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10.1186/s12977-017-0349-2

http://scihub22266oqcxt.onion/10.1186/s12977-017-0349-2
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suck abstract from ncbi


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pmid28415995      Retrovirology 2017 ; 14 (ä): ä
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  • Type I interferon signaling is required for the APOBEC3/Rfv3-dependent neutralizing antibody response but not innate retrovirus restriction #MMPMID28415995
  • Barrett BS; Harper MS; Jones ST; Guo K; Heilman KJ; Kedl RM; Hasenkrug KJ; Santiago ML
  • Retrovirology 2017[]; 14 (ä): ä PMID28415995show ga
  • Background: APOBEC3/Rfv3 restricts acute Friend retrovirus (FV) infection and promotes virus-specific neutralizing antibody (NAb) responses. Classical Rfv3 studies utilized FV stocks containing lactate-dehydrogenase elevating virus (LDV), a potent type I interferon inducer. Previously, we showed that APOBEC3 is required for the anti-FV activity of exogenous IFN-alpha treatment. Thus, type I interferon receptor (IFNAR) signaling may be required for the APOBEC3/Rfv3 response. Results: To test if the APOBEC3/Rfv3 response is dependent on type I IFN signaling, we infected IFNAR knockout versus IFNAR/APOBEC3 double-knockout mice with FV/LDV or LDV-free FV, and evaluated acute FV infection and subsequent NAb titers. We show that LDV co-infection and type I IFN signaling are not required for innate APOBEC3-mediated restriction. By contrast, removal of LDV and/or type I IFN signaling abrogated the APOBEC3-dependent NAb response. Conclusions: APOBEC3 can restrict retroviruses in a type I IFN-independent manner in vivo. By contrast, the ability of APOBEC3 to promote NAb responses is type I IFN-dependent. These findings reveal novel insights on the interplay between type I IFNs and APOBEC3 in vivo that may have implications for augmenting antiretroviral NAb responses. Electronic supplementary material: The online version of this article (doi:10.1186/s12977-017-0349-2) contains supplementary material, which is available to authorized users.
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