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Yunus M. Siddiqui

Researcher at Alfaisal University

Publications -  15
Citations -  460

Yunus M. Siddiqui is an academic researcher from Alfaisal University. The author has contributed to research in topics: Virus & Interferon. The author has an hindex of 11, co-authored 15 publications receiving 445 citations. Previous affiliations of Yunus M. Siddiqui include King Faisal Specialist Hospital & Research Centre.

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The α Chemokine, Interleukin 8, Inhibits the Antiviral Action of Interferon α

TL;DR: In an in vitro cytopathic effect assay for IFN, it is found that IL-8 can inhibit IFN-α activity in a dose-dependent manner and was associated with reduced 2′,5′-A oligoadenylate synthetase activity, a pathway well correlative with the anti– encephalomyocarditis virus action of IFN -α.
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Effect of deficiency of the double-stranded RNA-dependent protein kinase, PKR, on antiviral resistance in the presence or absence of ribonuclease L: HSV-1 replication is particularly sensitive to deficiency of the major IFN-mediated enzymes.

TL;DR: Results showed that PKR is an important mediator in constitutive resistance against HSV-1 and that RNAse L is also necessary for the full antiviral activity of IFN against a variety of viruses, and supported the existence of novel pathways aimed toward specific stages of the virus life cycle.
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RNase L mediates transient control of the interferon response through modulation of the double-stranded RNA-dependent protein kinase PKR

TL;DR: It is shown that the transient nature of the IFN response against acute viral infections is regulated, at least in part, by RNase L, and a role forRNase L in the transient control of theIFN response and possibly of other cytokine and stress responses is suggested.
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Interleukin-8 selectively enhances cytopathic effect (CPE) induced by positive-strand RNA viruses in the human WISH cell line.

TL;DR: It is found that IL-8 enhanced cytopathic effect induced by the positive strand RNA virus, encephalomyocarditis virus (EMCV), in the human WISH cell line, and the activity of constitutive 2',5'-oligoadenylate synthetase (OAS), a pathway that was implicated in protection from EMCV but not VSV, was examined.