Receptor modulation in viral replication: HIV, HSV, HHV-8 and HPV: same goal, different techniques to interfere with MHC-I antigen presentation.

Evasion of host immunity is a common objective of viruses that cause chronic infections. Viruses involved in sexually transmitted infections constitute no exception to this phenomenon. HIV, HPV, HSV, and HHV-8 subvert the class I major histocompatibility complex (MHC-I) antigen presentation pathway, thereby evading the cellular immune response. Although the goal of these viruses is the same and efficient MHC-I downregulation in infected cells is achieved, their techniques vary considerably. Whether viral inhibition occurs at the transcriptional level, during assembly of MHC-I complexes in the endoplasmic reticulum, during its journey to the cell surface, or after reaching the cell surface, each one of these viruses ingeniously achieves MHC-I downregulation and avoids the cellular immune response. Unraveling the mechanisms of interference with MHC-I antigen presentation employed by these viruses is not only crucial to understand their pathogenesis, but also reveals novel mechanisms of regulation of cellular receptors. When employed as modulators of cellular trafficking pathways, viruses become tools to dissect fundamental cell processes. In return, the precise dissection of these processes may offer new weapons against the ruses viruses employ to propagate and establish chronic infections.