Human papillomavirus infection is an infection by human papillomavirus (HPV). Most HPV infections cause no symptoms and disappear spontaneously. In some people, HPV infection persists and causes warts or precancerous lesions. Pre-cancerous lesions increase the risk of cervical cancer, vulva, vagina, penis, anus, mouth, or throat. Almost all cervical cancers are caused by HPV with two types, HPV16 and HPV18, accounting for 70% of cases. Between 60% and 90% of other cancers mentioned above are also associated with HPV. HPV6 and HPV11 are common causes of genital warts and laryngeal papillomatosis.
HPV infection is caused by human papillomavirus , a DNA virus from the papillomavirus family, of which more than 170 species are known. More than 40 species are transmitted through sexual contact and infect the anus and genitals. Risk factors for persistent HPV infection include early age of first sexual intercourse, multiple partners, smoking, and poor immune function. HPV usually spreads through skin-to-skin direct contact with vaginal and anal sex being the most common method. Sometimes, it can spread from mother to baby during pregnancy. It does not spread through common items like toilet seats. People can get infected with more than one type of HPV. HPV affects only humans.
The HPV vaccine can prevent the most common types of infections. To be most effective, they should be used before infection occurs and are therefore recommended between the ages of nine and 13. Cervical cancer screening, such as with the Papanicolaou test (pap) or seeing the cervix after using acetic acid, can detect early or abnormally developing cancers become cancerous. This allows for early care that produces better results. Screening has reduced the number and deaths of cervical cancer in developed countries. Warts can be removed by freezing.
HPV is the most common sexually transmitted infection globally. Most people get infected at some point in their lives. In 2012, about 528,000 new cases and 266,000 deaths occurred due to cervical cancer worldwide. About 85% of this happens in developing countries. In the United States, about 27,000 cases of cancer due to HPV occur every year. Approximately 1% of sexually active adults have genital warts. While the case of warts has been described since ancient Greece, the nature of their virus was not discovered until 1907.
Video Human papillomavirus infection
Signs and symptoms
More than 170 types of HPV have been identified, and they are designated by numbers.
Several types of HPV, such as HPV-5, can cause an infection that lasts an individual's lifetime without ever showing any clinical symptoms. HPV types 1 and 2 can cause warts in some infected individuals. HPV types 6 and 11 can cause genital warts and laryngeal papillomatosis. HPV types 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68, 73, and 82 are considered carcinogenic.
This table lists the common symptoms of HPV infection and associated HPV strains:
Warts
Skin infections ("cutaneous" infection) with HPV are extensive. Skin infections with HPV can cause non-cancerous skin growth called warts (verruca). Warts are caused by rapid cell growth in the outer layer of the skin. While the case of warts has been described since ancient Greece, the cause of their virus was not known until 1907.
Skin warts are most common in childhood and usually appear and spontaneously deteriorate for several weeks to months. About 10% of adults also suffer from recurrent skin warts. All HPVs are believed to be able to develop long term "latent" infections in small amounts of stem cells present in the skin. Although this latent infection may never be completely eradicated, immunological control is thought to inhibit the appearance of symptoms such as warts. Immunologic control is a specific type of HPV, which means one can become resistant to one type of HPV while remaining susceptible to another. In one study, infection with HPV types 2, 27, and 57 was found in people with warts, while infection with HPV types 1, 2, 63, and 27 was found in people with clinically normal skin.
Type of warts include:
- Common warts are usually found in the hands and feet, but can also occur in other areas, such as elbows or knees. Ordinary warts have a typical cauliflower-like surface and are usually slightly protruding above the surrounding skin. This type of cutaneous HPV can cause genital warts but is not associated with cancer progression.
- Plantar warts are found on the soles of the feet; they grow inward, generally causing pain when walking.
- Subungual or periungual warts are formed under the nail (subungual), around the nail, or on the cuticle (periungual). They are more difficult to treat than warts in other locations.
- Flat warts are most commonly found on the arms, face, or forehead. Like common warts, flat warts are most common in children and adolescents. In people with normal immune function, flat warts are not associated with cancer progression.
Genital warts are quite contagious, while plain, flat, and plantar warts are very unlikely to spread from person to person.
Genital warts
HPV infection of the skin in the genital area is the most common sexually transmitted infection worldwide. Such infections are associated with genital or anal warts (medically known as condylomata acuminata or genital warts), and this wart is the most recognizable sign of genital HPV infection.
HPV strains that can cause genital warts are usually different from those that cause warts on other body parts, such as the hands or feet, or even the inner thighs. Different types of HPV can cause genital warts, but types 6 and 11 together produce about 90% of all cases. However, a total of more than 40 types of HPV are transmitted through sexual contact and can infect anal and genital skin. Such infections can cause genital warts, although it may also show no symptoms.
Most genital HPV infections never cause clear symptoms and are cleared by the immune system in a matter of months. In addition, people can pass the virus on to others even if they do not show any obvious symptoms of the infection. Most people acquire genital HPV infection at some point in their lives, and about 10% of women are currently infected. A major increase in the incidence of genital HPV infection occurs at an age when individuals begin to engage in sexual activity. Like HPV skin, immunity to genital HPV is believed to be specific for certain strains of HPV.
Papillomatosis larynx
In addition to genital warts, infection by HPV types 6 and 11 can cause a rare condition known as recurrent laryngeal papillomatosis, where the warts form in the larynx or other areas of the respiratory tract. These warts often recur, can interfere with breathing, and in very rare cases can develop into cancer. For this reason, repeated surgery to remove warts may be recommended.
Cancer
About a dozen types of HPV (including types 16, 18, 31, and 45) are called "high-risk" types because persistent infections have been linked to cancers such as cancer of the oropharynx, larynx, vulva, vagina, cervix, penis, and anus. This cancer generally involves sexually transmitted HPV infection into epithelial tissue. Individuals infected with HPV and HIV have an increased risk of cervical or rectal cancer.
An estimated 561,200 new cases of cancer worldwide (5.2% of all new cancers) were caused by HPV in 2002, making HPV one of the most important causes of cancer infection. HPV-related cancers account for more than 5% of all cancer cases diagnosed worldwide, and this incidence is higher in developing countries where it is estimated to cause nearly half a million cases each year.
In the United States, about 27,000 cases of cancer due to HPV occur every year.
In some infected individuals, their immune system may fail to control HPV. Ongoing infection with high risk HPV types, such as types 16, 18, 31, and 45, can support cancer progression. Ko-factors such as cigarette smoke can also increase the risk of HPV-related cancers.
HPV is believed to cause cancer both by integrating into DNA and in non-integrated episodes. Some of the "early genes" carried by HPV viruses, such as E6 and E7 genes, act as oncogens that promote tumor growth and malignant transformation. Furthermore, HPV can induce a tumorigenic process through integration into the host genome associated with changes in the number of DNA copies.
E6 produces a protein (also called E6) that binds and inactivates proteins in a host cell called p53. Typically, p53 acts to prevent cell growth, and promotes cell death in the presence of DNA damage. p53 also improves the regulation of p21 protein, which blocks the formation of the D/Cdk4 cyclin complex, thus preventing RB phosphorylation, and in turn, stopping the development of cell cycle by preventing E2F activation. In short, p53 is a tumor suppressor protein that captures 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, cancer characteristics.
E6 also has a strong relationship with E6-associated protein (E6-AP) protein cells, which are involved in ubiquitin ligase pathways, a system that functions to degrade proteins. E6-AP binds ubiquitin to p53 protein, thus marking it for proteosomal degradation.
The study also showed an association between different types of HPV and squamous cell carcinoma of the skin. In such cases, the in vitro studies show that E6 proteins of the HPV virus can inhibit apoptosis caused by ultraviolet light.
Cervical Cancer
Almost all cases of cervical cancer are associated with HPV infection, with two types, HPV16 and HPV18, present in 70% of cases.
HPV type 16 is the most malignant strain, present in 41 to 54% of all cervical cancers, and in many cases vaginal/vulvar, penile, anal, and head and neck cancers.
In 2012, about 528,000 new cases and 266,000 deaths from cervical cancer occur worldwide. About 85% of this happens in developing countries.
Most HPV infections in the cervix are rapidly cleared by the immune system and do not develop into cervical cancer (see below Clearance subsection in Virology). Since the process of transforming normal cervical cells into cancer cells is slow, cancer occurs in people who have been infected with HPV for a long time, usually more than a decade or more (persistent infection).
Non-European (NE) HPV16 variants are significantly more carcinogenic than European (E) HPV16 variants.
Genital Cancer
Studies show an association between HPV infection and penile and rectal cancer. Sexually transmitted HPV is found in a large percentage of anal cancers. In addition, the risk of anal cancer was 17 to 31 times higher among gay and bisexual men than among heterosexual men - although one survey found no difference between male sex HPV infection rates compared with men those who have sex only with women.
Anal Pap smear screening for anal cancer may benefit some of the subpopulations of men or women involved in anal sex. There is no consensus, though, that such screening is beneficial, or who should get an anal Pap smear.
Cancer head and neck
High-risk carcinogenic HPV types (including HPV 16 and HPV 18) are associated with an increased number of head and neck cancers.
Sexually transmitted form of HPV for about 25% of upper cancers and throat (oropharynx). The latter is often present in the tonsils area, and HPV is associated with increased oral cancer in nonsmokers. Engaging in anal or oral sex with an HPV-infected partner may increase the risk of developing this type of cancer. Oral infection with several types of HPV, particularly type 16, has been found to be associated with oropharyngeal HPV-positive cancers, a form of head and neck cancer. This association does not depend on the use of tobacco and alcohol. In the United States, HPV is expected to replace tobacco as the main causative agent for oral cancer, and the number of newly diagnosed, head and neck cancers associated with HPV is expected to surpass cases of cervical cancer by 2020.
In recent years, the United States has seen an increase in the number of cases of throat cancer caused by HPV type 16. The HPV-related throat cancer has been estimated to increase from 0.8 cases per 100,000 people in 1988 to 2.6 per 100,000 years 2004. The researchers explain this latest data with increased oral sex. In addition, the findings suggest this type of cancer is much more common in men than in women, something that needs to be explored further. Currently, two immunizations, Gardasil and Cervarix, are recommended for girls to prevent HPV-related cervical cancer, but not as prevention of HPV-related throat cancer.
The profile of HPV-positive and HPV-negative cancer mutations have been reported, further demonstrating that they are essentially different diseases.
Lung cancer
Some evidence links HPV with benign and malignant tumors in the upper respiratory tract. The International Agency for Research on Cancer has found that people with lung cancer are significantly more likely to have some form of high-risk HPV antibodies compared to those who do not have lung cancer. The researchers looked for HPV among 1,633 lung cancer patients and 2,729 people without lung disease found that people with lung cancer had more HPV types than noncancer patients, and among lung cancer patients, probably had eight serious HPV types increased significantly.. In addition, the expression of structural HPV proteins by immunohistochemical and in vitro studies suggests the presence of HPV in bronchial cancer and precursor lesions. Another study detected HPV in EBC, brushing brushing tissue and neoplastic lung tissue, and found an HPV infection in 16.4% of subjects with non-cell lung cancer, but no control. The reported frequency of HPV in lung cancer was 17% and 15% in Europe and America, respectively, and the mean HPV count in Asian lung samples was 35.7%, with sufficient heterogeneity between certain countries and regions.
Uninterrupted individual
In very rare cases, HPV can cause verruciformis epidermodisplasia in individuals with weakened immune systems. Viruses, which are not checked by the immune system, cause excess production of keratin by skin cells, resulting in lesions resembling warts or skin horns.
Maps Human papillomavirus infection
Cause
Sexually transmitted HPV is divided into 2 categories: low risk and high risk. Low risk HPV causes warts in or around the genitals. Types 6 and 11 cause 90% of all genital warts and recurrent respiratory papillomatosis that cause benign tumors in the airways. HPV is a high-risk cause of cancer and consists of about a dozen identifiable species. Types 16 and 18 are the two responsible for causing the majority of cancers caused by HPV. This high-risk HPV causes 5% of cancer in the world. In the United States, high-risk HPV causes 3% of all cases of cancer in women and 2% in men.
Transmission
Risk factors for persistent genital HPV infection include early age of first sexual intercourse, multiple partners, smoking, and immunosuppression. Genital HPV is usually spread through continuous skin-to-skin contact, with vaginal and anal sex being the most common method although transmission of oral sex may occur. Sometimes it can spread from mother to baby during pregnancy. It does not spread through common items like toilet seats. The period of transmission is still unknown, but perhaps at least as long as the visible lesions are still present. HPV can still be transmitted even after lesions are treated and are no longer visible or present.
Perinatal
Although genital HPV types can be transmitted from mother to child during birth, the appearance of genital HPV-related disease in newborns is rare. However, the lack of appearance does not rule out asymptomatic latent infection, as the virus has proven able to hide for decades. Perineal HPV 6 and 11 perinatal transmission may result in the development of recurrent juvenile respiratory papillomatosis (JORRP). JORRP is very rare, with a rate of about 2 cases per 100,000 children in the United States. Although JORRP levels are much higher if a woman comes with genital warts at the time of delivery, the risk of JORRP in such cases is still less than 1%.
Genital Infections
Because genital cervical infection and women by specific HPV types are strongly associated with cervical cancer, this type of HPV infection has received most of the attention from scientific studies.
HPV infection in the area is transmitted primarily through sexual activity.
Of the known 120 known human papilloma viruses, 51 species and three subtypes infect the genital mucosa. 15 are classified as high-risk types (16, 18, 31, 33, 56, 58, 59, 68, 73, and 82), three as high-risk possibility (26, 53, 66), and 12 as low risk (6, 11, 40, 42, 43, 44, 54, 61, 70, 72, 81, and CP6108).
If a woman has at least one different partner per year for four years, it is likely that she will leave college with a HPV infection greater than 85%. Condoms do not fully protect from viruses because the area around the genitalia includes the inner thigh area is not closed, thus exposing this area to the skin of an infected person.
Hands
Studies have shown the transmission of HPV between the hands and genitals of the same person and sexual partners. Hernandez tested the genitals and the dominant hands of each person in 25 heterosexual couples each month for an average of seven months. He found two couples in which his male genitals infected her hand with high-risk HPV, two in which his hands infected his genitals, one where his genitals infected his hands, two where he infected his own hands, and he infected his own hands. Hands are not the main source of transmission in these 25 pairs, but they are meaningful.
Partridge reported male fingertips to be positive for high-risk HPV at more than half the rate (26% per 2 years) as their genitals (48%). Winer reported 14% of fingertip samples from sexually active women were positive.
Non-sexual hand contact seems to have little or no role in HPV transmission. Winer found all 14 fingertip samples from female virgin negative at the beginning of her fingertip study. In a separate report on genital HPV infection, 1% of virgin girls (1 in 76) without sexual contact tested positive for HPV, while 10% of virgin women reported positive non-penetrative sexual contact (7 of 72).
Sharing objects that may be contaminated, for example, a razor, can send HPV. Although possible, transmission by route other than sexual intercourse is less common for female genital HPV infection. Fingers-genital contact is a possible means of transmission but may not be a significant source.
Blood
Although it has traditionally been assumed that HPV can not be transmitted through blood - because it is thought to only infect skin and mucosal tissues - recent research has called this idea into question. Historically, HPV DNA has been detected in the blood of cervical cancer patients. In 2005, a group reported that, in frozen blood samples from 57 sexually naive children with vertical or transfusion HIV infection, 8 (14.0%) of these samples were tested positive for HPV-16. This seems to indicate that HPV can be transmitted through blood transfusions. However, as non-sexual HPV transmission in other ways is not uncommon, this can not be proven definitively. In 2009, a group examined blood samples of the Australian Red Cross from 180 healthy male donors for HPV, and then found DNA from one or more viral strains in 15 (8.3%) of the samples. However, it is important to note that detecting the presence of HPV DNA in the blood is not the same as detecting the virus itself in the blood, and whether the virus itself can or does not exist in the blood of an infected individual is still unknown. Thus, it remains to be determined whether or not HPV can be transmitted through the blood. This is of concern, as blood donors are currently not screened for HPV, and at least some organizations such as the American Red Cross and other Red Cross communities are currently not appearing to ban HPV-positive individuals from donating blood.
Surgery
Transmission of HPV in hospitals, especially for surgical staff, has been documented. Surgeons, including urologists and/or anyone in the room, are subject to HPV infection by inhaling harmful virus particles during electrocautery or laser ablation from a condyloma (warts). There is a case report of a laser surgeon who developed extensive laryngeal papillomatosis after providing laser ablation in patients with anogenital condylomata.
Virology
HPV infection is confined to epithelial basal cell stages, the only tissue in which they replicate. Viruses can not bind live tissue; on the contrary, it infects epithelial tissue through micro-abrasions or other epithelial trauma that expose the basement membrane segment. The infection process is slow, taking 12-24 hours to initiate transcription. It is believed that the antibodies involved play a major neutralizing role while the virions are still in the basement membrane and the cell surface.
HPV lesions are thought to arise from the proliferation of infected basal keratinocytes. Infection usually occurs when basal cells in the host are exposed to a contagious virus through an impaired epithelial barrier such as will occur during sexual intercourse or after minor skin blisters. HPV infection has not been proven to be cytolytic; more precisely, virus particles are released as a result of degeneration of desquamating cells. HPV can last for months and at low temperatures without hosts; therefore, an individual with plantar warts can spread the virus by walking barefoot.
HPV is a small double-stranded DNA DNA virus with a genome of about 8000 base pairs. The HPV life cycle closely follows the host keratinocyte differentiation program. It is thought that HPV virions infect epithelial tissue via micro-abrasion, where virions are associated with putative receptors such as integrin alpha, laminin, and annexin A2 which cause the entry of virions into basal epithelial cells through endocytosis mediated by clathrin and/or guaolin-mediated endocytosis depending on type of HPV. At this point, the viral genome is transported to the nucleus by an unknown mechanism and sets itself on the number of copies of 10-200 viral genomes per cell. A sophisticated transcriptional cascade then occurs when the master keratinocytes begin to divide and become more differentiated in the upper layers of the epithelium.
The phylogeny of various strains of HPV generally reflects the migratory pattern of Homo sapiens and suggests that HPV may have diversified along with the human population. Studies show that HPV evolved along five major branches that reflect the ethnicity of the human host, and are diversified along with the human population. The researchers have identified two major variants of HPV16, Europe (HPV16-E), and Non-Europe (HPV16-NE).
protein E6/E7
The two major oncoproteins of high-risk HPV types are E6 and E7. The "E" marking indicates that both of these proteins are expressed at the beginning of the HPV life cycle, whereas the term "L" indicates a delayed expression. The HPV genome consists of six open reading frames (E1, E2, E4, E5, E6, and E7) (ORF), two late ORFs (L1 and L2), and long codeless control areas (LCRs). Once the host cell is infected the initial viral activator is activated and the primary polycistronic RNA containing all six initial ORFs is transcribed. This polycistronic RNA then experiences an active RNA splicing to produce several mRNA isoforms. One connected RA isoform, E6 * I, serves as E7 mRNA to translate E7 protein. However, the initial viral transcription subject for viral E2 regulation and high E2 levels suppress transcription. The HPV genome integrates with the host genome with E2 ORF disorders, preventing E2 and E7 repression. Thus, the integration of the viral genome into the host DNA genome increases the expression of E6 and E7 to promote cellular proliferation and possible malignancy. The extent to which E6 and E7 are expressed is correlated with the type of cervical lesion that can eventually develop.
- Role in cancer
Protein E6/E7 disables two tumor suppressor proteins, p53 (attenuated by E6) and pRb (attenuated by E7). Virus oncogens E6 and E7 are thought to modify cell cycles thus maintaining different host keratinocytes in favorable circumstances for amplification of viral gene replication and consequent end-gene expression. E6 in association with the host E6-associated protein, which has ubiquitin ligase activity, acts for ubiquitinate p53, which causes proteosomal degradation. E7 (in oncogenic HPV) acts as a major transformation protein. E7 competes to bind to the retinoblastoma protein (pRb), freeing the transcription factor E2F to transact its targets, thus pushing the cell cycle forward. All HPV can induce temporary proliferation, but only strains 16 and 18 can perpetuate the cell line in vitro . It has also been shown that HPV 16 and 18 can not immortalize only primary mouse cells; there needs to be oncogene racial activation. In the upper layers of the host epithelium, the final genes L1 and L2 are transcribed and serve as structural proteins that enclose a reinforced genome of the virus. Once the genome is encapsulated, the capsid appears to experience a redox-dependent assembly/maturation event, which is bound to a natural redox gradient that extends both the suprabacial and cornified epithelial tissue layers. This assembly/maturation stabilizes the virions, and increases their specific infectivity. The virus can then be exfoliated in the dead squames of the host epitelium and the viral life cycle continues. A 2010 study found that E6 and E7 are involved in nuclear accumulation of beta-catenin and activation of Wnt signaling on cancer induced by HPV.
Latency period
After the HPV virion attacks the cell, active infection occurs, and the virus can be transmitted. A few months to years may pass before the intraepithelic squamous lesion (SIL) develops and can be detected clinically. The time from active infection to a clinically detectable disease may make it difficult for epidemiologists to determine which pair is the source of the infection.
Clearance
Most HPV infections are cleaned by most people without medical action or consequences. This table provides data for high-risk types (ie types found in cancer).
Cleaning the infection does not always create immunity if there is a source of new or continuous infection. Hernandez '2005-6 study of 25 couples reported "A number of cases showed clear reinfection [of partners] after viral eradication."
Diagnosis
There are several 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.
Health guidelines recommend HPV testing in patients with specific indications including certain abnormal Pap test results.
Cervical test
According to the National Cancer Institute, "The most common test detects DNA from some high risk HPV types, but can not identify the type (s) that exist.Other tests are specific for DNA of HPV types 16 and 18, both of which cause most cancers HPV-related third test can detect DNA from several high-risk HPV types and may indicate whether HPV-16 or HPV-18 is present. The fourth test detects RNA from the most common high-risk HPV types.These tests can detect HPV infection before cell abnormalities visible.
"Theoretically, HPV DNA and RNA testing can be used to identify HPV infection in cells taken from every part of the body, but the test is approved by the FDA for only two indications: for advanced testing of women who appear to have abnormal Pap test results and for cervical cancer screening in combination with Pap tests among women over the age of 30. "
In April 2011, the Food and Drug Administration approved the HPV Cobas test, produced by Roche. This cervical cancer screening test "specifically identifies the types of HPV 16 and HPV18 while simultaneously detecting residuals of high-risk types (31, 33, 35, 39, 59, 66 and 68)."
The HPV cobas test was evaluated in the ATHENA trial, which studied more than 47,000 US women aged 21 years and older who underwent routine cervical cancer screening. Results from the ATHENA trial showed that 1 in 10 women, age 30 and older, tested positive for HPV 16 and/or 18, actually had pre-cervical cancer even though they showed normal results with Pap tests.
In March 2003, the US Food and Drug Administration (FDA) approved a Hybrid Taking test 2 produced by Qiagen/Digene, which is a "hybrid-capture test" in addition to Pap testing. Tests can be done during regular Pap smears. Detecting DNA from 13 "high risk" HPV strains that most often affect the cervix, does not specify specific HPV types. Hybrid Capture 2 is the most commercially-studied HPV testing and most of the evidence for HPV primary testing in a population-based screening program is based on the Hybrid Capture 2 test.
Recent results in the identification of molecular pathways involved in cervical cancer provide useful information on new or oncogenic biophysical markers that allow monitoring of these important molecular events in cytologic, histological, or cytological specimens. Bio- or markers of this onset tend to improve detection of lesions that have a high risk of progression in both primary screening and triage settings. Detection of mRNA E6 and E7 PreTek HPV-Proofer (HPV OncoTect) or p16 cell level proteins are examples of these new molecular markers. According to published results, these markers, which are highly sensitive and specific, make it possible to identify cells through malignant transformation.
In October 2011 the US Food and Drug Administration approved the Aptima HPV Assay test for RNA was made when and if any strains of HPV started creating cancer (see virology).
The vulva/vagina has been sampled with a Dacron rag and shows more HPV than the cervix. Among women who were positive for HPV in both sites, 90% were positive in the vulvovaginal region, 46% in the cervix.
Oral testing
Research has found increased HPV in oral cell samples from people with oral squamous cell carcinoma. Studies have not found significant HPV in oral cells after sampling with a toothbrush (5 of 2,619 samples) and cytobrushes (no oral transmission was found).
Test people
Studies have tested and found HPV, including high-risk types (ie types found in cancer), in the fingers, mouth, saliva, anus, urethra, urine, semen, blood, scrotum and penis. However, most research tests have used Dacron swabs and custom analysis not available to the general public.
A study in Brazil using the Qiagen/Digene test is available on the off label to test the male penis, scrotum and anus. Each of the 50 people has been a partner for at least 6 months from a woman who is positive for high-risk HPV. They found high risk HPV in 60% of these men, especially the penis. "The specimens were obtained by using a strong movement of the cone brush that is included in the Digene kit after spraying the anogenital area with a saline solution."
A slightly different method also uses cytobrushes (but custom lab analysis) and found 37% of 582 Mexican soldiers recruit positive for high-risk HPV. They were told not to wash genitals for 12 hours before sampling. (Other studies are not vocal about washing, special gaps in hand study). They include the urethra as well as the scrotum and penis, but the urethra adds less than 1% at the HPV level. Studies like this make Giuliano suggest taking gland, stem and pleat samples between them and the scrotum, because very little urethral or anal sampling for diagnosis. Dunne recommends their glands, stems, folds, and foreskin.
A small study of cytobrushes in 10 US men where a wet brush, not a skin, found 2 out of 10 men positive for HPV (type not reported). Their lab analysis is not the same as the above study. This small study found 4 out of 10 positive men for HPV when the skin was rubbed with a 600 grit emery paper, then wiped with a Dacron wet cloth. Since the sandpaper and brush paper are analyzed together in the lab, it is not known whether the emery paper collects the virus or looses it for sampling.
Research has found collections by men of their own skin (with sandpaper and Dacron swabs) as effective as doctors, sometimes more, because patients are more willing to scrape off vigorously.
Other studies have used similar cytobrushes to sample fingertips and under the nails, though without wetting the area or brush.
Other studies analyzed urine, semen and blood and found HPV in varying amounts, but no tests were available to the public.
There is no assortment of tests even though HPV is common. Doctors rely on vaccines among young people and high permission levels (see Clearance section in Virology) to create a low risk of illness and death, and treat cancer when they appear. Others believe that reducing HPV infection in more men and women, even when it has no symptoms, is important (grazing immunity) to prevent more cancers than just treating them. Where tests are used, negative test results indicate the safety of the transmission, and positive test results show where a shield (condom, glove) is required to prevent transmission until the infection is lost.
Other tests
While it is possible to test HPV DNA in other types of infections, there are no FDA-approved tests for general examination in the United States or tests approved by the Canadian government, since the tests can not be concluded and are considered medically unnecessary.
Genital warts are the only visible sign of low-risk genital HPV and can be identified by visual examination. This visible growth, however, is the result of non-carcinogenic HPV types. Five percent acetic acid (vinegar) is used to identify both squamous and intraepithelic squamous (SIL) warts and neoplasia with limited success by causing abnormal white tissue, but most doctors have found this technique only helpful in humid areas, such as female genitalia. system. Currently, HPV testing for men is only used in research.
Research on testing for HPV by the presence of antibodies has been performed. This approach looks for immune responses in the blood, which will contain antibodies to HPV if the patient is HPV positive. The reliability of the test has not been proven, as there is no FDA-approved product in March 2014; blood testing would be a less invasive test for screening purposes.
Prevention
The HPV vaccine can prevent the most common types of infections. To be effective they should be used before infection occurs and are therefore recommended between the ages of nine and thirteen. Cervical cancer screening, such as with a Papanicolaou test (pap) or seeing the cervix after using acetic acid, can detect early cancer or abnormal cells that can progress to cancer. This allows for early care that produces better results. Screening has reduced the number and deaths of cervical cancer in developed countries. Warts can be removed by freezing.
Methods reduce the possibility of infection including sexual abstinence, condoms, and vaccinations.
Vaccines
Three vaccines are available to prevent infection by several types of HPV: Gardasil, Cervarix, and Gardasil 9. All protect against early infection with HPV types 16 and 18, which causes most cases of HPV-related cancers. Gardasil also protects against HPV types 6 and 11, which causes 90% of genital warts. Gardasil is a recombinant quadrivalent vaccine, while Cervarix is ​​bivalent, and is made from virus-like particles (VLP) from L1 capsid protein. Gardasil 9 nonavalent, has the potential to prevent about 90% of cervical, vulvar, vaginal, and rectal cancers. This can protect against HPV types 6, 11, 16, 18, 31, 33, 45, 52, and 58. These five additives account for up to 20% of cervical cancers, previously not previously discussed.
Vaccines provide few benefits for women who have been infected with HPV types 16 and 18. For this reason, vaccines are recommended especially for women who have not been exposed to HPV during sex. The World Health Organization's position paper on HPV vaccination clearly outlines the appropriate and cost-effective strategies for using HPV vaccine in public sector programs.
There is evidence of high certainty that HPV vaccine protects against pre-cancerous cervical lesions in young women, especially those vaccinated aged 15 to 26 years. The HPV vaccine does not increase the risk of serious side effects. A longer follow-up is needed to monitor the impact of HPV vaccine on cervical cancer.
The CDC recommends vaccines given in two shots, with an interval of at least 6 months between them, for those who are 11-12, and three doses for those older. In most countries, they are funded solely for the use of women, but are approved for the use of men in many countries, and are funded for boys in Australia. Vaccines have no therapeutic effect on existing HPV infections or cervical lesions. In 2010, 49% of teenage girls in the US received HPV vaccine.
After the study showed that the vaccine was more effective in younger women than older adolescents, the UK, Switzerland, Mexico, the Netherlands and Quebec began offering vaccines in a two-dose schedule for girls under 15 in 2014.
Recommended cervical cancer screening is unchanged for women receiving HPV vaccine. It remains a recommendation that women continue cervical screening, such as a Pap smear test, even after receiving the vaccine, as it does not prevent all types of cervical cancer.
Both men and women are carriers of HPV. The Gardasil vaccine also protects men from anal cancers, warts, and genital warts.
The duration of the success of both vaccines has been observed since it was first developed, and is expected to last forever.
In December 2014, the FDA approved nine-valent Gardasil-based vaccine, Gardasil 9, to protect against infection with four strains of HPV covered by Gardasil's first generation as well as five other strains responsible for 20% of cervical cancers (HPV-31, HPV -33, HPV-45, HPV-52, and HPV-58).
Condoms
The Centers for Disease Control and Prevention says that "the use of male condoms may reduce the risk of HPV infection" but provides a lower level of protection than other sexually transmitted diseases "because HPV can also be transmitted by exposure to the area (eg, infected skin or surface mucosa) that is not covered or protected by a condom. "
Female condoms provide somewhat greater protection than male condoms, because female condoms allow for fewer skin contacts.
Research has suggested that regular condom use can effectively limit persistent persistence and spread of HPV to additional genital sites in already infected individuals.
Disinfection
The virus is relatively strong and immune to many common disinfectants. 90% ethanol exposure for at least 1 min, 2% glutaraldehyde, 30% Savlon, and/or 1% sodium hypochlorite may disinfect the pathogen.
The virus is resistant to drying and heat, but is killed at 100 Ã, Â ° C (212Ã, Â ° F) and by ultraviolet radiation.
Treatment
There is currently no specific treatment for HPV infection. However, a viral infection, more often than not, clears to undetectable levels by itself. According to the Centers for Disease Control and Prevention, the immune system cleans the HPV naturally within two years for 90% of cases (see verse Clearance in Virology for more details). However, experts do not agree whether the virus is completely eliminated or reduced to undetectable levels, and it is difficult to know when the virus is contagious.
Advanced treatment is usually recommended and practiced by many health clinics. Follow-up sometimes does not work because some of those treated do not return for evaluation. In addition to the normal methods of phone calls and letters, text messages and emails can increase the number of people returning for treatment.
Epidemiology
Worldwide, HPV is estimated to infect about 12% of women at any given time. HPV infection is the most sexually transmitted disease in the world.
United States
HPV is thought to be the most common sexually transmitted infection in the United States. Most sexually active men and women may get genital HPV infection at some point in their lives. The American Social Health Association estimates that about 75-80% of sexually active Americans will be infected with HPV at some point in their lives. At the age of 50 years more than 80% of American women will experience at least one type of genital HPV. It is estimated that, in 2000, there were about 6.2 million new HPV infections among Americans aged 15-44; of this, an estimated 74% occur in people aged between 15 and 24 years. Of the STD studied, genital HPV is the most commonly obtained. In the United States, it is estimated that 10% of the population has active HPV infection, 4% have infections that cause cytological abnormalities, and an additional 1% have infections that cause genital warts.
Estimates of HPV prevalence vary from 14% to over 90%. One reason for the difference is that some studies report women who currently have detected infections, while other studies report women who have had a detectable infection. Another cause of the difference is the difference in the strain 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 is higher than previously thought; 15.2% are infected with one or more of the high risk types that can cause cancer.
Prevalence for high-risk and low-risk types is almost the same over time.
Human papillomavirus is not among the diseases normally reported to CDC in 2011.
History
In 1972, the human papillomavirus relationship with skin cancer in the verruciformis epidermodisplasia was proposed by Stefania Jabofalo in Poland. In 1978, Jab? O? Ska and Gerard Orth at the Pasteur Institute found HPV-5 in skin cancer. 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.
The HeLa cell line contains extra DNA in its genome derived from HPV type 18.
Research
Ludwig-McGill HPV Cohort, a large longitudinal study of the natural history of human papillomavirus infection and the risk of cervical cancer
One study found transient evidence to support the extract from garlic.
References
External links
- Human papillomavirus infection in Curlie (based on DMOZ)
- Information Center on HPV and Cancer , ICO .
- HPV fact sheet , Centers for Disease Control and Prevention .
- "Human Papillomavirus (HPV) vaccine", National Cancer Institute Fact Sheet, US National Institutes of Health, October 22, 2009.
Source of the article : Wikipedia
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