Papillomavirus Infection

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Papillomaviruses are thought to have two methods of replication:
• Stable replication of the episomal genome in basal cells
• Runaway, or vegetative, replication in more differentiated cells to generate progeny virus.

“Viral multiplication is confined to the nucleus. Consequently, infected cells exhibit a high degree of nuclear atopia. Koilocytosis (from Greek koilos “empty”) describes a combination of perinuclear clearing (halo) with a pyknotic or shrunken (raisinoid) nucleus and is a characteristic feature of productive papillomavirus infection.” (Peter A Gearhart, MD, 2007-2016).

“In malignant lesions, the genomes of high-risk HPV types 16 and 18 are typically integrated into the host cell DNA. Integration of the viral genome into the host cell genome is
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It is incredibly difficult to detect HPV in its latent stage, so it is impossible to know whether the immune system can get rid of the virus in its entirety or if the virus can remain latent at undetectable levels, ready to re-emerge later on (Ministry of Health, 2014). Another unresolved issue is when and for how long HPV infection remains contagious. It has been said that, “if the patient has been successfully treated for genital warts and has had no new warts or cervical abnormalities for a year or more, the risk of HPV transmission is very low.” (HPV, The New Zealand HPV Project, 2007-2016). Generally, people with more than one sexual partner, as well as those who have had a persistent HPV infection, are at a greater risk for acquiring additional HPV strains. Peter A Gearhart believes that, “HPV infections have not been shown to be cytolytic; rather, viral particles are released as a result of degeneration of desquamating cells. The HPV virus can survive for many months and at low temperatures without a

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