Beyond SHM and CSR: AID and related cytidine deaminases in the host response to viral infection.
Beyond SHM and CSR: AID and related cytidine deaminases in the host response to viral infection.
复制标题
DOI：
10.1016/s0065-2776(06)94007-3
复制
发表时间：
2007-01-01
影响因子：
--
通讯作者：
Papavasiliou, F Nina
中科院分区：
文献类型：
--
作者：
Rosenberg, Brad R;Papavasiliou, F Nina
活化诱导的胞苷脱氨酶（AID）作为免疫球蛋白体细胞超突变（SHM）和类别转换重组（CSR）的主要效应子，在获得性免疫应答中发挥重要作用。最近的进展表明，AID和一组密切相关的胞苷脱氨酶，APOBEC 3蛋白，也在先天宿主对病毒感染的反应中起作用。抗病毒活性首先归因于APOBEC 3G作为HIV的有效抑制剂。现在很明显，APOBEC 3蛋白的靶点超出了HIV，其家族成员可以对抗多种病毒以及宿主编码的逆转录转座遗传因子。虽然它似乎通过不同的机制发挥作用，但AID也具有抗病毒特性。独立于其抗体多样化功能，AID可防止Abelson鼠白血病病毒（Ab-MLV）（一种致癌逆转录病毒）的转化。此外，艾滋病还与宿主对其他病原性病毒的反应有关。AID/APOBEC胞苷脱氨酶在病毒感染中的这些新兴作用表明先天性和适应性免疫机制之间存在有趣的进化联系。
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.