Human+Papillomavirus+(HPV)

=** Human papillomavirus **=

**A. Name of disease:** Human papillomavirus

**B. Root cause of disease:** Papillomaviruses are a class of virus that replicate exclusively through the basal layer (deepest epidermal layer) of body surface tissues. Human papillomavirus is no except to this rule. In practice, human papillomavirus is spread through genital contact as a consequence of vaginal, anal, and oral sex. In extraneous cases, HPV can also be spread through direct genital contact and during delivery from an infected mother to her child. [2] On a cellular level, HPV infection occurs when the virus gains access to the basal epithelial cells of the penis, scrotum, vulva, vagina, cervix, anus, or bladder. In order to replicate and spread, human papillomavirus particles must first pass through the squamous epithelial cells (the most superficial layer) through micro-wounds or micro-abrasions that expose the basement membrane. Past the point of entrance, the HPV virion interacts with the ** α ** 6 ** β ** 4 integrins, leading to the subsequent internalization of the virus through a papillomavirus capsid protein L1. [4]

**C. Affected cell types/tissues/organs/systems:** The Skin [2]


 * D. Historical background: ** Human papillomavirus was first identified by the scientific world in the 1950’s. However, it was not until Stefania Ginsburg-Jablonska, a polish physician and dermatologist, first connected HPV onset to skin cancer in 1972 that real gains were made into the pathology of the disease. In her investigation of skin cancer Ginsburg-Jablonska continually came across a specific strain of HPV, HPV-5. In 1976, a virologist by the name of Harald zur Hausen made additional strides in the investigation of the connection between human papillomavirus and cancer. He and his team discovered two strains of HPV, HPV-16 and HPV-18, which were common amongst all cervical cancer cases. [7] Through the following years, growing numbers of scientists would perform additional research on human papillomavirus only to discover that of the 120 known types of HPV isolated in humans, HPV 16, 18, 31, 33, 35, 45, 52, and 58 are known to be the most high-risk oncogenic strains and are pivotal to the development of cervical cancer. [4]

Although there is little information on famous individuals who are infected solely with the human papillomavirus, there is an abundance of information on those who suffer from cancers derived from the virus. Farah Fawcett, a well-known actress, passed away in 2009 after becoming infected with HPV-derived anal cancer. Evita Peron, the wife of Juan Peron the Argentinian leader, passed away of HPV-derived cervical cancer in her early 30’s. [5] These women and countless like them all developed cancer as a result of persistent infections with such high-risk strains that ultimately led to cell abnormalities and malignant conformations. The high-risk strains aid in the development of carcinoma by inactivating cellular tumor suppressor proteins p53 and retinoblastoma protein (pRb). Such inactivation leads to an amassing of DNA damage, which can then undergo cell division due to the absence of pRb. Eventually, over years, the number of malignant cells grows and presents itself as cancer. [4]


 * E. Common symptoms: ** In general, human papillomavirus can present as a slew of various symptoms. However, genital warts far exceed any other sign or symptom. Warts appear as small bumps in the genital area, and appear within weeks or months after sexual contact with an infected partner, regardless of whether the partner has visible indication of the disease. The types of HPV that causes warts are not the same strains that lead to the development of cancer. [3]

**F. Standard Treatments:** While there are no standard treatments for the virus itself, there are those that address the symptoms of viral infection. Genital warts are typically asymptomatic, but can be painful in select cases. In such situations, removal through application of creams or gels or provider-administered cryotherapy with liquid nitrogen, surgical removal, or podophyllin resin or trichloroacetic acid application might be preferred. In non-issue situations though, patients can leave the warts untreated and the visible warts can resolve on their own. Genital warts should be allowed three months to recover fully through treatment and modulation. [3]

**G. Current research:** As it stands, there is still much research to be conducted if scientists are to fully understand the human papillomavirus. Due to the wide extensiveness of the effect that HPV can have upon human health and wellness, scientists have investigated a range of further topics related to HPV infection including, but not limited to, advances in diagnostic technology and links between cancer and HPV. Increases in HPV infections in the past 30 years have been ties to the similar rise in HPV-related cancers, and in an effort to curb the rate of cancer development, scientists are pushing for more practical, wide-spread administration of the HPV vaccine. [1] [6]

Figure 1: In order for HPV to replicate, it must first gain access to the basal epithelial cells. In order to do so, it targets the squamous epithelium found beneath the foreskin of the penis or the skin of the cervix. HPV particles gain access through microabrasians or microwoundings that expose the basement membrane. Once inside, the L1 capsid protein on the surface of the virion interacts with the **α**6**β**4 integrins that are regulated by basal epithelial cells during wound repair. These integrins cause the internalization of the virus, which allows it to propagate and spread. Adapted from [4]

Figure 2: HPV utilizes the differentiation pathway of keratinocytes (anoikis) to establish infection of basal epithelial cells. An infection soon develops, and the virus experiences low levels of replication and protein expression so as not to activate the immune system. After the keratinocytes differentiate, the HPV genes are expressed, and viral late protein expression and assembly finally occurs. During the terminal differentiation of the keratinocyte, the viruses are shed from the outermost layer of epithelial cells. Adapted from [4]

References [1] (2006). Epidemiology Of HPV 16 And Cervical Cancer In Finland And The Potential Impact Of Vaccination: Mathematical Modeling Analyses. //PLoS Medicine//, //3//(5), e138. Retrieved December 6, 2013, from http://dx.doi.org/10.1371/journal.pmed.0030138 [2] Genital HPV Infection - Fact Sheet. (2013, July 25). //Centers for Disease Control and Prevention//. Retrieved December 8, 2013, from http://www.cdc.gov/std/HPV/STDFact-HPV.htm [3] Genital Warts. (2012, February 8). //Centers for Disease Control and Prevention//. Retrieved December 9, 2013, from http://www.cdc.gov/std/treatment/2010/genital-warts.htm [4] Human Papilloma Virus (HPV). (n.d.). //Human Papilloma Virus (HPV)//. Retrieved December 7, 2013, from http://immunopaedia.org.za/index.php?id=799 [5] Nilsen, R. (n.d.). Famous People With HPV. //LIVESTRONG.COM//. Retrieved December 8, 2013, from http://www.livestrong.com/article/26370-famous-people-hpv/ [6] Roden, R., & Wu, T. (2006). How Will HPV Vaccines Affect Cervical Cancer?. //Nature Reviews Cancer//, //6//(10), 753-763. Retrieved December 6, 2013, from http://dx.doi.org/10.1038/nrc1973 [7] Who Discovered HPV?. (n.d.). //Who Discovered HPV?//. Retrieved December 8, 2013, from http://discovery.yukozimo.com/who-discovered-hpv/