الفهرس 
Human papillomavirusesOnly 14 pages are availabe for public view
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Abstract
As the infected cells differentiate, E1 and E2 which are DNA binding proteins regulate transcription and replication of the viral genome. E4 is thought to be involved in activating the productive phase of the HPV life cycle. E5 is another viral protein involved in transformation. As the cells approach terminal differentiation the late genes, L1 and L2, are activated. They encode the major and minor viral capsid proteins (respectively). By this point, the viral copy number has been drastically increased so that thousands of virus particles are produced per cell. As these cells approach the surface of the skin they are shed into the environmentand the virus particles are released to infect other cells and spread to other hosts. Often this lytic process is associated with inflammation, which might trigger immune attack against the virus.
In low-grade infections, the high-riskHPVgenomes are present as episomes, while during progressionto high-grade lesions or carcinomas, the genome is often foundintegrated into host sequences. This integration usually occurswithin the E2 ORF and results in loss of E2 repressive actionleading to higher levels of E6 and E7 expression.The E6 and E7 proteins of the high-risk HPV types act as viraloncoproteins, high-risk E6binds the p53 tumor suppressor protein leading tothe rapid turnover of p53. E7 binds to the retinoblastoma(Rb) family of tumor suppressors, involved in cell cycle regulationleading to the progression to malignancy. E4 and E5 involved in regulation of lateviral functions (Fehrmannet al., 2003).Figure (d)shows the life cycle of HPV.