Coronavirus Interplay With Lipid Rafts and Autophagy Unveils Promising Therapeutic Targets.

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The plasma membrane microdomain lipid rafts have been found by researchers to be involved in the replication cycle of numerous viruses, including coronaviruses. Indeed, some pathogen recognition receptors for coronaviruses as for other viruses cluster into lipid rafts, and it is therefore conceivable that the first contact between virus and host cells occurs into these specialized regions, representing a port of cell entry for viruses. Recent data highlighted the peculiar pro-viral or anti-viral role played by autophagy in the host immune responses to viral infections. Coronaviruses, like other viruses, were reported to be able to exploit the autophagic machinery to increase their replication or to inhibit the degradation of viral products. Agents known to disrupt lipid rafts, such as metil-β-cyclodextrins or statins, as well as autophagy inhibitor agents, were shown to have an anti-viral role. In this review, we briefly describe the involvement of lipid rafts and autophagy in coronavirus infection and replication. We also hint how lipid rafts and autophagy may represent a potential therapeutic target to be investigated for the treatment of coronavirus infections.

During co-evolution with their natural hosts, viruses developed the ability to hijack autophagic mechanisms to their advantage by using them for immune escaping, or using autophagosomes as a replicative niche. However, data on autophagy interplay with coronaviruses are scant so far, related on no more than 50 works published between 2004 and 2015. In general, it is suggested that CoVs can interact with some components of the autophagic pathway in an opposite way with a dual effect: utilizing autophagy components to promote viral replication and/or to inhibit degradation of viral products through the autophagic pathway.

Fecchi K, Anticoli S, Peruzzu D, et al. Coronavirus Interplay With Lipid Rafts and Autophagy Unveils Promising Therapeutic Targets. Front Microbiol. 2020;11:1821. Published 2020 Aug 11. doi:10.3389/fmicb.2020.01821

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