Abstract
Background Host cells have developed a broad range of mechanisms to counteract retroviral infection. Besides Trim5a (tripartite motif-containing protein 5alpha) and Tetherin, APOBEC3 proteins (apolipoprotein B mRNA editing enzyme catalytic polypeptide-like 3), especially APOBEC3G and APOBEC3F, are major factors in the post entry inhibition of retroviruses. These proteins are incorporated into budding virions and exhibit inhibitory activity by interfering with reverse transcription and/or by deamination of cytosine to uracil in the proviral minus strand, resulting in hypermutation of the viral DNA. Mouse mammary tumor virus, MMTV, is a murine pathogen causing mammary adenocarcinomas and Tcell lymphomas in infected animals. The betaretrovirus, which is transmitted from mother to pubs via milk, infects dendritic cells, T-cells, B-cells and mammary epithelial cells (MEC). Previous studies showed that MMTV is inhibited by mouse APOBEC3 and human APOBEC3G proteins. However, the virus is also known to replicate in cells expressing APOBEC3 proteins, suggesting a partial resistance to the APOBEC-mediated antiviral effect. Therefore, we sought to analyse the anti-MMTV activity of APOBEC3 proteins derived from various species and compare it to the antiviral activity imposed on ΔVif HIV-1.
Highlights
Host cells have developed a broad range of mechanisms to counteract retroviral infection
We sought to analyse the anti-MMTV activity of APOBEC3 proteins derived from various species and compare it to the antiviral activity imposed on ΔVif HIV-1
We found these variants to show low activity against both MMTV and ΔVif HIV-1
Summary
Host cells have developed a broad range of mechanisms to counteract retroviral infection. Besides Trim5a (tripartite motif-containing protein 5alpha) and Tetherin, APOBEC3 proteins (apolipoprotein B mRNA editing enzyme catalytic polypeptide-like 3), especially APOBEC3G and APOBEC3F, are major factors in the post entry inhibition of retroviruses. These proteins are incorporated into budding virions and exhibit inhibitory activity by interfering with reverse transcription and/or by deamination of cytosine to uracil in the proviral minus strand, resulting in hypermutation of the viral DNA. MMTV, is a murine pathogen causing mammary adenocarcinomas and Tcell lymphomas in infected animals. The virus is known to replicate in cells expressing APOBEC3 proteins, suggesting a partial resistance to the APOBEC-mediated antiviral effect. We sought to analyse the anti-MMTV activity of APOBEC3 proteins derived from various species and compare it to the antiviral activity imposed on ΔVif HIV-1
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
