Beyond SHM and CSR: AID and related cytidine deaminases in the host response to viral infection.
As the primary effector of immunoglobulin somatic hypermutation (SHM) and class switch recombination (CSR), activation-induced cytidine deaminase (AID) serves an important function in the adaptive immune response. Recent advances have demonstrated that AID and a group of closely related cytidine deaminases, the APOBEC3 proteins, also act in the innate host response to viral infection. Antiviral activity was first attributed to APOBEC3G as a potent inhibitor of HIV. It is now apparent that the targets of the APOBEC3 proteins extend beyond HIV, with family members acting against a wide variety of viruses as well as host-encoded retrotransposable genetic elements. Although it appears to function through a different mechanism, AID also possesses antiviral properties. Independent of its antibody diversification functions, AID protects against transformation by Abelson murine leukemia virus (Ab-MLV), an oncogenic retrovirus. Additionally, AID has been implicated in the host response to other pathogenic viruses. These emerging roles for the AID/APOBEC cytidine deaminases in viral infection suggest an intriguing evolutionary connection of innate and adaptive immune mechanisms.
Rosenberg
Brad R
BR
Laboratory of Lymphocyte Biology, The Rockefeller University, New York, New York, USA.
Papavasiliou
F Nina
FN
D000818:Animals; D003564:Cytidine Deaminase / Q000276:immunology*; D015658:HIV Infections / Q000276:immunology; D006801:Humans; D017578:Immunoglobulin Class Switching; D027041:Somatic Hypermutation, Immunoglobulin; D014777:Virus Diseases / Q000276:immunology*; D000098830:AICDA (Activation-Induced Cytidine Deaminase)
D000098830:AICDA (Activation-Induced Cytidine Deaminase); D003564:Cytidine Deaminase