Abstract
Human papillomaviruses (HPVs) cause diseases ranging from benign warts to invasive cancers. HPVs infect epithelial cells and their replication cycle is tightly linked with the differentiation process of the infected keratinocyte. The normal replication cycle involves an early and a late phase. The early phase encompasses viral entry and initial genome replication, stimulation of cell division and inhibition of apoptosis in the infected cell. Late events in the HPV life cycle include viral genome amplification, virion formation, and release into the environment from the surface of the epithelium. The main proteins required at the late stage of infection for viral genome amplification include E1, E2, E4 and E5. The late proteins L1 and L2 are structural proteins that form the viral capsid. Regulation of these late events involves both cellular and viral proteins. The late viral mRNAs are expressed from a specific late promoter but final late mRNA levels in the infected cell are controlled by splicing, polyadenylation, nuclear export and RNA stability. Viral late protein expression is also controlled at the level of translation. This review will discuss current knowledge of how HPV late gene expression is regulated.
Highlights
Over 210 human papillomavirus (HPV) genotypes have been characterized
Infection is usually transient because the virus is eventually recognized by the immune system and the infection is cleared without causing significant disease [2]
If infection with one of the so-called “high risk” (HR) anogenital-infective HPV genotypes becomes persistent, it can cause cellular changes that can lead to cancer formation [3]
Summary
Over 210 human papillomavirus (HPV) genotypes have been characterized. Most HPVs do not cause any symptoms or disease. If infection with one of the so-called “high risk” (HR) anogenital-infective HPV genotypes becomes persistent, it can cause cellular changes that can lead to cancer formation [3]. Initial infection is targeted to dividing cells in the basal the viral life cycle and epithelial differentiation. Once an infected basal epithelial cell genome divides, these replicated and segregated into daughter cells. The viral genome the cell expression events are linked to different epithelial layers (Figure 1). Viral late proteins are required to accomplish productive viral genome amplification and virion These late events in the viralinlife in the differentiating upper layers the production. This review article willwill explore current knowledge of the viral andand cellular molecular mechanisms of of gene regulation that are required for the virus to accomplish late events in its life cycle.
Sign-in/Register to view highlights & summary 
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call