|March 26, 2016|
Taxobox_begin | color = violet | name = Human papillomavirus
Taxobox image | image =Image:Hpv16b.gif|240px|Genome organisation of Human papillomavirus type 16 | caption = Genome of HPV-16. E1-E7 early genes, L1-L2 late genes (capsid)
Taxobox_familia_entry | taxon = Papillomaviridae
Taxobox_genus_entry | taxon = Papillomavirinae
Taxobox_species_entry | taxon = Human papillomavirus
Human papillomavirus (HPV) is a virus that infects humans. Some of its effects are classed as sexually transmitted disease (STD).
Scientists have identified more than 100 strain (biology)|strains of HPV, most of which are harmless. Some can produce common skin warts on the hands and feet. About 30 strains are spread through sexual contact; some can cause visible genital warts, while others can cause cervical cancer and other genital cancers.
HPV is by far the most common sexually transmitted infection. It is estimated that 80% of sexually active adults have been infected with one or more genital HPV strains at some time.http://www.hpv.org.nz/pdf/hpvguidelines2004.pdf The vast majority of infected people suffer no ill effects and never even know that they have been infected, but may be able to infect others. The immune system typically clears the virus from the body within a year, after which the person will be immune to that particular HPV strain.http://www2.niaid.nih.gov/Newsroom/Releases/hpv.htm
HPV is an almost unavoidable and invisible consequence of sexual activity. Many health authorities recommend that women have an annual pap smear following their first sexual activity, to ensure early detection of cervical cancer.
Though the different types of HPV virus differ to a small extent, they all have some characteristics in common. The viruses are all small and enveloped virus|nonenveloped, meaning they have no lipid bilayer surrounding their capsid, the protein coat surrounding the genome (M??nger et al., 2004; Sinal and Woods, 2005; Greenblatt, 2005). Their capsid is an icosahedron, or a polygon with 20 faces, that is 55-nanometer|nm in diameter (M??nger et al., 2004; Greenblatt, 2005; Sinal and Woods, 2005).
The genome of all HPV viruses is circular (Greenblatt, 2005; Sinal and Woods, 2005) and double stranded, with about 8000 base pairs (de Villiers et al., 2004; M??nger et al., 2004; Greenblatt, 2005; Moljin et al., 2005; Sinal and Woods, 2005). The genome has eight open reading frames , which overlap to an extent (Greenblatt, 2005; Moljin et al., 2005) and which code for ten proteins (Sinal and Woods, 2005). The genes for these are divided into an early region containing eight genes, that are expressed in the skin's infected basal cells that have yet to cell differentiation|differentiate, and a late region with two genes whose protein products exist only in cells after they have differentiated (Greenblatt, 2005; Sinal and Woods, 2005).
The proteins coded by the late genes, L1 and L2, form the virus's capsid (Moljin et al., 2005; Sinal and Woods, 2005). The proteins coded by the early genes, E1 through E8, commandeer the host cell???s replication machinery for viral replication (Moljin et al., 2005; Sinal and Woods, 2005). The incorrectly named E4 protein is actually a late gene (Greenblatt, 2005) that spurs the cell to produce and release mature virions, viruses capable of existing outside the cell and infecting other hosts (Sinal and Woods, 2005).
Though viruses are not actually alive, their development progresses through stages intrinsically linked to the cell cycle of the host cell (Sinal and Woods, 2005; Stern, 2005).
Since the virus's propagation is dependent on its replication by the host's DNA replication machinery, which is only in use when the host's genome is being copied (M??nger and Howley, 2002; Rapp and Chen, 1998), it is advantageous for the virus to speed cell division and rid the cell of factors that prevent DNA replication (Rapp and Chen, 1998; Greenblatt, 2005). Unfortunately, this leads to the abrogation of processes that exist to ensure that DNA containing errors is not copied, which can lead to the formation of warts and cancer.
Skin cells in the outermost layer of the epidermis are constantly being lost and replaced by cells in the stratum basale, which divide and move up outward the skin's layers. As they move outward, these cells differentiate and usually withdraw from the cell cycle (Rapp and Chen, 1998; Wu et al., 2003). The viral proteins E6 and E7 from high-risk HPV types prevent cells from differentiating and withdrawing from the cell cycle as they move outward through the cell layers, while those from low risk types do not (Baseman and Koutsky, 2005). Differentiating cells begin to produce more and more HPV-encoded proteins until, when they reach the skin surface, they produce complete virions, mature viruses that can survive outside of the host cell (Greenblatt, 2005; Sinal and Woods, 2005). Virions flake off with the discarded skin cells and can go on to infect other hosts and other areas on the same host (Greenblatt, 2005).
Common skin warts
Some strains of HPV, called cutaneous strains, (e.g., HPV 1) cause common skin warts. They are most commonly found on the hands and the feet. These strains of HPV do not cause genital warts.
Genital warts (condylomata acuminata or venereal warts) are the most easily recognised sign of genital HPV infection. However, of the 30 strains of genital HPV, only two can cause warts (HPV 6 and 11); and most people who acquire those strains never develop warts or any other symptoms.
It is important to note that the strains of HPV that can cause genital warts are NOT the same ones that can cause cervical cancer. These strains are called low-risk types.
About 15 strains of HPV (including 16, 18, and 31) are called high-risk types because they can cause cervical cancer, anal cancer, vulvar cancer, head and neck cancers, and (rarely) penile cancer. High-risk types of HPV can cause intraepithelial neoplasias, or abnormal and precancerous cell growth, in the vulva and cervix, which can progress to cancer. These tumours often have HPV viral sequences integrated into the cellular DNA. Some of the genes encoded by these viruses are known to act as oncogenes. The viral E6 protein from high-risk HPV types binds to and causes the degradation of the cellular protein p53 while the high-risk E7 protein interferes with the retinoblastoma protein.
A history of HPV infection is believed to be a prerequisite for the development of cervical cancer; according to the American Cancer Society, women with no history of the virus do not develop this type of cancer. However, most HPV infections do not progress to cervical cancer. Because the process of transforming normal cervical cells into cancerous ones is slow, cancer occurs in people who have been infected with HPV for a long time, usually over a decade (Greenblatt, 2005; Sinal and Woods, 2005).
High-risk HPV types 16 and 18 are together responsible for over 70% of cervical cancer cases (Baseman and Koutsky, 2005; Cohen, 2005). Type 16 causes 41 to 54% of cervical cancers (Noel et al., 2001; Baseman and Koutsky, 2005) and is also the usual cause of VIN (Edwards et al., 2005) and oropharyngeal cancers (Bolt et al., 2005).
If a woman has cervical intraepithelial neoplasia, or abnormal (possibly precancerous) cervical cells, a Pap smear can detect them. It is particularly important for women who have abnormal cervical cells to undergo colposcopy so that precancerous and cancerous lesions can be detected and treated early.
Throat cancers and tumors
HPV can also cause laryngeal papillomatosis, or warts in the respiratory tract (Wu et al., 2003; Sinal and Woods, 2005). These warts often recur frequently, may require repetitive surgery (Moore et al., 1999; Sinal and Woods, 2005), may interfere with breathing, and in rare cases can progress to cancer (Moore et al., 1999). HPV types 30 and 40 cause laryngeal carcinoma.
Viral sites may be distributed widely over the pelvic area, and transmission can occur even when there are no visible symptoms; thus, the only sure way to prevent genital HPV infection is to abstain from any contact with the genitals of another.
The American Cancer Society advises that condoms offer only limited protection against HPV. Both Planned Parenthood and the Centers for Disease Control recommend condom use to reduce the risk of HPV, and the latter advises that condom use has been associated with a lower rate of cervical cancer. Since the virus infects the skin and is transmitted by skin-to-skin contact, covering even part of the skin (as with a condom) reduces the opportunity for infection, as the area of contact would be reduced for both partners.
Risk factors linked to acquiring HPV include sex at an early age and having many sexual partners.
At least two pharmaceutical company|pharmaceutical companies are currently testing vaccines against the human papillomavirus (HPV), in hopes of preventing this very common viral infection and eradicating cervical cancer in women.
# Baseman J.G. and Koutsky L.A. 2005. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15753008&query_hl=4 The epidemiology of human papillomavirus infections. Journal of Clinical Virology, 32(1): 16-24. Abstract available.
# Bolt J., Vo Q.N., Kim W.J., McWhorter A.J., Thomson J., Hagensee M.E., Friedlander P., Brown K.D., and Gilbert J. 2005. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=16139561&dopt=Citation 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): 1013-1020. Abstract available.
# Cohen J. 2005. High Hopes and Dilemmas for a Cervical Cancer Vaccine. Science, 308(5722): 618-621.
# de Villiers E.M., Fauquet C, Broker TR, Bernard HU., and zur Hausen H. 2004. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15183049&dopt=Citation Classification of papillomaviruses. Virology, 324(1): 17-27. Absstract available.
# Edwards Q.T., Saunders-Goldson S., Morgan P.D., Maradiegue A., and Macri C. 2005. Vulvar Intraepithelial Neoplasia. Advance for Nurse Practitioners. March, 2005 issue. pp. 49-52.
# Greenblatt R.J. 2005. http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T5D-4H6P7Y9-1&_user=10&_handle=V-WA-A-W-W-MsSAYZA-UUA-U-AABAVZDCWU-AAWEUVYBWU-BEAYVEYEY-W-U&_fmt=summary&_coverDate=09%2F15%2F2005&_rdoc=1&_orig=browse&_srch=%23toc%235000%232005%23999729981%23607092!&_cdi=5000&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=42b5289fd6b206fd7ae9269741210c39 Human papillomaviruses: Diseases, diagnosis, and a possible vaccine. Clinical Microbiology Newsletter, 27(18), 139-145. Abstract available.
# Molijn A., Kleter B., Quint W., and van Doorn L.J. 2005. Molecular diagnosis of human papillomavirus (HPV) infections. Journal of Clinical Virology, 32(1): 43-51.
# Moore C.E., Wiatrak B.J., McClatchey K.D., Koopmann C.F., Thomas G.R., Bradford C.R. and Carey T.E. 1999. High-risk human papillomavirus types and squamous cell carcinoma in patients with respiratory papillomas. Otolaryngology, 120(5): 698-705.
# M??nger, K. and Howley, P.M., 2002. Human papillomavirus immortalization and transformation functions. Virus Research, 89: 213???228.
# Noel J.C., Lespagnard L., Fayt I., Verhest A., and Dargent J.L. 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): 135-138.
# Rapp L. and Chen J.J. 1998. The papillomavirus E6 proteins. Biochimica et Biophysica Acta, 1378(1): F1-F19.
# Sinal S.H. and Woods C.R. 2005. Human papillomavirus infections of the genital and respiratory tracts in young children. Seminars in Pediatric Infectious Diseases, 16(4): 306-316.
# Wu R. Sun S., Steinberg B.M. 2003. http://www.molmed.org/content/2003/77.pdf Requirement of STAT3 activation for differentiation of mucosal stratified squamous epithelium. Molecular Medicine, 9(3/4), 77-84. Available.
Category:Sexually-transmitted diseasesCategory:VirusesCategory:Infectious diseases
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