Human Papilloma Virus: Difference between revisions

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4.Galinski C. Human Papillomavirus (HPV). Austin Community College.
4.Galinski C. Human Papillomavirus (HPV). Austin Community College.
Created by Hannah Wilson (student of Tyrrell Conway at the University of Oklahoma).

Revision as of 08:55, 26 July 2015

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University of Oklahoma Study Abroad Microbiology in Arezzo, Italy[1][http://cas.ou.edu/study-abroad/

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Atomic model of papillomavirus capsid.[2] From: www.virology.wisc.edu [http://www.virology.wisc.edu/virusworld/images/hpv-green-blue-mesh.jpg

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Etiology/Bacteriology

Taxonomy

|Family = Papillomaviridae
|Genus = Alphapapillomavirus
|species = Human Papillomavirus
NCBI: Taxonomy Genome: Genome

Description

Papillomavirus are small virus with DNA from the family papovavirdae which measure 50 nm in diameter, lack membrane, and their capsids have an icosahedral form composed of 72 capsomeres [3].The DNA of HPV is circular, double chain, and contains approximately 8000 base pairs [3]. Persistent infection by human papilloma virus (HPV) is considered the main causative agent of cervical cancer. According to their oncogenic risk, HPV are classified as low-risk HPV (LR-HPV) or high-risk HPV (HR-HPV) [3]. Classification is based on the origin and degree of homogeneity of the DNA.

Pathogenesis

Transmission

Transmission of HPV occurs most commonly during sexual activity. During sexual activity, micro-trauma or the genital epithelium, particularly in the transformation areas of the cervical epithelium, allows exposure of basal cells to active proliferation of the various types of HPV [3]. The union between receptor of the basal cells with the protein of the HPV infection occurs via direct contact between skin and mucous membranes. Though sexual relationships are the main form of contact, transmission can occur between mother and child during the time of childbirth [3]. In order for infection to develop, the complete virus must be transmitted and not only DNA fragments.

Steps of Pathogenesis

Virulence Factors

The virulence factors of HPV include proteins E6 and E7 that are heavily present in high risk papillomavirus. These proteins have been shown to inactivate the host's tumor suppressor proteins p53 and Rb. This inactivation of tumor suppresser proteins results in the host cells dividing at rate that cannot be regulated. In HR-HPV malignant transformation occurs in the quickly proliferating cells and causing the formation of cervical cancer [4]

Epidemiology

Clinical Features

Symptoms

Morbidity and Mortality

Diagnosis

Treatment

Prevention

Host Immune Response

Damage Response Framework

References

1. College of Arts and Sciences | The University of Oklahoma. Study Abroad.

2. Virology.wisc.edu. 2002. Atomic Model of papillomavirus capsid.

3. Alba A, Cararach M, Rodriguez-Cerdeira C. 2009. The Human Papillomavirus (HPV) in Human Pathology: Description, Pathogenesis, Oncogenic Role, Epidemiology and Detection Techniques. TODJ 3:90-102.

4.Galinski C. Human Papillomavirus (HPV). Austin Community College.

Created by Hannah Wilson (student of Tyrrell Conway at the University of Oklahoma).