Regulation of human papillomavirus gene expression in the vegetative life cycle

• Published in: Perspectives in Medical Virology Vol. 8; pp. 31 - 51
• Main Authors: Peña, Loren del Mar, Laimins, Laimonis A.
• Format: Book Chapter
• Language: English
• Published: Elsevier B.V 2002
• ISBN: 9780444506269; 0444506268
• ISSN: 0168-7069; 1875-791X
• DOI: 10.1016/S0168-7069(02)08015-1

The chapter discusses regulation of human papillomavirus (HPVs) gene expression in the vegetative life cycle. HPVs infect epithelial or mucosal tissue at specific anatomical locations. Over 100 HPVs have been identified to date, of which approximately 30 types infect the genital tract. Genital types are divided into two categories based on their potential for malignant transformation. Infection by low-risk viruses, such as HPV-6, and 11, can lead to genital warts, while high-risk types (HPV-16, 18, 31, 33, and 45, among others) can induce oncogenesis in infected tissue of the anogenital tract. HPVs are members of a small group of viruses that link their life-cycle to the differentiation status of the host cell. It may occur through microwounds of the epithelium and to utilize a heparin-like molecule on basal cells for the initial binding event. Following entry, viral DNA is established as episomes in basal cells at approximately 50–100 copies per cell. Early viral gene expression occurs at low levels at this stage, and viral DNA replication is synchronized to the host chromosomes. As infected cells migrate through the suprabasal strata, they differentiate and the viral DNA continues to replicate. Late gene expression occurs upon terminal differentiation, and progeny virions are produced in suprabasal cells. The use of organotypic raft culture and other methods for differentiation has facilitated analysis of transcription and DNA synthesis throughout the HPV lifecycle, while growth of submerged monolayer cultures is a model for growth in the basal layers of the epithelium.