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Human and murine APOBEC3s restrict replication of koala retrovirus by different mechanisms


Takayuki Nitta1,2,3*, Dat Ha1,2, Felipe Galvez1,2, Takayuki Miyazawa4 and Hung Fan1,2*

 

1 Department of Molecular Biology and Biochemistry, University of California, Irvine, Irvine, CA 92697-3905, USA.

2 Cancer Research Institute, University of California, Irvine, Irvine, CA 92697-3905, USA.

3 Department of Biology, Savannah State University, 3219 College St, Savannah, GA 31404-5254, USA.

4 Laboratory of Signal Transduction, Department of Cell Biology, Institute for Virus Research, Kyoto University, 53 Shogoin-Kawaharacho, Sakyo-ku, Kyoto 606-8507, Japan.


ABSTRACT
Background   Koala retrovirus (KoRV) is an endogenous and exogenous retrovirus of koalas that may cause lymphoma. As for many other gammaretroviruses, the KoRV genome can potentially encode an alternate form of Gag protein, glyco-gag.
Results   In this study, a convenient assay for assessing KoRV infectivity in vitro was employed: the use of DERSE cells (initially developed to search for infectious xenotropic murine leukemia-like viruses). Using infection of DERSE and other human cell lines (HEK293T), no evidence for expression of glyco-gag by KoRV was found, either in expression of glyco-gag protein or changes in infectivity when the putative glyco-gag reading frame was mutated. Since glyco-gag mediates resistance of Moloney murine leukemia virus to the restriction factor APOBEC3, the sensitivity of KoRV (wt or putatively mutant for glyco-gag) to restriction by murine (mA3) or human APOBEC3s was investigated. Both mA3 and hA3G potently inhibited KoRV infectivity. Interestingly, hA3G restriction was accompanied by extensive GA hypermutation during reverse transcription while mA3 restriction was not. Glyco-gag status did not affect the results.
Conclusions   These results indicate that the mechanisms of APOBEC3 restriction of KoRV by hA3G and mA3 differ (deamination dependent vs. independent) and glyco-gag does not play a role in the restriction.

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