VIRAL MUTATIONS, TCR ANTAGONISM AND ESCAPE FROM THE IMMUNE-RESPONSE

Persistent viruses use several mechanisms to evade the immune response , including the generation of mutations that affect TCR recognition. I t has recently been reported that spontaneous mutations at TCR contact sites within individual viral epitopes in certain persistent human vi ruses can abrogate or antagonize the recognition of the corresponding wild-type epitope, and it has been suggested that such mutations may c ontribute to viral persistence.