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Haris Mirza

Researcher at Yale University

Publications -  22
Citations -  1011

Haris Mirza is an academic researcher from Yale University. The author has contributed to research in topics: Blastocystis & Medicine. The author has an hindex of 10, co-authored 17 publications receiving 533 citations. Previous affiliations of Haris Mirza include Agency for Science, Technology and Research & National University of Singapore.

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Inflammasome activation in infected macrophages drives COVID-19 pathology

TL;DR: In this article , the authors showed that SARS-CoV-2 infection and replication in lung resident human macrophages is a critical driver of lung pathology, as inhibition of the NLRP3 inflammasome pathway reversed chronic lung pathology.
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Current Views on the Clinical Relevance of Blastocystis spp.

TL;DR: The controversial pathogenesis of Blastocystis is attributed to subtype variations in virulence; although current studies seem to support this idea, evidence suggests other factors also contribute to the clinical outcome of the infection.
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Inflammasome activation in infected macrophages drives COVID-19 pathology

TL;DR: In this paper , the authors showed that SARS-CoV-2 infection and replication in lung resident human macrophages is a critical driver of lung pathology, as inhibition of the NLRP3 inflammasome pathway reversed chronic lung pathology.
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A Rapid, High-Throughput Viability Assay for Blastocystis spp. Reveals Metronidazole Resistance and Extensive Subtype-Dependent Variations in Drug Susceptibilities

TL;DR: The need to reevaluate established treatment regimens for Blastocystis infections and offer clear new treatment options for Mz treatment failures is highlighted and the first study to report extensive variations in drug sensitivities among two clinically important subtypes is reported.
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Blastocystis exhibits inter- and intra-subtype variation in cysteine protease activity

TL;DR: Differences in virulence between Blastocystis subtypes have been reported recently in both animal models and clinical studies, although cellular mechanisms for these differences are currently unknown.