TY - CHAP
T1 - Beyond SHM and CSR
T2 - AID and Related Cytidine Deaminases in the Host Response to Viral Infection
AU - Rosenberg, Brad R.
AU - Papavasiliou, F. Nina
N1 - Funding Information:
We wish to thank Dr. Charles Rice, Dr. Christian Munz, and Dr. Lynn Dustin for critical review of the chapter and helpful advice. We also thank Joanna Spencer and Robert McGinty for additional editorial assistance. BRR is supported by NIH MSTP grant GM07739. NPP is supported in part by NIH/NIAID grant AI071029.
PY - 2007
Y1 - 2007
N2 - 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.
AB - 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.
UR - https://www.scopus.com/pages/publications/34249781408
U2 - 10.1016/S0065-2776(06)94007-3
DO - 10.1016/S0065-2776(06)94007-3
M3 - Chapter
C2 - 17560276
AN - SCOPUS:34249781408
SN - 0123737060
SN - 9780123737069
T3 - Advances in Immunology
SP - 215
EP - 244
BT - AID for Immunoglobulin Diversity
A2 - Alt, Frederick
A2 - Honjo, Tasuku
ER -