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dc.contributor.authorRex, Devasahayam Arokia Balaya
dc.contributor.authorKeshava Prasad, Thottethodi Subrahmanya
dc.contributor.authorKandasamy, Richard Kumaran
dc.date.accessioned2023-02-06T14:39:20Z
dc.date.available2023-02-06T14:39:20Z
dc.date.created2022-09-22T14:05:32Z
dc.date.issued2022
dc.identifier.citationInternational Journal of Molecular Sciences. 2022, 23 (13), .en_US
dc.identifier.issn1661-6596
dc.identifier.urihttps://hdl.handle.net/11250/3048664
dc.description.abstractThe fate of a viral infection in the host begins with various types of cellular responses, such as abortive, productive, latent, and destructive infections. Apoptosis, necroptosis, and pyroptosis are the three major types of regulated cell death mechanisms that play critical roles in viral infection response. Cell shrinkage, nuclear condensation, bleb formation, and retained membrane integrity are all signs of osmotic imbalance-driven cytoplasmic swelling and early membrane damage in necroptosis and pyroptosis. Caspase-driven apoptotic cell demise is considered in many circumstances as an anti-inflammatory, and some pathogens hijack the cell death signaling routes to initiate a targeted attack against the host. In this review, the selected mechanisms by which viruses interfere with cell death were discussed in-depth and were illustrated by compiling the general principles and cellular signaling mechanisms of virus–host-specific molecule interactions.en_US
dc.language.isoengen_US
dc.publisherMDPIen_US
dc.rightsNavngivelse 4.0 Internasjonal*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/deed.no*
dc.titleRevisiting Regulated Cell Death Responses in Viral Infectionsen_US
dc.title.alternativeRevisiting Regulated Cell Death Responses in Viral Infectionsen_US
dc.typePeer revieweden_US
dc.typeJournal articleen_US
dc.description.versionpublishedVersionen_US
dc.source.pagenumber34en_US
dc.source.volume23en_US
dc.source.journalInternational Journal of Molecular Sciencesen_US
dc.source.issue13en_US
dc.identifier.doi10.3390/ijms23137023
dc.identifier.cristin2054395
dc.relation.projectNorges forskningsråd: 223255en_US
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode1


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