human papillomavirus and cancer - immunological consequences of mhc class i down-regulation

few studies have been conducted on the causative factors associated with the development of cancer. infection by high risk human papillomaviruses (hpvs) have been implicated as causative agents in a variety of cancers. hpv is capable of evading immune system and establishing persistent infections. prolonged infection and lesion maintenance are associated with higher risk of neoplastic progression. hence, curtailing the ability of the virus to escape host immunosurveilance should reduce this risk by accelerating resolution of infection and lesion progression. one of the potential effectors of hpv escape from host immunosurveilance is the e5 oncoprotein, which we have shown to down-regulate surface major histocompatibility complex class i (mhc i), without apparent effect on non-classical mhc. these effects would interfere with both cytotoxic t lymphocyte (ctl) killing of the virally infected cells, and with the natural killer (nk) cell illumination of infected cells. in this review we address mechanisms of immunomodulation by papillomavirus and discuss our current findings on the association of hpv and cancers.