Hudson Laboratory

We are interested in how viruses escape detection by the immune system.

As a response to selective pressures exerted by the host immune system, many viruses have developed an equally complex set of immunoevasive strategies. Perhaps most interesting is the array of unique strategies that viruses employ to interfere with the presentation of viral antigens on the surface of host cells for recognition by cytotoxic T lymphocytes.

Many viruses, including all known members of the Herpesvirus family, target antigen presentation by class I MHC molecules as a means of undermining the anti-viral immune response. We focus on two recently discovered human herpesviruses, HHV-6 and -7. Little is known about the immunobiology of these two beta-herpesviruses. They are most closely related to human cytomegalovirus (HCMV), and like all other herpesviruses, HHV-6 and -7 remain latent or establish persistent infections. Thus, it seemed likely that HHV-6 and -7 would also encode unique mechanisms of immune evasion. Because so many of the viral immunoevasins affect trafficking or stability of class I MHC molecules, we took a biochemical approach to examine the maturation and stability of class I molecules in HHV-7-infected T cells.