This article is part of the supplement: Frontiers of Retrovirology: Complex retroviruses, retroelements and their hosts
Invited speaker presentation
The fallout from crossing paths with cellular cytidine deaminases
Retrovirology 2009, 6(Suppl 2):I9 doi:10.1186/1742-4690-6-S2-I9
Published: 24 September 2009First paragraph (this article has no abstract)
Humans are unique in encoding eleven APOBEC cytidine deaminases that edit single stranded DNA (ssDNA). So far no other species encodes so many. To be exact, prime face evidence has been found for 8, the remaining 3 proving to be recalcitrant. Single stranded DNA is synonymous with replication and transcription and might suggest a role in epigenetic modification. The most widely known member goes by a different name, AID, and is responsible for class switch recombination and somatic hypermutation of rearranged immunoglobulin V region loci. Retroviral cDNA is of course, single stranded and an anti-viral activity possible. In fact the lentiviruses and one of their precursors were so vulnerable to some of the APOBEC3 enzymes that they evolved the vif gene more than 10 M years ago to effectively take them out. By contrast, HTLV-1 and other retroviruses seem not to be bothered. By contrast several human APOBEC3 genes do act as major restriction factors for hepatitis B virus in vivo. Some of the APOBEC3 genes are upregulated by interferon-α, which goes a long with an anti-viral role for certain APOBEC3 members. Finally some of the human genes at least, may also restrict some other human viruses in vivo presumably during replication and/or transcription. Indeed, a rather eclectic ensemble.