Ab initial predictions of both the rA2-GC12 and –GC4 CCR clearly show a different folding profile suggesting that these proteins may be unable to interact with surface CX3CR1, thus explaining the lack of SOCS-1/-3 induction in mutant virus infection and emphasizing the need for an intact CX3C motif for G protein-mediated immunosuppression. The gene discussed is SOCS1; the disease is viral infectious disease.