Novel immune evasion strategy of CMV: targeting of an adhesion molecule involved in leukocyte recruitment/activation.

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Herpesviruses cause persistent lifelong infection. To achieve this they have evolved a variety of mechanisms to evade the immune response mounted to combat them. They also minimise the expression of their gene products to a minimal suite of latency associated proteins. One member of the herpesvirus family is cytomegalovirus. While in healthy individuals it causes aymptomatic infection, it causes significant disease and mortality in individuals whose immune systems are suppressed such as transplant and AIDS patients, and also in the fetus which has a poorly developed immune system. Cytomegaloviruses set up persistent and latent lifelong infections. In the current proposal we will be assessing a viral gene present in mouse cytomegalovirus that codes for a protein that binds to a cellular adhesion molecule. This adhesion molecule called CD44 is involved in the migration of immune effector cell to sites of infection and in their activation. The viral gene thus represents a potential immune evasion molecule with the ability to subvert the host's immune response by reducing the infiltration and-or activation of cells that clear virus infection. The results from these studies could help us design anti-viral drugs that interfere with the effect of this viral protein, thus providing a novel anti-viral treatment strategy.