Host immune responses to HPV are generally low-level because the virus, being confined to basal epithelial cells is shielded from the circulating immune cells during initial stages of infection. In this location there is only a limited expression of viral proteins. Other factors contributing to the low level of host immunity are that HPV infection is non-lytic (does not cause death of the infected cell); that a functionally active immune response is generated only at later stages of HPV infection, in post-mitotic suprabasal keratinocytes where all viral genes are expressed; and that only in suprabasal keratinocytes has the HPV DNA been sufficiently amplified to be detected by the host immune-surveillance cells. In addition to the natural low-level immune responses towards HPV, HPV also employs several mechanisms to down-regulate innate and cell-mediated immunity, thus facilitating host immune evasion and persistent infection. The environment, lifestyle, the genetic make-up of the host, and the viral genomic characteristics can also influence the persistence of HPV infection, and consequential diseases. Persistent infection with high-risk HPV is associated with increased risk of developing HPV-mediated premalignancy and malignancy. It is not clear if the natural humoral immune response as opposed to vaccination is effective in eliminating primary HPV infection or in preventing progression of infection; but after initial infection, the host develops HPV-specific T cell immune responses that appear to be capable of clearing established infection, of protecting against progression of early HPV-associated intraepithelial neoplastic lesions to squamous cell carcinoma, and of preventing reinfection.
|Number of pages||3|
|Journal||SADJ : journal of the South African Dental Association = tydskrif van die Suid-Afrikaanse Tandheelkundige Vereniging|
|Publication status||Published - Jul 2010|