Human papillomavirus (HPV) is a viral infection passed from one person to the other through contact with the skin. More than 100 varieties of HPV exist, with about 40 being transmitted through sexual contact. HPV passed through sexual intercourse can affect the mouth, throat, and genitals (Chaturvedi et al. 265). The Centers for Disease Control and Prevention opines that HPV is the most common sexually transmitted infection in the United States (Human Papillomavirus (HPV) Infection). HPV is classified into different forms and exists in various structures, each with its unique functions.
By classification, HPV belongs to the family of Papillomaviridae. The genera under this family include Alphapapillomavirus, Betapapillomavirus, Gammapapillomavirus, and Deltapapillomavirus. This family contains viruses that have circular double-stranded DNA genomes (Patel et al.). Incidentally, each of these genera contains papillomaviruses that typically share their hosts’ biological properties and specificity. This includes the diseases that the members of the genus cause.
Structurally, the Human papillomavirus genome contains 8000 base pairs divided into the early or late gene. W1, E2, E4, E5, E6, and E7 are encoded by the early genome, whereas the late genome encodes the L1 and the L2. Meanwhile, the E6 and E7 oncoproteins function by degrading the p53 and pRb tumor suppressors, respectively (Patel et al.). The HPV capsid structure protein is built using L1 and L2.
If the L1 is expressed, it can produce virus-like particles (VLPs) in mammalian and non-mammalian systems of expression. This can be achieved if it is expressed independently or blended with L2. All HPV-type genomes contain about 8 ORFs, which are transcribed from a single strand of DNA. There are three functional parts upon which ORX is divided. The first one is the early (E) region in which the (E1-E7) proteins essential for the replication of proteins are encoded (Wu et al. 538). The second is the late (L) region, where the (L1-L2) structural proteins are encoded for virion assembly. Finally, there is the non-coding part known as the long control region (LCR). This contains the elements of cis, which are significant for the transcription and replication of the viral DNA. Incidentally, it is from the early promoter, such as the HPV 31’s P97, that the viral E proteins are transcribed (Human Papillomavirus (HPV) Infection). On the other hand, the late promoter, like the P742, assists in the transcription of the L proteins.
The structure of the HPV illustrates that each protein molecule contained therein has its specific function. The E1 protein acts as a binding site for DNA, while E2 controls DNA replication, viral genomes segregation, and viral transcription. On its part, the E4 supports and favors the amplification of the HPV genome (Wu et al.). It also regulates the expression of late genes, facilitates the release of virions, and controls the maturation of the virus.
E5 enhances the E6 and E7 activity of transformation in addition to promoting cell fusion and contributing to the evasion of the immune response. Meanwhile, the E6 serves to bind and degrade the E5 protein, which is known to bind and degrade tumor suppressors. The E7 also binds and degrades another tumor suppressor, the pRB protein, in addition to increasing the CDK activity (Chaturvedi et al.). The L1 is a capsid protein, while the L2 is a minor capsid protein. The L1 comprises a significant cell-surface receptors attachment determinant, whereas the L2 contributes to the virion binding in the cell receptor (Human Papillomavirus (HPV) Infection). This supports the transportation and uptake of the nucleus as well as delivering the viral DNA to the centers for replication. From the above illustrations, it is apparent that each structure of HPV has its own function.
Works Cited
Chaturvedi, Anil K, et al. “Effect of Prophylactic Human Papillomavirus (HPV) Vaccination on Oral HPV Infections Among Young Adults in the United States.” Journal of Clinical Oncology, vol. 36, no. 3, 2018, pp. 262–267.
“Human Papillomavirus (HPV) Infection.” Centers for Diseases Control and Prevention, 2021. Web.
Patel, Cyra , et al. “The Impact of 10 years of Human Papillomavirus (HPV) Vaccination in Australia: What Additional Disease Burden Will a Nonavalent Vaccine Prevent?” Eurosurveillance , vol. 23, no. 41, 2018.
Wu, Zeni, et al. “Association Between Human Papillomavirus (HPV) 16, HPV18, and Other HR-HPV Viral Load And The Histological Classification Of Cervical Lesions: Results From a Large-Scale Cross-Sectional Study.” Journal of Medical Virology, vol. 89, no. 3, 2017, pp. 535-541.