Ubiquitin-Mediated Regulation of Autophagy During Viral Infection.

Autor: Nag J; Department of Microbiology & Cell Biology, Indian Institute of Science, Bengaluru, 560012 India.; Centre for Infectious Disease Research, Indian Institute of Science, Bengaluru, 560012 India., Patel J; Department of Microbiology & Cell Biology, Indian Institute of Science, Bengaluru, 560012 India.; Centre for Infectious Disease Research, Indian Institute of Science, Bengaluru, 560012 India., Tripathi S; Department of Microbiology & Cell Biology, Indian Institute of Science, Bengaluru, 560012 India.; Centre for Infectious Disease Research, Indian Institute of Science, Bengaluru, 560012 India.
Jazyk: angličtina
Zdroj: Current clinical microbiology reports [Curr Clin Microbiol Rep] 2023; Vol. 10 (1), pp. 1-8. Date of Electronic Publication: 2023 Jan 13.
DOI: 10.1007/s40588-022-00186-y
Abstrakt: Purpose of Review: Virus infections skew the host autophagic response to meet their replication and transmission demands by tapping into the critical host regulatory mechanisms that control the autophagic flux. This review is a compendium of previous reports highlighting the mechanisms that viruses adapt to hijack the host ubiquitination machinery to repurpose autophagy for their sustenance.
Recent Findings: Emerging evidence suggests a critical role of host ubiquitin machinery in the manifestation of the antiviral or proviral functions of autophagy. Lately, more emphasis has been laid to identify specific host E3 ubiquitin ligases, their targets (viral or host), and characterizing corresponding ubiquitin linkages by biochemical or genome-wide genetic screening approaches.
Summary: Here, we highlight how viruses ingeniously engage and subvert the host ubiquitin-autophagy system to promote virus replication and antagonize intracellular innate immune responses.
Competing Interests: Conflict of InterestThe authors declare no competing interests.
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Databáze: MEDLINE
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