TABLE 25.3.
Mechanism | Example |
---|---|
Interference with viral antigen processing and presentation | HSV (ICP47), EBV (EBNA-1), HIV (Nef, Tat), HPV (E5), CMV (UL6) |
Evasion of NK cell function | HIV (Nef), EBV (EBNA-1), CMV (UL40, UL18) |
Inhibition of cell apoptosis | Adenovirus (RID complex and E1B), HIV (Nef), EBV (BHRF-1) |
Destruction of T cells | HIV |
Interference with antiviral cytokines and chemokines | EBV (IL-10 homologue), CMV(US28 chemokine receptor homologue), vaccinia virus (IL-18-binding protein), HIV (Tat chemokine activity) |
Inhibition of complement action | HSV, pox viruses |
Inhibition of DC maturation | HSV, vaccinia virus |
Frequent antigenic variation | Influenza virus, HIV |
Infection of immune privileged site | Measles virus, VZV and HSV (neurons) |
Immune exhaustion | HIV, HCV, HBV |
CMV, cytomegalovirus; DC, dendritic cell; EBV, Epstein–Barr virus; HBV, hepatitis B virus; HCV, hepatitis C virus; HIV, human immunodeficiency virus; HPV, human papillomavirus; HSV, herpes simplex virus; IL-18, interleukin-18; NK, natural killer; RID, receptor internalization and degradation; VZV, varicella-zoster virus.