Pathogenic Role of Immune Evasion and Integration of Human Papillomavirus in Oropharyngeal Cancer

Abstract

The incidence of oropharyngeal cancer (OPC) is increasing remarkably among all head and neck cancers, mainly due to its association with the human papillomavirus (HPV). Most HPVs are eliminated by the host’s immune system; however, because HPV has developed an effective immune evasion mechanism to complete its replication cycle, a small number of HPVs are not eliminated, leading to persistent infection. Moreover, during the oncogenic process, the extrachromosomal HPV genome often becomes integrated into the host genome. Integration involves the induction and high expression of E6 and E7, leading to cell cycle activation and increased genomic instability in the host. Therefore, integration is an important event in oncogenesis, although the associated mechanism remains unclear, especially in HPV-OPC. In this review, we summarize the current knowledge on HPV-mediated carcinogenesis, with special emphasis on immune evasion and integration mechanisms, which are crucial for oncogenesis.

Immune Responses in Oral Papillomavirus Clearance in the MmuPV1 Mouse Model

“…Intriguingly, across species, females tend to develop a stronger innate and adaptive immune response to contagions [51]. Sex difference in immune responses to infectious diseases has been reported [70,71]. HPV infection and associated OPC also showed higher incidence in males when compared with females [1].…”

Injectable catechin-based supramolecular hydrogel for highly efficient application in HPV-associated OSCC

“…Disruption of normal cell cycle processes plays an important role in carcinogenesis. 4,[42][43][44] Therefore, it is of great importance to reveal the concrete influence of the CPBisoG gel on the cell cycles of HPV + OSCC. Flow cytometry further revealed that CPBisoG significantly induced S and G2/M arrest and G0/G1 reduce in HPV + OSCC after 24 h (Fig.…”

HPV co‐infections with other pathogens in cancer development: A comprehensive review

“…The E7 protein degrades retinoblastoma (Rb) family members (i.e., p105, p107, and p130) leading to the release of the E2F transcription factor which promotes gene expression in the S phase, and elicits hyperproliferation. 26 Viral assembly occurs in the maturing squamous epithelium leading to the release of amplified viruses from the terminally differentiated squamous cells. This 3-week process refers to the maturation of a basal cell to the superficial cells.…”