TRIM5α Modulates Immunodeficiency Virus Control in Rhesus Monkeys

摘要: The cytoplasmic TRIM5α proteins of certain mammalian lineages efficiently recognize the incoming capsids particular retroviruses and potently restrict infection in a species-specific manner. Successful have evolved that are less recognized by natural hosts. To address whether contributes to outcome retroviral susceptible host species, we investigated impact TRIM5 polymorphisms rhesus monkeys on course simian immunodeficiency virus (SIV) infection. Full-length cDNAs were derived from each 79 outbred sequenced. Associations explored between expression alleles both permissiveness cells SIV vitro clinical sequelae vivo. Natural variation B30.2(SPRY) domain influenced efficiency SIVmac capsid binding susceptibility We also show importance vivo interaction with different allelic forms TRIM5, demonstrating associated as much 1.3 median log difference set-point viral loads SIVmac-infected monkeys. Moreover, these extent loss central memory (CM) CD4+ T rate progression AIDS infected These findings demonstrate role for limiting replication an primate host.