The Antiviral Factor SERINC5 Impairs the Expression of Non-Self-DNA

SERINC5 is a restriction factor that becomes incorporated into nascent retroviral particles, impairing their ability to infect target cells. In turn, retroviruses have evolved countermeasures against SERINC5. For instance, the primate lentiviruses (HIV and SIV) use Nef, Moloney Murine Leukemia Virus...

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Bibliographic Details
Published in:	Viruses Vol. 15; no. 9; p. 1961
Main Authors:	Shi, Yuhang, Simpson, Sydney, Ahmed, Shahad K, Chen, Yuexuan, Tavakoli-Tameh, Aidin, Janaka, Sanath Kumar, Evans, David T, Serra-Moreno, Ruth
Format:	Journal Article
Language:	English
Published:	Switzerland MDPI AG 01-09-2023 MDPI
Subjects:	Animals Antiviral Agents Cell Membrane Classical Swine Fever Virus Deoxyribonucleic acid DNA ectopic DNA Equine infectious anemia Extrachromosomal DNA Gene expression Genomes Health aspects Hepatitis B HIV HIV Infections Hog cholera Horses Human immunodeficiency virus Infections Leukemia Life cycles Medical research Medicine, Experimental Membrane proteins Mice non-self-DNA Pathogens Penicillin Physiological aspects Plasmids Proteins Proviruses Retroviridae SERINC5 Swine transcriptional restriction Virions Viruses United States United States > US transcriptional restriction non-self-DNA HIV SERINC5 ectopic DNA
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Summary:	SERINC5 is a restriction factor that becomes incorporated into nascent retroviral particles, impairing their ability to infect target cells. In turn, retroviruses have evolved countermeasures against SERINC5. For instance, the primate lentiviruses (HIV and SIV) use Nef, Moloney Murine Leukemia Virus (MLV) uses GlycoGag, and Equine Infectious Anemia Virus (EIAV) uses S2 to remove SERINC5 from the plasma membrane, preventing its incorporation into progeny virions. Recent studies have shown that SERINC5 also restricts other viruses, such as Hepatitis B Virus (HBV) and Classical Swine Fever Virus (CSFV), although through a different mechanism, suggesting that SERINC5 can interfere with multiple stages of the virus life cycle. To investigate whether SERINC5 can also impact other steps of the replication cycle of HIV, the effects of SERINC5 on viral transcripts, proteins, and virus progeny size were studied. Here, we report that SERINC5 causes significant defects in HIV gene expression, which impacts virion production. While the underlying mechanism is still unknown, we found that the restriction occurs at the transcriptional level and similarly affects plasmid and non-integrated proviral DNA (ectopic or non-self-DNA). However, SERINC5 causes no defects in the expression of viral RNA, host genes, or proviral DNA that is integrated in the cellular genome. Hence, our findings reveal that SERINC5's actions in host defense extend beyond blocking virus entry.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	1999-4915 1999-4915
DOI:	10.3390/v15091961