][needs update]

In one study researchers sampled subjects' urethra, scrotum and penis.[123][124][needs update] Samples taken from the urethra added less than 1% to the HPV rate. Studies like this led Giuliano to recommend sampling the glans, shaft and crease between them, along with the scrotum, since sampling the urethra or anus added very little to the diagnosis.[86] Dunne recommends the glans, shaft, their crease, and the foreskin.[118]

In one study the subjects were asked not to wash their genitals for 12 hours before sampling, including the urethra as well as the scrotum and the penis.[123] Other studies are silent on washing - a particular gap in studies of the hands.

One small study used wet cytobrushes, rather than wet the skin.[124] It found a higher proportion of men to be HPV-positive when the skin was rubbed with a 600 grit emery paper before being swabbed with the brush, rather than swabbed with no preparation. It's unclear whether the emery paper collected the virions or simply loosened them for the swab to collect.

Studies have found self-collection (with emery paper and Dacron swabs) as effective as collection done by a clinician, and sometimes more so, since patients were more willing than a clinician to scrape vigorously.[125][needs update][126] Women had similar success in self-sampling using tampons, swabs, cytobrushes and lavage.[127][needs update]

Several studies used cytobrushes to sample fingertips and under fingernails, without wetting the area or the brush.[87][91][128][needs update]

Other studies analyzed urine, semen, and blood and found varying amounts of HPV,[118] but there isn't a publicly available test for those yet.

Other testing[edit]

Although it is possible to test for HPV DNA in other kinds of infections,[129] there are no FDA-approved tests for general screening in the United States[130] or tests approved by the Canadian government,[131] since the testing is inconclusive and considered medically unnecessary.[132]

Genital warts are the only visible sign of low-risk genital HPV and can be identified with a visual check. These visible growths, however, are the result of non-carcinogenic HPV types. Five percent acetic acid (vinegar) is used to identify both warts and squamous intraepithelial neoplasia (SIL) lesions with limited success[citation needed] by causing abnormal tissue to appear white, but most doctors have found this technique helpful only in moist areas, such as the female genital tract.[citation needed] At this time, HPV tests for males are used only in research.[citation needed]

Research into testing for HPV by antibody presence has been done. The approach is looking for an immune response in blood, which would contain antibodies for HPV if the patient is HPV positive.[133][134][135][136] The reliability of such tests hasn't been proven, as there hasn't been a FDA approved product as of August 2018;[137] testing by blood would be a less invasive test for screening purposes.


The HPV vaccines can prevent the most common types of infection.[3] To be effective they must be used before an infection occurs and are therefore recommended between the ages of nine and thirteen. Cervical cancer screening, such as with the Papanicolaou test (pap) or looking at the cervix after using acetic acid, can detect early cancer or abnormal cells that may develop into cancer. This allows for early treatment which results in better outcomes.[1] Screening has reduced both the number and deaths from cervical cancer in the developed world.[11] Warts can be removed by freezing.[4]

Methods of reducing the chances of infection include sexual abstinence, condoms, and vaccination.[138]


Three vaccines are available to prevent infection by some HPV types: Gardasil, Gardasil 9 and Cervarix; all three protect against initial infection with HPV types 16 and 18, which cause most of the HPV-associated cancer cases. Gardasil also protects against HPV types 6 and 11, which cause 90% of genital warts. Gardasil is a recombinant quadrivalent vaccine, whereas Cervarix is bivalent, and is prepared from virus-like particles (VLP) of the L1 capsid protein. Gardasil 9 is nonavalent, it has the potential to prevent about 90% of cervical, vulvar, vaginal, and anal cancers. It can protect for HPV types 6, 11, 16, 18, 31, 33, 45, 52, and 58; the latter five cause up to 20% of cervical cancers which were not previously covered.[139]

The vaccines provide little benefit to women already infected with HPV types 16 and 18.[140] For this reason, the vaccine is recommended primarily for those women not yet having been exposed to HPV during sex. The World Health Organization position paper on HPV vaccination clearly outlines appropriate, cost-effective strategies for using HPV vaccine in public sector programs.[141]

There is high-certainty evidence that HPV vaccines protect against precancerous cervical lesions in young women, particularly those vaccinated aged 15 to 26.[142] HPV vaccines do not increase the risk of serious adverse events.[142] Longer follow-up is needed to monitor the impact of HPV vaccines on cervical cancer.[142]

The CDC recommends the vaccines be delivered in two shots at an interval of least 6 months for those aged 11–12, and three doses for those 13 and older.[143] In most countries, they are funded only for female use, but are approved for male use in many countries, and funded for teenage boys in Australia. The vaccine does not have any therapeutic effect on existing HPV infections or cervical lesions.[144] In 2010, 49% of teenage girls in the US got the HPV vaccine.

Following studies suggesting that the vaccine is more effective in younger girls[145] than in older teenagers, the United Kingdom, Switzerland, Mexico, the Netherlands and Quebec began offering the vaccine in a two-dose schedule for girls aged under 15 in 2014.

Cervical cancer screening recommendations have not changed for females who receive HPV vaccine. It remains a recommendation that women continue cervical screening, such as Pap smear testing, even after receiving the vaccine, since it does not prevent all types of cervical cancer.[144][146]

Both men and women are carriers of HPV.[147] The Gardasil vaccine also protects men against anal cancers and warts and genital warts.[148]

Duration of both vaccines' efficacy has been observed since they were first developed, and is expected to be longlasting.[149]

In December 2014, the FDA approved a nine-valent Gardasil-based vaccine, Gardasil 9, to protect against infection with the four strains of HPV covered by the first generation of Gardasil as well as five other strains responsible for 20% of cervical cancers (HPV-31, HPV-33, HPV-45, HPV-52, and HPV-58).[150]


The Centers for Disease Control and Prevention says that male 'condom use may reduce the risk for genital human papillomavirus (HPV) infection' but provides a lesser degree of protection compared with other sexual transmitted diseases 'because HPV also may be transmitted by exposure to areas (e.g., infected skin or mucosal surfaces) that are not covered or protected by the condom.'[151]

Female condoms provide somewhat greater protection than male condoms, as the female condom allows for less skin contact.[152]

Studies have suggested that regular condom use can effectively limit the ongoing persistence and spread of HPV to additional genital sites in individuals already infected.[needs update]


The virus is unusually hardy, and is immune to most common disinfectants. It is the first virus ever shown to be resistant to inactivation by glutaraldehyde, which is among the most common strong disinfectants used in hospitals.[153] Diluted sodium hypochlorite bleach is effective,[153] but cannot be used on some types of re-usable equipment, such as ultrasound transducers.[77] As a result of these difficulties, there is developing concern about the possibility of transmitting the virus on healthcare equipment, particularly reusable gynecological equipment that cannot be autoclaved.[154][155] For such equipment, some health authorities encourage use of UV disinfection[156] or a non-hypochlorite 'oxidizing‐based high‐level disinfectant [bleach] with label claims for non‐enveloped viruses',[157] such as a strong hydrogen peroxide solution[158][156] or chlorine dioxide wipes.[156] Such disinfection methods are expected to be relatively effective against HPV.


There is currently no specific treatment for HPV infection.[159][160][161] However, the viral infection, more often than not, clears to undetectable levels by itself.[162] According to the Centers for Disease Control and Prevention, the body's immune system clears HPV naturally within two years for 90% of cases (see Clearance subsection in Virology for more detail).[159] However, experts do not agree on whether the virus is completely eliminated or reduced to undetectable levels, and it is difficult to know when it is contagious.[163]

Follow up care is usually recommended and practiced by many health clinics.[164] Follow-up is sometimes not successful because a portion of those treated do not return to be evaluated. In addition to the normal methods of phone calls and mail, text messaging and email can improve the number of people who return for care.[165]


Worldwide, HPV is estimated to infect about 12% of women at any given time.[166] HPV infection is the most frequently sexually transmitted disease in the world.[167]

United States[edit]

HPV prevalence among women by age, including 20 low-risk types and 23 high-risk types[168]
Age (years)Prevalence (%)
14 to 1924.5%
20 to 2444.8%
25 to 2927.4%
30 to 3927.5%
40 to 4925.2%
50 to 5919.6%
14 to 5926.8%

HPV is estimated to be the most common sexually transmitted infection in the United States.[168] Most sexually active men and women will probably acquire genital HPV infection at some point in their lives.[37] The American Social Health Association estimates that about 75–80% of sexually active Americans will be infected with HPV at some point in their lifetime.[169][170] By the age of 50 more than 80% of American women will have contracted at least one strain of genital HPV.[168][171] It was estimated that, in the year 2000, there were approximately 6.2 million new HPV infections among Americans aged 15–44; of these, an estimated 74% occurred to people between ages of 15 and 24.[172] Of the STDs studied, genital HPV was the most commonly acquired.[172] In the United States, it is estimated that 10% of the population has an active HPV infection, 4% has an infection that has caused cytological abnormalities, and an additional 1% has an infection causing genital warts.[173]

Estimates of HPV prevalence vary from 14% to more than 90%.[174] One reason for the difference is that some studies report women who currently have a detectable infection, while other studies report women who have ever had a detectable infection.[175][176] Another cause of discrepancy is the difference in strains that were tested for.

One study found that, during 2003–2004, at any given time, 26.8% of women aged 14 to 59 were infected with at least one type of HPV. This was higher than previous estimates; 15.2% were infected with one or more of the high-risk types that can cause cancer.[168][177]

The prevalence for high-risk and low-risk types is roughly similar over time.[168]

Human papillomavirus is not included among the diseases that are typically reportable to the CDC as of 2011.[178][179]

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On average 538 cases of HPV-associated cancers were diagnosed per year in Ireland during the period 2010 to 2014.[180] Cervical cancer was the most frequent HPV-associated cancer with on average 292 cases per year (74% of the female total, and 54% of the overall total of HPV-associated cancers).[180] A study of 996 cervical cytology samples in an Irish urban female, opportunistically screened population, found an overall HPV prevalence of 19.8%, HPV 16 at 20% and HPV 18 at 12% were the commonest high-risk types detected. In Europe, types 16 and 18 are responsible for over 70% of cervical cancers.[181] Overall rates of HPV-associated invasive cancers may be increasing. Between 1994 and 2014, there was a 2% increase in the rate of HPV-associated invasive cancers per year for both sexes in Ireland.[180]

As HPV is known to be associated with ano-genital warts, these are notifiable to the Health Protection Surveillance Centre (HPSC). Genital warts are the second most common STI in Ireland.[182] There were 1,281 cases of ano-genital warts notified in 2017, which was a decrease on the 2016 figure of 1,593.[183] The highest age-specific rate for both male and female was in the 25-29 year old age range, 53% of cases were among males.[183]


In 1972, the association of the human papillomaviruses with skin cancer in epidermodysplasia verruciformis was proposed by Stefania Jabłońska in Poland. In 1978, Jabłońska and Gerard Orth at the Pasteur Institute discovered HPV-5 in skin cancer.[184][page needed] In 1976 Harald zur Hausen published the hypothesis that human papilloma virus plays an important role in the cause of cervical cancer. In 1983 and 1984 zur Hausen and his collaborators identified HPV16 and HPV18 in cervical cancer.[185]

The HeLa cell line contains extra DNA in its genome that originated from HPV type 18.[186]


Ludwig-McGill HPV Cohort, large longitudinal study of the natural history of human papillomavirus infection and cervical cancer risk

One study found tentative evidence in support of an extract from garlic.[187]


  1. ^ abcdefghijklmnopq'Human papillomavirus (HPV) and cervical cancer'. WHO. June 2016. Archived from the original on 5 August 2016. Retrieved 10 August 2016.Cite uses deprecated parameter deadurl= (help)
  2. ^ abcdeLjubojevic S, Skerlev M (2014). 'HPV-associated diseases'. Clinics in Dermatology. 32 (2): 227–34. doi:10.1016/j.clindermatol.2013.08.007. PMID24559558.
  3. ^ abcdefghij'What is HPV?'. CDC. 28 December 2015. Archived from the original on 7 August 2016. Retrieved 10 August 2016.Cite uses deprecated parameter deadurl= (help)
  4. ^ abcdefMilner, Danny A. (2015). Diagnostic Pathology: Infectious Diseases. Elsevier Health Sciences. p. 40. ISBN9780323400374. Archived from the original on 11 September 2017.Cite uses deprecated parameter deadurl= (help)
  5. ^'Fact Sheet for Public Health Personnel Condom Effectiveness CDC'. 25 March 2013. Archived from the original on 27 May 2017. Retrieved 1 May 2017.Cite uses deprecated parameter deadurl= (help)
  6. ^ abc'The Link Between HPV and Cancer'. CDC. 30 September 2015. Archived from the original on 9 November 2015. Retrieved 11 August 2016.
  7. ^ abBzhalava D, Guan P, Franceschi S, Dillner J, Clifford G (October 2013). 'A systematic review of the prevalence of mucosal and cutaneous human papillomavirus types'. Virology. 445 (1–2): 224–31. doi:10.1016/j.virol.2013.07.015. PMID23928291.
  8. ^ abcd'Human Papillomavirus (HPV) Questions and Answers'. CDC. 28 December 2015. Archived from the original on 11 August 2016. Retrieved 11 August 2016.Cite uses deprecated parameter deadurl= (help)
  9. ^'Human Papilloma Virus (HPV)'(PDF). WRHA. 18 November 2019. Retrieved 26 March 2019.
  10. ^'Pink Book (Human Papillomavirus)'(PDF). Archived(PDF) from the original on 21 March 2017. Retrieved 18 April 2017.Cite uses deprecated parameter deadurl= (help)
  11. ^ abSawaya GF, Kulasingam S, Denberg TD, Qaseem A (June 2015). 'Cervical Cancer Screening in Average-Risk Women: Best Practice Advice From the Clinical Guidelines Committee of the American College of Physicians'. Annals of Internal Medicine. 162 (12): 851–9. doi:10.7326/M14-2426. PMID25928075.
  12. ^'Global Cancer Observatory: International Agency for Research on Cancer'(PDF). IARC. Archived from the original(PDF) on 11 October 2018. Retrieved 16 March 2019.
  13. ^ abcdeViens, LJ; Henley, SJ; Watson, M; Markowitz, LE; Thomas, CC; Thompson, TD; Razzaghi, H; Saraiya, M (8 July 2016). 'Human Papillomavirus-Associated Cancers - United States, 2008-2012'. MMWR. Morbidity and Mortality Weekly Report. 65 (26): 661–6. doi:10.15585/mmwr.mm6526a1. PMID27387669.
  14. ^ abTyring S, Moore AY, Lupi O (2016). Mucocutaneous Manifestations of Viral Diseases: An Illustrated Guide to Diagnosis and Management (2 ed.). CRC Press. p. 207. ISBN9781420073133.
  15. ^EHPV, archived from the original on 17 December 2014Cite uses deprecated parameter deadurl= (help)
  16. ^ abChaturvedi, Anil; Maura L. Gillison (4 March 2010). 'Human Papillomavirus and Head and Neck Cancer'. In Andrew F. Olshan (ed.). Epidemiology, Pathogenesis, and Prevention of Head and Neck Cancer (1st ed.). New York: Springer. ISBN978-1-4419-1471-2.
  17. ^Muñoz N, Bosch FX, de Sanjosé S, Herrero R, Castellsagué X, Shah KV, Snijders PJ, Meijer CJ, et al. (International Agency for Research on Cancer Multicenter Cervical Cancer Study Group) (February 2003). 'Epidemiologic classification of human papillomavirus types associated with cervical cancer'. The New England Journal of Medicine. 348 (6): 518–27. doi:10.1056/NEJMoa021641. hdl:2445/122831. PMID12571259.
  18. ^ abcKumar, Vinay; Abbas, Abul K.; Fausto, Nelson; Mitchell, Richard (2007). 'Chapter 19 The Female Genital System and Breast'. Robbins Basic Pathology (8 ed.). Philadelphia: Saunders. ISBN978-1-4160-2973-1.
  19. ^Palefsky JM, Holly EA, Ralston ML, Jay N (February 1998). 'Prevalence and risk factors for human papillomavirus infection of the anal canal in human immunodeficiency virus (HIV)-positive and HIV-negative homosexual men'. The Journal of Infectious Diseases. 177 (2): 361–7. doi:10.1086/514194. PMID9466522.
  20. ^ abMuñoz N, Castellsagué X, de González AB, Gissmann L (August 2006). 'Chapter 1: HPV in the etiology of human cancer'. Vaccine. 24 (3): S3/1–10. doi:10.1016/j.vaccine.2006.05.115. PMID16949995.
  21. ^Antonsson A, Forslund O, Ekberg H, Sterner G, Hansson BG (December 2000). 'The ubiquity and impressive genomic diversity of human skin papillomaviruses suggest a commensalic nature of these viruses'. Journal of Virology. 74 (24): 11636–41. doi:10.1128/JVI.74.24.11636-11641.2000. PMC112445. PMID11090162.
  22. ^Mayo, Common warts, 17 October 2011 at the Wayback Machine
  23. ^StatPearls. StatPearls Publishing. January 2018.
  24. ^de Koning MN, Quint KD, Bruggink SC, Gussekloo J, Bouwes Bavinck JN, Feltkamp MC, Quint WG, Eekhof JA (January 2015). 'High prevalence of cutaneous warts in elementary school children and the ubiquitous presence of wart-associated human papillomavirus on clinically normal skin'. The British Journal of Dermatology. 172 (1): 196–201. doi:10.1111/bjd.13216. PMID24976535.
  25. ^Lountzis NI, Rahman O (July 2008). 'Images in clinical medicine. Digital verrucae'. The New England Journal of Medicine. 359 (2): 177. doi:10.1056/NEJMicm071912. PMID18614785.
  26. ^MedlinePlus, Warts, 5 June 2016 at the Wayback Machine (general reference with links). Also, see
  27. ^ abcWorld Cancer Report 2014. World Health Organization. 2014. pp. Chapter 5.12. ISBN978-9283204299.
  28. ^Greer CE, Wheeler CM, Ladner MB, Beutner K, Coyne MY, Liang H, Langenberg A, Yen TS, Ralston R (August 1995). 'Human papillomavirus (HPV) type distribution and serological response to HPV type 6 virus-like particles in patients with genital warts'. Journal of Clinical Microbiology. 33 (8): 2058–63. PMC228335. PMID7559948.
  29. ^ ab'Human Papillomavirus'. Medscape. 16 October 2018. Archived from the original on 29 November 2016.Cite uses deprecated parameter deadurl= (help)
  30. ^'Photos of larynx Papillomas — Voice Medicine, New York'. Archived from the original on 12 June 2010. Retrieved 29 August 2010.Cite uses deprecated parameter deadurl= (help)
  31. ^ abcdSinal SH, Woods CR (October 2005). 'Human papillomavirus infections of the genital and respiratory tracts in young children'. Seminars in Pediatric Infectious Diseases. 16 (4): 306–16. doi:10.1053/j.spid.2005.06.010. PMID16210110.
  32. ^Wu R, Sun S, Steinberg BM (2003). 'Requirement of STAT3 activation for differentiation of mucosal stratified squamous epithelium'. Molecular Medicine. 9 (3–4): 77–84. doi:10.2119/2003-00001.Wu. PMC1430729. PMID12865943.
  33. ^Moore CE, Wiatrak BJ, McClatchey KD, Koopmann CF, Thomas GR, Bradford CR, Carey TE (May 1999). 'High-risk human papillomavirus types and squamous cell carcinoma in patients with respiratory papillomas'. Otolaryngology–Head and Neck Surgery. 120 (5): 698–705. doi:10.1053/hn.1999.v120.a91773. PMID10229596.
  34. ^ abcdefParkin DM (June 2006). 'The global health burden of infection-associated cancers in the year 2002'. International Journal of Cancer. 118 (12): 3030–44. doi:10.1002/ijc.21731. PMID16404738.
  35. ^ abcdPahud BA, Ault KA (December 2015). 'The Expanded Impact of Human Papillomavirus Vaccine'. Infectious Disease Clinics of North America (Review). 29 (4): 715–24. doi:10.1016/j.idc.2015.07.007. PMID26610422.
  36. ^Nowińska K, Ciesielska U, Podhorska-Okołów M, Dzięgiel P (2017). 'The role of human papillomavirus in oncogenic transformation and its contribution to the etiology of precancerous lesions and cancer of the larynx: A review'. Advances in Clinical and Experimental Medicine. 26 (3): 539–547. doi:10.17219/acem/67461. PMID28791831.
  37. ^ abcBaseman JG, Koutsky LA (March 2005). 'The epidemiology of human papillomavirus infections'. Journal of Clinical Virology. 32 Suppl 1 (Suppl 1): S16–24. doi:10.1016/j.jcv.2004.12.008. PMID15753008. Overall, these DNA-based studies, combined with measurements of type-specific antibodies against HPV capsid antigens, have shown that most (>50%) sexually active women have been infected by one or more genital HPV types at some point in time [S17].
  38. ^Noel J, Lespagnard L, Fayt I, Verhest A, Dargent J (January 2001). 'Evidence of human papilloma virus infection but lack of Epstein-Barr virus in lymphoepithelioma-like carcinoma of uterine cervix: report of two cases and review of the literature'. Human Pathology. 32 (1): 135–8. doi:10.1053/hupa.2001.20901. PMID11172309.
  39. ^'Vulvar Intraepithelial Neoplasia: Varied signs, varied symptoms: what you need to know'. Archived from the original on 16 July 2012. Retrieved 5 August 2009.Cite uses deprecated parameter deadurl= (help)
  40. ^Bolt J, Vo QN, Kim WJ, McWhorter AJ, Thomson J, Hagensee ME, Friedlander P, Brown KD, Gilbert J (November 2005). 'The ATM/p53 pathway is commonly targeted for inactivation in squamous cell carcinoma of the head and neck (SCCHN) by multiple molecular mechanisms'. Oral Oncology. 41 (10): 1013–20. doi:10.1016/j.oraloncology.2005.06.003. PMID16139561.
  41. ^Schiffman M, Castle PE (November 2005). 'The promise of global cervical-cancer prevention'. The New England Journal of Medicine. 353 (20): 2101–4. doi:10.1056/NEJMp058171. PMID16291978.
  42. ^Alam S, Conway MJ, Chen HS, Meyers C (January 2008). 'The cigarette smoke carcinogen benzo[a]pyrene enhances human papillomavirus synthesis'. Journal of Virology. 82 (2): 1053–8. doi:10.1128/JVI.01813-07. PMC2224590. PMID17989183.
  43. ^Lu B, Hagensee ME, Lee JH, Wu Y, Stockwell HG, Nielson CM, Abrahamsen M, Papenfuss M, Harris RB, Giuliano AR (February 2010). 'Epidemiologic factors associated with seropositivity to human papillomavirus type 16 and 18 virus-like particles and risk of subsequent infection in men'. Cancer Epidemiology, Biomarkers & Prevention. 19 (2): 511–6. doi:10.1158/1055-9965.EPI-09-0790. PMID20086109.
  44. ^Liu Y, Lu Z, Xu R, Ke Y (February 2016). 'Comprehensive mapping of the human papillomavirus (HPV) DNA integration sites in cervical carcinomas by HPV capture technology'. Oncotarget. 7 (5): 5852–64. doi:10.18632/oncotarget.6809. PMC4868726. PMID26735580.
  45. ^Parfenov M, Pedamallu CS, Gehlenborg N, Freeman SS, Danilova L, Bristow CA, Lee S, Hadjipanayis AG, Ivanova EV, Wilkerson MD, Protopopov A, Yang L, Seth S, Song X, Tang J, Ren X, Zhang J, Pantazi A, Santoso N, Xu AW, Mahadeshwar H, Wheeler DA, Haddad RI, Jung J, Ojesina AI, Issaeva N, Yarbrough WG, Hayes DN, Grandis JR, El-Naggar AK, Meyerson M, Park PJ, Chin L, Seidman JG, Hammerman PS, Kucherlapati R (October 2014). 'Characterization of HPV and host genome interactions in primary head and neck cancers'. Proceedings of the National Academy of Sciences of the United States of America. 111 (43): 15544–9. Bibcode:2014PNAS.11115544P. doi:10.1073/pnas.1416074111. PMC4217452. PMID25313082.
  46. ^Karagas MR, Waterboer T, Li Z, Nelson HH, Michael KM, Bavinck JN, Perry AE, Spencer SK, Daling J, Green AC, Pawlita M (July 2010). 'Genus beta human papillomaviruses and incidence of basal cell and squamous cell carcinomas of skin: population based case-control study'. BMJ. 341: c2986. doi:10.1136/bmj.c2986. PMC2900549. PMID20616098. Archived from the original on 15 July 2010.Cite uses deprecated parameter deadurl= (help)
  47. ^Cohen J (April 2005). 'Public health. High hopes and dilemmas for a cervical cancer vaccine'. Science. 308 (5722): 618–21. doi:10.1126/science.308.5722.618. PMID15860602.
  48. ^ abcAult KA (2006). 'Epidemiology and natural history of human papillomavirus infections in the female genital tract'. Infectious Diseases in Obstetrics and Gynecology. 2006: 1–5. doi:10.1155/IDOG/2006/40470. PMC1581465. PMID16967912.
  49. ^Kreimer AR, Clifford GM, Boyle P, Franceschi S (February 2005). 'Human papillomavirus types in head and neck squamous cell carcinomas worldwide: a systematic review'. Cancer Epidemiology, Biomarkers & Prevention. 14 (2): 467–75. doi:10.1158/1055-9965.EPI-04-0551. PMID15734974.
  50. ^International Collaboration of Epidemiological Studies of Cervical Cancer (2007). 'Comparison of risk factors for invasive squamous cell carcinoma and adenocarcinoma of the cervix: Collaborative reanalysis of individual data on 8,097 women with squamous cell carcinoma and 1,374 women with adenocarcinoma from 12 epidemiological studies'. International Journal of Cancer. 120 (4): 885–891. doi:10.1002/ijc.22357. ISSN1097-0215. PMID17131323.
  51. ^Denny, Lynette A.; Franceschi, Silvia; de Sanjosé, Silvia; Heard, Isabelle; Moscicki, Anna Barbara; Palefsky, Joel (20 November 2012). 'Human Papillomavirus, Human Immunodeficiency Virus and Immunosuppression'. Vaccine. Comprehensive Control of HPV Infections and Related Diseases. 30: F168–F174. doi:10.1016/j.vaccine.2012.06.045. ISSN0264-410X. PMID23199960.
  52. ^Dugué, Pierre-Antoine; Rebolj, Matejka; Garred, Peter; Lynge, Elsebeth (1 January 2013). 'Immunosuppression and risk of cervical cancer'. Expert Review of Anticancer Therapy. 13 (1): 29–42. doi:10.1586/era.12.159. ISSN1473-7140. PMID23259425.
  53. ^Greenblatt, R. J. (2005). 'Human papillomaviruses: Diseases, diagnosis, and a possible vaccine'. Clinical Microbiology Newsletter. 27 (18): 139–145. doi:10.1016/j.clinmicnews.2005.09.001.
  54. ^Freitas LB, Chen Z, Muqui EF, Boldrini NA, Miranda AE, Spano LC, Burk RD (1 July 2014). 'Human papillomavirus 16 non-European variants are preferentially associated with high-grade cervical lesions'. PLOS ONE. 9 (7): e100746. Bibcode:2014PLoSO..9j0746F. doi:10.1371/journal.pone.0100746. PMC4077691. PMID24983739.
  55. ^ abcdeBurd, E. M.; Dean, C. L. (1 January 2016), Hayden, Randall T.; Wolk, Donna M.; Carroll, Karen C.; Tang, Yi-Wei (eds.), 'Human Papillomavirus', Diagnostic Microbiology of the Immunocompromised Host, Second Edition, American Society of Microbiology, 4 (4), pp. 177–195, doi:10.1128/microbiolspec.dmih2-0001-2015, ISBN9781555819033, PMID27726787
  56. ^Chin-Hong PV, Vittinghoff E, Cranston RD, Browne L, Buchbinder S, Colfax G, Da Costa M, Darragh T, Benet DJ, Judson F, Koblin B, Mayer KH, Palefsky JM (June 2005). 'Age-related prevalence of anal cancer precursors in homosexual men: the EXPLORE study'. Journal of the National Cancer Institute. 97 (12): 896–905. doi:10.1093/jnci/dji163. PMID15956651.
  57. ^'AIDSmeds Web Exclusives : Pap Smears for Anal Cancer? — by David Evans'. 10 June 2008. Archived from the original on 7 July 2011. Retrieved 29 August 2010.Cite uses deprecated parameter deadurl= (help)
  58. ^Goldie SJ, Kuntz KM, Weinstein MC, Freedberg KA, Palefsky JM (June 2000). 'Cost-effectiveness of screening for anal squamous intraepithelial lesions and anal cancer in human immunodeficiency virus-negative homosexual and bisexual men'. The American Journal of Medicine. 108 (8): 634–41. doi:10.1016/S0002-9343(00)00349-1. PMID10856411.
  59. ^ abcDyne; et al. (24 August 2018). 'Trends in Human Papillomavirus–Associated Cancers — United States, 1999–2015'(PDF). Centers for Disease Control and Prevention, Morbidity and Mortality Weekly Report.
  60. ^ abD'Souza G, Kreimer AR, Viscidi R, Pawlita M, Fakhry C, Koch WM, Westra WH, Gillison ML (May 2007). 'Case-control study of human papillomavirus and oropharyngeal cancer'. The New England Journal of Medicine. 356 (19): 1944–56. doi:10.1056/NEJMoa065497. PMID17494927.
  61. ^ abRidge JA, Glisson BS, Lango MN, et al. 'Head and Neck Tumors'Archived 20 July 2009 at the Wayback Machine in Pazdur R, Wagman LD, Camphausen KA, Hoskins WJ (Eds) Cancer Management: A Multidisciplinary ApproachArchived 4 October 2013 at the Wayback Machine. 11 ed. 2008.
  62. ^Gillison ML, Koch WM, Capone RB, Spafford M, Westra WH, Wu L, Zahurak ML, Daniel RW, Viglione M, Symer DE, Shah KV, Sidransky D (May 2000). 'Evidence for a causal association between human papillomavirus and a subset of head and neck cancers'. Journal of the National Cancer Institute. 92 (9): 709–20. doi:10.1093/jnci/92.9.709. PMID10793107.
  63. ^Gillison ML (December 2006). 'Human papillomavirus and prognosis of oropharyngeal squamous cell carcinoma: implications for clinical research in head and neck cancers'. Journal of Clinical Oncology. 24 (36): 5623–5. doi:10.1200/JCO.2006.07.1829. PMID17179099.
  64. ^Goodman, Marc T.; Altekruse, Sean; Saber, Maria Sibug; Huang, Youjie; Peters, Edward S.; Cozen, Wendy; Copeland, Glenn; Hopenhayn, Claudia; Wilkinson, Edward J. (1 June 2015). 'US Assessment of HPV Types in Cancers: Implications for Current and 9-Valent HPV Vaccines'. JNCI Journal of the National Cancer Institute. 107 (6): djv086. doi:10.1093/jnci/djv086. ISSN0027-8874. PMC4838063. PMID25925419.
  65. ^Anantharaman, Devasena; Abedi‐Ardekani, Behnoush; Beachler, Daniel C.; Gheit, Tarik; Olshan, Andrew F.; Wisniewski, Kathy; Wunsch‐Filho, Victor; Toporcov, Tatiana N.; Tajara, Eloiza H. (2017). 'Geographic heterogeneity in the prevalence of human papillomavirus in head and neck cancer'. International Journal of Cancer. 140 (9): 1968–1975. doi:10.1002/ijc.30608. ISSN1097-0215. PMID28108990.
  66. ^Chaturvedi AK, Engels EA, Pfeiffer RM, Hernandez BY, Xiao W, Kim E, Jiang B, Goodman MT, Sibug-Saber M, Cozen W, Liu L, Lynch CF, Wentzensen N, Jordan RC, Altekruse S, Anderson WF, Rosenberg PS, Gillison ML (November 2011). 'Human papillomavirus and rising oropharyngeal cancer incidence in the United States'. Journal of Clinical Oncology. 29 (32): 4294–301. doi:10.1200/JCO.2011.36.4596. PMC3221528. PMID21969503.
  67. ^Ernster JA, Sciotto CG, O'Brien MM, Finch JL, Robinson LJ, Willson T, Mathews M (December 2007). 'Rising incidence of oropharyngeal cancer and the role of oncogenic human papilloma virus'. The Laryngoscope. 117 (12): 2115–28. doi:10.1097/MLG.0b013e31813e5fbb. PMID17891052.
  68. ^Lechner M, Frampton GM, Fenton T, Feber A, Palmer G, Jay A, Pillay N, Forster M, Cronin MT, Lipson D, Miller VA, Brennan TA, Henderson S, Vaz F, O'Flynn P, Kalavrezos N, Yelensky R, Beck S, Stephens PJ, Boshoff C (2013). 'Targeted next-generation sequencing of head and neck squamous cell carcinoma identifies novel genetic alterations in HPV+ and HPV- tumors'. Genome Medicine. 5 (5): 49. doi:10.1186/gm453. PMC4064312. PMID23718828.
  69. ^'Lung Cancer Risk Rises in the Presence of HPV Antibodies'. Archived from the original on 27 April 2012.Cite uses deprecated parameter deadurl= (help)
  70. ^'Lung Cancer Patients More Likely to Have High-Risk Human Papillomavirus'. NPIN. Archived from the original on 27 July 2012.Cite uses deprecated parameter deadurl= (help)
  71. ^Syrjänen K, Syrjänen S, Kellokoski J, Kärjä J, Mäntyjärvi R (1989). 'Human papillomavirus (HPV) type 6 and 16 DNA sequences in bronchial squamous cell carcinomas demonstrated by in situ DNA hybridization'. Lung. 167 (1): 33–42. doi:10.1007/BF02714928. PMID2537916.
  72. ^Carpagnano GE, Koutelou A, Natalicchio MI, Martinelli D, Ruggieri C, Di Taranto A, Antonetti R, Carpagnano F, Foschino-Barbaro MP (October 2011). 'HPV in exhaled breath condensate of lung cancer patients'. British Journal of Cancer. 105 (8): 1183–90. doi:10.1038/bjc.2011.354. PMC3208494. PMID21952627.
  73. ^Klein F, Amin Kotb WF, Petersen I (July 2009). 'Incidence of human papilloma virus in lung cancer'. Lung Cancer. 65 (1): 13–8. doi:10.1016/j.lungcan.2008.10.003. PMID19019488.
  74. ^Moore, Matthew (12 November 2007). 'Tree man 'who grew roots' may be cured'. The Daily Telegraph. London. Archived from the original on 13 November 2007.Cite uses deprecated parameter deadurl= (help)
  75. ^ abTyring, Stephen; Rady, Peter; Morrison, L. Katie; Patel, Tejas (2010). 'Epidermodysplasia Verruciformis and Susceptibility to HPV'. Disease Markers. 29 (3–4): 199–206. doi:10.3233/dma-2010-0733. PMC3835378. PMID21178278.
  76. ^'HPV and Cancer'. National Cancer Institute. 15 May 2015. Archived from the original on 18 April 2017. Retrieved 18 April 2017.Cite uses deprecated parameter deadurl= (help)
  77. ^ abMiyague AH, Mauad FM, Martins W, Benedetti AC, Ferreira AE, Mauad-Filho F (5 February 2019). 'Ultrasound scan as a potential source of nosocomial and crossinfection: a literature review'. Radiologia Brasileira. 48 (5): 319–23. doi:10.1590/0100-3984.2014.0002. PMC4633077. PMID26543284.
  78. ^ abHeymann, MD, David (2015). Control of Communicable Diseases Manual (20th ed.). Washington D.C.: Apha Press. pp. 299–300. ISBN978-0-87553-018-5.
  79. ^ abBurchell AN, Winer RL, de Sanjosé S, Franco EL (August 2006). 'Chapter 6: Epidemiology and transmission dynamics of genital HPV infection'. Vaccine. 24 (Suppl 3): S3/52–61. doi:10.1016/j.vaccine.2006.05.031. PMID16950018.
  80. ^Schmitt M, Depuydt C, Benoy I, Bogers J, Antoine J, Arbyn M, Pawlita M (May 2013). 'Prevalence and viral load of 51 genital human papillomavirus types and three subtypes'. International Journal of Cancer. 132 (10): 2395–403. doi:10.1002/ijc.27891. PMID23034864.
  81. ^Muñoz N, Bosch FX, de Sanjosé S, Herrero R, Castellsagué X, Shah KV, Snijders PJ, Meijer CJ (February 2003). 'Epidemiologic classification of human papillomavirus types associated with cervical cancer'. The New England Journal of Medicine. 348 (6): 518–27. doi:10.1056/NEJMoa021641. hdl:2445/122831. PMID12571259.
  82. ^ abEgendorf, Laura. Sexually Transmitted Diseases (At Issue Series). New York: Greenhaven Press, 2007.
  83. ^ abcWiner RL, Lee SK, Hughes JP, Adam DE, Kiviat NB, Koutsky LA (February 2003). 'Genital human papillomavirus infection: incidence and risk factors in a cohort of female university students'. American Journal of Epidemiology. 157 (3): 218–26. doi:10.1093/aje/kwf180. PMID12543621.
  84. ^ abcHernandez BY, Wilkens LR, Zhu X, Thompson P, McDuffie K, Shvetsov YB, Kamemoto LE, Killeen J, Ning L, Goodman MT (June 2008). 'Transmission of human papillomavirus in heterosexual couples'. Emerging Infectious Diseases. 14 (6): 888–94. doi:10.3201/eid1406.070616. PMC2600292. PMID18507898.
  85. ^Hernandez BY, Wilkens LR, Zhu X, Thompson P, McDuffie K, Shvetsov YB, Kamemoto LE, Killeen J, Ning L, Goodman MT (June 2008). 'Transmission of human papillomavirus in heterosexual couples'. Emerging Infectious Diseases. 14 (6): 888–94. doi:10.3201/eid1406.070616. PMC2600292. PMID18507898.
  86. ^ abGiuliano AR, Nielson CM, Flores R, Dunne EF, Abrahamsen M, Papenfuss MR, Markowitz LE, Smith D, Harris RB (October 2007). 'The optimal anatomic sites for sampling heterosexual men for human papillomavirus (HPV) detection: the HPV detection in men study'. The Journal of Infectious Diseases. 196 (8): 1146–52. doi:10.1086/521629. PMC3904649. PMID17955432.
  87. ^ abcdWiner RL, Hughes JP, Feng Q, Xi LF, Cherne S, O'Reilly S, Kiviat NB, Koutsky LA (July 2010). 'Detection of genital HPV types in fingertip samples from newly sexually active female university students'. Cancer Epidemiology, Biomarkers & Prevention. 19 (7): 1682–5. doi:10.1158/1055-9965.EPI-10-0226. PMC2901391. PMID20570905.
  88. ^Tay SK (July 1995). 'Genital oncogenic human papillomavirus infection: a short review on the mode of transmission'(Free full text). Annals of the Academy of Medicine, Singapore. 24 (4): 598–601. PMID8849195. Archived from the original on 27 July 2012.Cite uses deprecated parameter deadurl= (help)
  89. ^Pao CC, Tsai PL, Chang YL, Hsieh TT, Jin JY (March 1993). 'Possible non-sexual transmission of genital human papillomavirus infections in young women'. European Journal of Clinical Microbiology & Infectious Diseases. 12 (3): 221–2. doi:10.1007/BF01967118. PMID8389707.
  90. ^Tay SK, Ho TH, Lim-Tan SK (August 1990). 'Is genital human papillomavirus infection always sexually transmitted?'(Free full text). The Australian & New Zealand Journal of Obstetrics & Gynaecology. 30 (3): 240–2. doi:10.1111/j.1479-828X.1990.tb03223.x. PMID2256864. Archived from the original on 6 April 2016.Cite uses deprecated parameter deadurl= (help)
  91. ^ abSonnex C, Strauss S, Gray JJ (October 1999). 'Detection of human papillomavirus DNA on the fingers of patients with genital warts'. Sexually Transmitted Infections. 75 (5): 317–9. doi:10.1136/sti.75.5.317. PMC1758241. PMID10616355.
  92. ^ abHans Krueger; Gavin Stuart; Richard Gallagher; Dan Williams, Jon Kerner (12 April 2010). HPV and Other Infectious Agents in Cancer:Opportunities for Prevention and Public Health: Opportunities for Prevention and Public Health. Oxford University Press. p. 34. ISBN978-0-19-973291-3. Archived from the original on 9 June 2013. Retrieved 24 December 2012.Cite uses deprecated parameter deadurl= (help)
  93. ^Bodaghi S, Wood LV, Roby G, Ryder C, Steinberg SM, Zheng ZM (November 2005). 'Could human papillomaviruses be spread through blood?'. Journal of Clinical Microbiology. 43 (11): 5428–34. doi:10.1128/JCM.43.11.5428-5434.2005. PMC1287818. PMID16272465.
  94. ^Chen AC, Keleher A, Kedda MA, Spurdle AB, McMillan NA, Antonsson A (October 2009). 'Human papillomavirus DNA detected in peripheral blood samples from healthy Australian male blood donors'. Journal of Medical Virology. 81 (10): 1792–6. doi:10.1002/jmv.21592. PMID19697401.
  95. ^'Eligibility Criteria by Topic - American Red Cross'. Archived from the original on 1 January 2017.Cite uses deprecated parameter deadurl= (help)
  96. ^ abcWatson RA (2005). 'Human Papillomavirus: Confronting the Epidemic-A Urologist's Perspective'. Reviews in Urology. 7 (3): 135–44. PMC1477576. PMID16985824.
  97. ^Guan, J; Bywaters, SM; Brendle, SA; Ashley, RE; Makhov, AM; Conway, JF; Christensen, ND; Hafenstein, S (7 February 2017). 'Cryoelectron Microscopy Maps of Human Papillomavirus 16 Reveal L2 Densities and Heparin Binding Site'. Structure (London, England : 1993). 25 (2): 253–263. doi:10.1016/j.str.2016.12.001. PMID28065506.
  98. ^ abcSchiller JT, Day PM, Kines RC (June 2010). 'Current understanding of the mechanism of HPV infection'. Gynecologic Oncology. 118 (1): S12–7. doi:10.1016/j.ygyno.2010.04.004. PMC3493113. PMID20494219.
  99. ^ abScheurer ME, Tortolero-Luna G, Adler-Storthz K (2005). 'Human papillomavirus infection: biology, epidemiology, and prevention'. International Journal of Gynecological Cancer. 15 (5): 727–46. doi:10.1111/j.1525-1438.2005.00246.x. PMID16174218.
  100. ^Woodham AW, Da Silva DM, Skeate JG, Raff AB, Ambroso MR, Brand HE, Isas JM, Langen R, Kast WM (2012). 'The S100A10 subunit of the annexin A2 heterotetramer facilitates L2-mediated human papillomavirus infection'. PLOS ONE. 7 (8): e43519. Bibcode:2012PLoSO..743519W. doi:10.1371/journal.pone.0043519. PMC3425544. PMID22927980.
  101. ^Raff AB, Woodham AW, Raff LM, Skeate JG, Yan L, Da Silva DM, Schelhaas M, Kast WM (June 2013). 'The evolving field of human papillomavirus receptor research: a review of binding and entry'. Journal of Virology. 87 (11): 6062–72. doi:10.1128/JVI.00330-13. PMC3648114. PMID23536685.
  102. ^Chen Z, Schiffman M, Herrero R, Desalle R, Anastos K, Segondy M, Sahasrabuddhe VV, Gravitt PE, Hsing AW, Burk RD (2011). 'Evolution and taxonomic classification of human papillomavirus 16 (HPV16)-related variant genomes: HPV31, HPV33, HPV35, HPV52, HPV58 and HPV67'. PLOS ONE. 6 (5): e20183. Bibcode:2011PLoSO..620183C. doi:10.1371/journal.pone.0020183. PMC3103539. PMID21673791.
  103. ^Zuna RE, Tuller E, Wentzensen N, Mathews C, Allen RA, Shanesmith R, Dunn ST, Gold MA, Wang SS, Walker J, Schiffman M (October 2011). 'HPV16 variant lineage, clinical stage, and survival in women with invasive cervical cancer'. Infectious Agents and Cancer. 6: 19. doi:10.1186/1750-9378-6-19. PMC3226431. PMID22035468.
  104. ^Zanier, K; Charbonnier, S; Sidi, AO; McEwen, AG; Ferrario, MG; Poussin-Courmontagne, P; Cura, V; Brimer, N; Babah, KO; Ansari, T; Muller, I; Stote, RH; Cavarelli, J; Vande Pol, S; Travé, G (8 February 2013). 'Structural basis for hijacking of cellular LxxLL motifs by papillomavirus E6 oncoproteins'. Science. 339 (6120): 694–8. doi:10.1126/science.1229934. PMC3899395. PMID23393263.
  105. ^Ganguly N, Parihar SP (March 2009). 'Human papillomavirus E6 and E7 oncoproteins as risk factors for tumorigenesis'. Journal of Biosciences. 34 (1): 113–23. doi:10.1007/s12038-009-0013-7. PMID19430123.
  106. ^Zheng ZM, Baker CC (September 2006). 'Papillomavirus genome structure, expression, and post-transcriptional regulation'. Frontiers in Bioscience. 11: 2286–302. doi:10.2741/1971. PMC1472295. PMID16720315.
  107. ^Tang S, Tao M, McCoy JP, Zheng ZM (May 2006). 'The E7 oncoprotein is translated from spliced E6*I transcripts in high-risk human papillomavirus type 16- or type 18-positive cervical cancer cell lines via translation reinitiation'. Journal of Virology. 80 (9): 4249–63. doi:10.1128/JVI.80.9.4249-4263.2006. PMC1472016. PMID16611884.
  108. ^Münger K, Howley PM (November 2002). 'Human papillomavirus immortalization and transformation functions'. Virus Research. 89 (2): 213–28. doi:10.1016/S0168-1702(02)00190-9. PMID12445661.
  109. ^Conway MJ, Alam S, Ryndock EJ, Cruz L, Christensen ND, Roden RB, Meyers C (October 2009). 'Tissue-spanning redox gradient-dependent assembly of native human papillomavirus type 16 virions'. Journal of Virology. 83 (20): 10515–26. doi:10.1128/JVI.00731-09. PMC2753102. PMID19656879.
  110. ^Bryan JT, Brown DR (March 2001). 'Transmission of human papillomavirus type 11 infection by desquamated cornified cells'. Virology. 281 (1): 35–42. doi:10.1006/viro.2000.0777. PMID11222093.
  111. ^Rampias T, Boutati E, Pectasides E, Sasaki C, Kountourakis P, Weinberger P, Psyrri A (March 2010). 'Activation of Wnt signaling pathway by human papillomavirus E6 and E7 oncogenes in HPV16-positive oropharyngeal squamous carcinoma cells'. Molecular Cancer Research. 8 (3): 433–43. doi:10.1158/1541-7786.MCR-09-0345. PMID20215420.
  112. ^Giuliano AR, Lu B, Nielson CM, Flores R, Papenfuss MR, Lee JH, Abrahamsen M, Harris RB (September 2008). 'Age-specific prevalence, incidence, and duration of human papillomavirus infections in a cohort of 290 US men'. The Journal of Infectious Diseases. 198 (6): 827–35. doi:10.1086/591095. PMID18657037.
  113. ^Schiffman M, Castle PE (August 2003). 'Human papillomavirus: epidemiology and public health' [1 January 2017]. Archives of Pathology & Laboratory Medicine. 127 (8): 930–4. doi:10.1043/1543-2165(2003)127<930:HPEAPH>2.0.CO;2 (inactive 18 August 2019). PMID12873163. Archived from the original on 14 April 2013.Cite uses deprecated parameter dead-url= (help)
  114. ^'HPV Human Papillomavirus Pap Smear MedlinePlus'. Retrieved 7 November 2018.
  115. ^Smith, Robert A.; Andrews, Kimberly S.; Brooks, Durado; Fedewa, Stacey A.; Manassaram‐Baptiste, Deana; Saslow, Debbie; Brawley, Otis W.; Wender, Richard C. (2017). 'Cancer screening in the United States, 2017: A review of current American Cancer Society guidelines and current issues in cancer screening'. CA: A Cancer Journal for Clinicians. 67 (2): 100–121. doi:10.3322/caac.21392. ISSN1542-4863. PMID28170086.
  116. ^'National Cancer Institute Fact Sheet: HPV and Cancer'. Archived from the original on 31 October 2013. Retrieved 23 October 2013.Cite uses deprecated parameter deadurl= (help)
  117. ^Pan, Cassie; Issaeva, Natalia; Yarbrough, Wendell G. (December 2018). 'HPV-driven oropharyngeal cancer: current knowledge of molecular biology and mechanisms of carcinogenesis'. Cancers of the Head & Neck. 3 (1): 12. doi:10.1186/s41199-018-0039-3. ISSN2059-7347. PMC6460765. PMID31093365.
  118. ^ abcdDunne EF, Nielson CM, Stone KM, Markowitz LE, Giuliano AR (October 2006). 'Prevalence of HPV infection among men: A systematic review of the literature'. The Journal of Infectious Diseases. 194 (8): 1044–57. doi:10.1086/507432. PMID16991079.
  119. ^Burchell AN, Richardson H, Mahmud SM, Trottier H, Tellier PP, Hanley J, Coutlée F, Franco EL (March 2006). 'Modeling the sexual transmissibility of human papillomavirus infection using stochastic computer simulation and empirical data from a cohort study of young women in Montreal, Canada'. American Journal of Epidemiology. 163 (6): 534–43. doi:10.1093/aje/kwj077. PMID16421235.
  120. ^Kim JJ (October 2007). 'Vaccine policy analyses can benefit from natural history studies of human papillomavirus in men'. The Journal of Infectious Diseases. 196 (8): 1117–9. doi:10.1086/521199. PMID17955427.
  121. ^'FAQs for Men'. Archived from the original on 5 September 2012. Retrieved 24 August 2012.Cite uses deprecated parameter deadurl= (help)
  122. ^ abNicolau SM, Camargo CG, Stávale JN, Castelo A, Dôres GB, Lörincz A, de Lima GR (February 2005). 'Human papillomavirus DNA detection in male sexual partners of women with genital human papillomavirus infection'. Urology. 65 (2): 251–5. doi:10.1016/j.urology.2004.09.031. PMID15708032.
  123. ^ abcAguilar LV, Lazcano-Ponce E, Vaccarella S, Cruz A, Hernández P, Smith JS, Muñoz N, Kornegay JR, Hernández-Avila M, Franceschi S (February 2006). 'Human papillomavirus in men: comparison of different genital sites'. Sexually Transmitted Infections. 82 (1): 31–3. doi:10.1136/sti.2005.015131. PMC2563819. PMID16461598.
  124. ^ abcWeaver BA, Feng Q, Holmes KK, Kiviat N, Lee SK, Meyer C, Stern M, Koutsky LA (February 2004). 'Evaluation of genital sites and sampling techniques for detection of human papillomavirus DNA in men'. The Journal of Infectious Diseases. 189 (4): 677–85. doi:10.1086/381395. PMID14767822.
  125. ^Hernandez BY, McDuffie K, Goodman MT, Wilkens LR, Thompson P, Zhu X, Wong W, Ning L (February 2006). 'Comparison of physician- and self-collected genital specimens for detection of human papillomavirus in men'. Journal of Clinical Microbiology. 44 (2): 513–7. doi:10.1128/JCM.44.2.513-517.2006. PMC1392697. PMID16455906.
  126. ^Ogilvie GS, Taylor DL, Achen M, Cook D, Krajden M (June 2009). 'Self-collection of genital human papillomavirus specimens in heterosexual men'. Sexually Transmitted Infections. 85 (3): 221–5. doi:10.1136/sti.2008.033068. PMID19066196.
  127. ^Petignat P, Faltin DL, Bruchim I, Tramèr MR, Franco EL, Coutlée F (May 2007). 'Are self-collected samples comparable to physician-collected cervical specimens for human papillomavirus DNA testing? A systematic review and meta-analysis'. Gynecologic Oncology. 105 (2): 530–5. doi:10.1016/j.ygyno.2007.01.023. PMID17335880.
  128. ^Partridge JM, Hughes JP, Feng Q, Winer RL, Weaver BA, Xi LF, Stern ME, Lee SK, O'Reilly SF, Hawes SE, Kiviat NB, Koutsky LA (October 2007). 'Genital human papillomavirus infection in men: incidence and risk factors in a cohort of university students'. The Journal of Infectious Diseases. 196 (8): 1128–36. doi:10.1086/521192. PMID17955430.
  129. ^Dunne EF, Nielson CM, Stone KM, Markowitz LE, Giuliano AR (October 2006). 'Prevalence of HPV infection among men: A systematic review of the literature'. The Journal of Infectious Diseases. 194 (8): 1044–57. doi:10.1086/507432. PMID16991079.
  130. ^'HPV and Men — CDC Fact Sheet'. Centers for Disease Control and Prevention (CDC). 3 April 2008. Archived from the original on 17 October 2009. Retrieved 13 November 2009.Cite uses deprecated parameter deadurl= (help)
  131. ^'Human Papillomavirus (HPV) and Men: Questions and Answers'. 2007. Archived from the original on 14 September 2008. Retrieved 10 September 2008. Currently, in Canada there is an HPV DNA test approved for women but not for men.Cite uses deprecated parameter deadurl= (help)
  132. ^'What Men Need to Know About HPV'. 2006. Archived from the original on 7 April 2007. Retrieved 4 April 2007. There is currently no FDA-approved test to detect HPV in men. That is because an effective, reliable way to collect a sample of male genital skin cells, which would allow detection of HPV, has yet to be developed.Cite uses deprecated parameter deadurl= (help)
  133. ^Storey R, Joh J, Kwon A, Jenson AB, Ghim SJ, Kloecker GH (2013). 'Detection of Immunoglobulin G against E7 of Human Papillomavirus in Non-Small-Cell Lung Cancer'. Journal of Oncology. 2013: 1–5. doi:10.1155/2013/240164. PMC3603668. PMID23533408.
  134. ^Rocha-Zavaleta L, Ambrosio JP, Mora-Garcia M, Cruz-Talonia F, Hernandez-Montes J, Weiss-Steider B, Ortiz-Navarrete V, Monroy-Garcia A (September 2004). 'Detection of antibodies against a human papillomavirus (HPV) type 16 peptide that differentiate high-risk from low-risk HPV-associated low-grade squamous intraepithelial lesions'(PDF). The Journal of General Virology. 85 (Pt 9): 2643–50. doi:10.1099/vir.0.80077-0. PMID15302958.[permanent dead link]
  135. ^Bolhassani A, Zahedifard F, Taslimi Y, Taghikhani M, Nahavandian B, Rafati S (November 2009). 'Antibody detection against HPV16 E7 & GP96 fragments as biomarkers in cervical cancer patients'(PDF). The Indian Journal of Medical Research. 130 (5): 533–41. PMID20090101. Archived(PDF) from the original on 16 December 2010. Retrieved 18 March 2014.Cite uses deprecated parameter deadurl= (help)
  136. ^Fitzgerald, Kelly (18 June 2013). 'Blood Test May Detect Sexually Transmitted Throat Cancer'. Medical News Today. Archived from the original on 7 April 2014. Retrieved 18 March 2014.Cite uses deprecated parameter deadurl= (help)
  137. ^'HPV (Human Papilloma Virus) Diagnosis and Tests'. Cleveland Clinic. 18 September 2018. Retrieved 8 February 2019.
  138. ^'Genital Human Papillomavirus (HPV) Infection - Ready-to-Use - Faculty Notes'(PDF). Retrieved 7 February 2018.[permanent dead link]
  139. ^'FDA approves Gardasil 9 for prevention of certain cancers caused by five additional types of HPV'. 10 December 2014. Archived from the original on 10 January 2015. Retrieved 8 March 2015.Cite uses deprecated parameter deadurl= (help)
  140. ^'Human Papillomavirus Epidemiology and Prevention of Vaccine-Preventable Diseases'. Archived from the original on 3 February 2014. Retrieved 30 January 2014.Cite uses deprecated parameter deadurl= (help)
  141. ^'Human papillomavirus vaccines. WHO position paper'(PDF). Releve Epidemiologique Hebdomadaire. 84 (15): 118–31. April 2009. PMID19360985. Archived(PDF) from the original on 24 December 2010.Cite uses deprecated parameter deadurl= (help)
  142. ^ abcKoliopoulos G, Nyaga VN, Santesso N, Bryant A, Martin-Hirsch PP, Mustafa RA, Schünemann H, Paraskevaidis E, Arbyn M (August 2017). 'Cytology versus HPV testing for cervical cancer screening in the general population'. The Cochrane Database of Systematic Reviews. 8: CD008587. doi:10.1002/14651858.CD008587.pub2. PMC6483676. PMID28796882.
  143. ^'CDC recommends only two HPV shots for younger adolescents'. CDC. 20 October 2016. Archived from the original on 23 March 2017. Retrieved 24 March 2017.Cite uses deprecated parameter deadurl= (help)
  144. ^ abMarkowitz LE, Dunne EF, Saraiya M, Lawson HW, Chesson H, Unger ER (March 2007). 'Quadrivalent Human Papillomavirus Vaccine: Recommendations of the Advisory Committee on Immunization Practices (ACIP)'. MMWR. Recommendations and Reports. 56 (RR-2): 1–24. PMID17380109. Archived from the original on 20 May 2017.Cite uses deprecated parameter deadurl= (help)
  145. ^Dobson SR, McNeil S, Dionne M, Dawar M, Ogilvie G, Krajden M, Sauvageau C, Scheifele DW, Kollmann TR, Halperin SA, Langley JM, Bettinger JA, Singer J, Money D, Miller D, Naus M, Marra F, Young E (May 2013). 'Immunogenicity of 2 doses of HPV vaccine in younger adolescents vs 3 doses in young women: a randomized clinical trial'. JAMA. 309 (17): 1793–802. doi:10.1001/jama.2013.1625. PMID23632723.
  146. ^'HPV Vaccine Information For Young Women'. CDC. 3 January 2017. Archived from the original on 25 March 2017. Retrieved 24 March 2017.Cite uses deprecated parameter deadurl= (help)
  147. ^'HPV Virus: Information About Human Papillomavirus'. WebMD. Archived from the original on 8 March 2008.Cite uses deprecated parameter deadurl= (help)
  148. ^'Gardasil patient information leaflet'(PDF). April 2015. Retrieved 11 July 2018.
  149. ^Deleré Y, Wichmann O, Klug SJ, van der Sande M, Terhardt M, Zepp F, Harder T (September 2014). 'The efficacy and duration of vaccine protection against human papillomavirus: a systematic review and meta-analysis'. Deutsches Arzteblatt International. 111 (35–36): 584–91. doi:10.3238/arztebl.2014.0584. PMC4174682. PMID25249360.
  150. ^'FDA approves Gardasil 9 for prevention of certain cancers caused by five additional types of HPV' (press release). 10 December 2014. Archived from the original on 10 January 2015. Retrieved 28 February 2015.Cite uses deprecated parameter deadurl= (help)
  151. ^'CDC — Condom Effectiveness — Male Latex Condoms and Sexually Transmitted Diseases'. Centers for Disease Control and Prevention (CDC). 22 October 2009. Archived from the original on 17 October 2009. Retrieved 23 October 2009.Cite uses deprecated parameter deadurl= (help)
  152. ^'Information About What is Human Papillomavirus (HPV)?'. City of Toronto Public Health Agency. September 2010. Retrieved 20 July 2011.[permanent dead link]
  153. ^ abMeyers J, Ryndock E, Conway MJ, Meyers C, Robison R (June 2014). 'Susceptibility of high-risk human papillomavirus type 16 to clinical disinfectants'. The Journal of Antimicrobial Chemotherapy. 69 (6): 1546–50. doi:10.1093/jac/dku006. PMC4019329. PMID24500190.
  154. ^Liu Z, Rashid T, Nyitray AG (February 2016). 'Penises not required: a systematic review of the potential for human papillomavirus horizontal transmission that is non-sexual or does not include penile penetration'. Sexual Health. 13 (1): 10–21. doi:10.1071/sh15089. PMID26433493.
  155. ^Sabeena S, Bhat P, Kamath V, Arunkumar G (March 2017). 'Possible non-sexual modes of transmission of human papilloma virus'. The Journal of Obstetrics and Gynaecology Research. 43 (3): 429–435. doi:10.1111/jog.13248. PMID28165175.
  156. ^ abcHSE Quality Improvement Division — Decontamination Safety Programme (January 2017). Health Service Executive Guidance for Decontamination of Semi‐critical Ultrasound Probes; Semi‐invasive and Non‐invasive Ultrasound Probes(PDF) (Report). Department of Health United Kingdom. QPSD‐GL‐028‐1.
  157. ^Provincial Health Services Authority, Provincial Infection Control Network of British Columbia (2 June 2016). 'Recommendations for Cleaning and Disinfection in Medical Ultrasound to Prevent Human Papillomavirus (HPV) Transmission'(PDF).Cite journal requires journal= (help)
  158. ^College of Physicians and Surgeons of British Columbia (December 2017). 'Reprocessing Requirements for Ultrasound Probes'(PDF).Cite journal requires journal= (help)
  159. ^ ab'Genital HPV Infection Fact Sheet'. Centers for Disease Control and Prevention (CDC). 10 April 2008. Archived from the original on 11 September 2012. Retrieved 13 November 2009.Cite uses deprecated parameter deadurl= (help)
  160. ^'HPV Vaccine Information For Young Women'. Centers for Disease Control and Prevention (CDC). 26 June 2008. Archived from the original on 26 October 2009. Retrieved 13 November 2009.Cite uses deprecated parameter deadurl= (help)
  161. ^American Cancer Society. 'What Are the Risk Factors for Cervical Cancer?'. Archived from the original on 19 February 2008. Retrieved 21 February 2008.
  162. ^'Cure for HPV'. Archived from the original on 18 August 2010. Retrieved 29 August 2010.Cite uses deprecated parameter deadurl= (help)
  163. ^Gilbert LK, Alexander L, Grosshans JF, Jolley L (March 2003). 'Answering frequently asked questions about HPV'. Sexually Transmitted Diseases. 30 (3): 193–4. doi:10.1097/00007435-200303000-00002. PMID12616133. Archived from the original on 24 December 2011.Cite uses deprecated parameter deadurl= (help)
  164. ^'Updated U.S. Public Health Service guidelines for the management of occupational exposures to HIV and recommendations for postexposure prophylaxis'. Centers for Disease Control and Prevention. Archived from the original on 16 November 2015. Retrieved 23 October 2015.Cite uses deprecated parameter deadurl= (help)
  165. ^Desai M, Woodhall SC, Nardone A, Burns F, Mercey D, Gilson R (August 2015). 'Active recall to increase HIV and STI testing: a systematic review'. Sexually Transmitted Infections. 91 (5): 314–23. doi:10.1136/sextrans-2014-051930. PMID25759476.
  166. ^'Human papillomavirus vaccines: WHO position paper, October 2014'(PDF). Releve Epidemiologique Hebdomadaire. 89 (43): 465–91. October 2014. PMID25346960. Archived(PDF) from the original on 19 October 2015.Cite uses deprecated parameter deadurl= (help)
  167. ^Gavillon N, Vervaet H, Derniaux E, Terrosi P, Graesslin O, Quereux C (March 2010). '[How did I contract human Papillomavirus (HPV)?]'. Gynecologie, Obstetrique & Fertilite. 38 (3): 199–204. doi:10.1016/j.gyobfe.2010.01.003. PMID20189438.
  168. ^ abcdeDunne EF, Unger ER, Sternberg M, McQuillan G, Swan DC, Patel SS, Markowitz LE (February 2007). 'Prevalence of HPV infection among females in the United States'. JAMA. 297 (8): 813–9. doi:10.1001/jama.297.8.813. PMID17327523.
  169. ^'American Social Health Association — HPV Resource Center'. Archived from the original on 18 July 2007. Retrieved 17 August 2007.Cite uses deprecated parameter deadurl= (help)
  170. ^'American Social Health Association — National HPV and Cervical Cancer Prevention Resource Center'. Archived from the original on 19 June 2008. Retrieved 1 July 2008.Cite uses deprecated parameter deadurl= (help)
  171. ^'HPV vaccine report', STD, HIV, Planned Parenthood, In fact, the lifetime risk for contracting HPV is at least 50 percent for all sexually active women and men, and, it is estimated that, by the age of 50, at least 80 percent of women will have acquired sexually transmitted HPV (CDC, 2004; CDC, 2006).
  172. ^ abWeinstock H, Berman S, Cates W (January–February 2004). 'Sexually transmitted diseases among American youth: incidence and prevalence estimates, 2000'. Perspectives on Sexual and Reproductive Health. 36 (1): 6–10. doi:10.1363/3600604. PMID14982671. Archived from the original on 4 July 2008.Cite uses deprecated parameter deadurl= (help)
  173. ^Koutsky, LA (1997). 'Epidemiology of human papilomavirus infection'. The American Journal of Medicine. 102 (5): 3–8. doi:10.1016/s0002-9343(97)00177-0. PMID9217656.
  174. ^Revzina NV, Diclemente RJ (August 2005). 'Prevalence and incidence of human papillomavirus infection in women in the USA: a systematic review'. International Journal of STD & AIDS. 16 (8): 528–37. doi:10.1258/0956462054679214. PMID16105186. The prevalence of HPV reported in the assessed studies ranged from 14% to more than 90%.
  175. ^McCullough, Marie (28 February 2007). 'Cancer-virus strains rarer than first estimated'. The Philadelphia Inquirer. Archived from the original on 10 March 2007. Retrieved 2 March 2007.
  176. ^Brown, David (28 February 2007) [The Washington Post, 'More American Women Have HPV Than Previously Thought']. 'Study finds more women than expected have HPV'. San Francisco Chronicle. Archived from the original on 9 November 2007. Retrieved 2 March 2007.Cite uses deprecated parameter deadurl= (help)
  177. ^Tanner, Lindsey (11 March 2008). 'Study Finds 1 in 4 US Teens Has a STD'. Newsvine. Associated Press. Archived from the original on 16 March 2008. Retrieved 17 March 2008.Cite uses deprecated parameter deadurl= (help)
  178. ^'MMWR: Summary of Notifiable Diseases'. Morbidity and Mortality Weekly Report. CDC. Archived from the original on 17 August 2014. Retrieved 18 August 2014.Cite uses deprecated parameter deadurl= (help)
  179. ^Reportable diseasesArchived 12 April 2016 at the Wayback Machine, from MedlinePlus, a service of the U.S. National Library of Medicine, from the National Institutes of Health. Update: 19 May 2013 by Jatin M. Vyas. Also reviewed by David Zieve.
  180. ^ abc'Health Information Quality Authority (HIQA)'(PDF).
  181. ^'HSE vaccination guidelines'(PDF).
  182. ^'STI Statistics – HIV Ireland'. Retrieved 11 January 2019.
  183. ^ ab'Ano-genital warts in Ireland, 2017'(PDF). Annual Epidemiological Report. HSE Health Protection Surveillance Centre. October 2018. Retrieved 11 January 2019.
  184. ^Human papillomaviruses. World Health Organization, International Agency for Research on Cancer. 2007. ISBN978-92-832-1290-4.
  185. ^'HPV — the Shy Virus' (radio program). Sound print. 6 December 2008. Archived from the original on 28 March 2009. Retrieved 6 December 2008.Cite uses deprecated parameter deadurl= (help)
  186. ^Picken RN, Yang HL (December 1987). 'The integration of HPV-18 into HeLa cells has involved duplication of part of the viral genome as well as human DNA flanking sequences'. Nucleic Acids Research. 15 (23): 10068. doi:10.1093/nar/15.23.10068. PMC306572. PMID2827110.
  187. ^Lipke MM (December 2006). 'An armamentarium of wart treatments'. Clinical Medicine & Research. 4 (4): 273–93. doi:10.3121/cmr.4.4.273. PMC1764803. PMID17210977.

External links[edit]

  • ICD-10: B97.7
  • ICD-9-CM: 078.1079.4
  • MeSH: D030361
  • DiseasesDB: 6032
External resources
  • Human papillomavirus infection at Curlie
  • Information Centre on HPV and Cancer—ICO
  • HPV Fact sheets at the Centers for Disease Control and Prevention
  • 'Human Papillomavirus (HPV) Vaccines', National Cancer Institute Fact Sheet, US National Institutes of Health, 22 October 2009.

How Is Hpv Transmitted Treatment

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