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APOBEC3G and other proteins in the same family are able to act as a [[cytidine deaminase]], inducing numerous '''[[Cytidine|C]]''' to '''[[Uracil|U]]''' mutations in the [[DNA#Strand_direction|negative strand]] of the HIV DNA. This results in many inviable virions. HIV appears to have evolved the Vif gene in order to counteract this effect. Vif does not halt APOBEC activity: it only down-regulates it, perhaps increasing overall HIV success by elevating the mutation rate. It is also able to function as | |||
'''APOBEC3G''' is a [[human]] [[protein]] belonging to the APOBEC superfamily of proteins<ref name=Malim>[http://www.nature.com/nature/journal/v418/n6898/abs/nature00939.html;jsessionid=054486BDC87BDF5630B18BF8D5B3F3B8 Sheehy AM, Gaddis NC, Choi JD, Malim MH.'''Isolation of a human gene that inhibits HIV-1 infection and is suppressed by the viral Vif protein'''. Nature. 2002 Aug 8;418(6898):646-50.]</ref>that interferes with the replication of [[HIV]] and other [[retrovirus]]es. This family of proteins has been suggested to play an important role in innate anti-viral [[immunity (medical)|immunity]].<ref name=Uirusu>[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=16557012&query_hl=3&itool=pubmed_docsum Takaori A.'''Antiviral defense by APOBEC3 family proteins.'''Uirusu. 2005 Dec;55(2):267-72.]</ref> | |||
APOBEC3G and other proteins in the same family are able to act as a [[cytidine deaminase]], inducing numerous '''[[Cytidine|C]]''' to '''[[Uracil|U]]''' mutations in the [[DNA#Strand_direction|negative strand]] of the HIV DNA. This results in many inviable virions. HIV appears to have evolved the Vif gene in order to counteract this effect. Vif does not halt APOBEC activity: it only down-regulates it, perhaps increasing overall HIV success by elevating the mutation rate. It is also able to function as anti-viral protein when its [[active site]] has been mutated so it can no longer mutate retroviral DNA. | |||
It was first identified in 2002 as a cellular factor able to restrict replication of HIV-1 lacking the viral accessory [[protein]] [[Viral infectivity factor|Vif]]. Soon after, it was shown that APOBEC3G belonged to a family of proteins grouped together due to their homology with the [[cytidine deaminase]] [[APOBEC1]]. | It was first identified in 2002 as a cellular factor able to restrict replication of HIV-1 lacking the viral accessory [[protein]] [[Viral infectivity factor|Vif]]. Soon after, it was shown that APOBEC3G belonged to a family of proteins grouped together due to their homology with the [[cytidine deaminase]] [[APOBEC1]]. | ||
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APOBEC3G is a human protein belonging to the APOBEC superfamily of proteins[1]that interferes with the replication of HIV and other retroviruses. This family of proteins has been suggested to play an important role in innate anti-viral immunity.[2]
APOBEC3G and other proteins in the same family are able to act as a cytidine deaminase, inducing numerous C to U mutations in the negative strand of the HIV DNA. This results in many inviable virions. HIV appears to have evolved the Vif gene in order to counteract this effect. Vif does not halt APOBEC activity: it only down-regulates it, perhaps increasing overall HIV success by elevating the mutation rate. It is also able to function as anti-viral protein when its active site has been mutated so it can no longer mutate retroviral DNA.
It was first identified in 2002 as a cellular factor able to restrict replication of HIV-1 lacking the viral accessory protein Vif. Soon after, it was shown that APOBEC3G belonged to a family of proteins grouped together due to their homology with the cytidine deaminase APOBEC1.
References
http://www.eurekalert.org/pub_releases/2006-12/uosc-utr122206.php
Bibliography
Sheehy AM, Gaddis NC, Choi JD, Malim MH. Isolation of a human gene that inhibits HIV-1 infection and is suppressed by the viral Vif protein. NATURE 418 (6898): 646-650 AUG 8 2002