SARS-CoV-2 Mac1 is required for IFN antagonism and efficient virus replication in cell culture and in mice Article Swipe
Yousef M. Alhammad
,
Srivatsan Parthasarathy
,
Roshan Ghimire
,
Catherine M. Kerr
,
Joseph J. O’Connor
,
Jessica J. Pfannenstiel
,
Debarati Chanda
,
Caden A. Miller
,
Nathalie Baumlin
,
Matthias Salathé
,
Robert L. Unckless
,
Sonia Zúñiga
,
Luis Enjuanes
,
Sunil More
,
Rudragouda Channappanavar
,
Anthony R. Fehr
·
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.1073/pnas.2302083120
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.1073/pnas.2302083120
Several coronavirus (CoV) encoded proteins are being evaluated as targets for antiviral therapies for COVID-19. Included in these drug targets is the conserved macrodomain, or Mac1, an ADP-ribosylhydrolase and ADP-ribose binding protein encoded as a small domain at the N terminus of nonstructural protein 3. Utilizing point mutant recombinant viruses, Mac1 was shown to be critical for both murine hepatitis virus (MHV) and severe acute respiratory syndrome (SARS)-CoV virulence. However, as a potential drug target, it is imperative to understand how a complete Mac1 deletion impacts the replication and pathogenesis of different CoVs. To this end, we created recombinant bacterial artificial chromosomes (BACs) containing complete Mac1 deletions (ΔMac1) in MHV, MERS-CoV, and SARS-CoV-2. While we were unable to recover infectious virus from MHV or MERS-CoV ΔMac1 BACs, SARS-CoV-2 ΔMac1 was readily recovered from BAC transfection, indicating a stark difference in the requirement for Mac1 between different CoVs. Furthermore, SARS-CoV-2 ΔMac1 replicated at or near wild-type levels in multiple cell lines susceptible to infection. However, in a mouse model of severe infection, ΔMac1 was quickly cleared causing minimal pathology without any morbidity. ΔMac1 SARS-CoV-2 induced increased levels of interferon (IFN) and IFN-stimulated gene expression in cell culture and mice, indicating that Mac1 blocks IFN responses which may contribute to its attenuation. ΔMac1 infection also led to a stark reduction in inflammatory monocytes and neutrophils. These results demonstrate that Mac1 only minimally impacts SARS-CoV-2 replication, unlike MHV and MERS-CoV, but is required for SARS-CoV-2 pathogenesis and is a unique antiviral drug target.
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Metadata
- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1073/pnas.2302083120
- OA Status
- green
- Cited By
- 53
- References
- 75
- Related Works
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- OpenAlex ID
- https://openalex.org/W4386065929
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4386065929Canonical identifier for this work in OpenAlex
- DOI
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https://doi.org/10.1073/pnas.2302083120Digital Object Identifier
- Title
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SARS-CoV-2 Mac1 is required for IFN antagonism and efficient virus replication in cell culture and in miceWork title
- Type
-
articleOpenAlex work type
- Language
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enPrimary language
- Publication year
-
2023Year of publication
- Publication date
-
2023-08-22Full publication date if available
- Authors
-
Yousef M. Alhammad, Srivatsan Parthasarathy, Roshan Ghimire, Catherine M. Kerr, Joseph J. O’Connor, Jessica J. Pfannenstiel, Debarati Chanda, Caden A. Miller, Nathalie Baumlin, Matthias Salathé, Robert L. Unckless, Sonia Zúñiga, Luis Enjuanes, Sunil More, Rudragouda Channappanavar, Anthony R. FehrList of authors in order
- Landing page
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https://doi.org/10.1073/pnas.2302083120Publisher landing page
- Open access
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YesWhether a free full text is available
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greenOpen access status per OpenAlex
- OA URL
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https://pmc.ncbi.nlm.nih.gov/articles/PMC10468617/pdf/pnas.202302083.pdfDirect OA link when available
- Concepts
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Virology, Biology, Recombinant DNA, Breakpoint, Virus, Viral replication, Gene, Mutant, Pathogenesis, Genetics, Immunology, Chromosomal translocationTop concepts (fields/topics) attached by OpenAlex
- Cited by
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53Total citation count in OpenAlex
- Citations by year (recent)
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2025: 22, 2024: 19, 2023: 12Per-year citation counts (last 5 years)
- References (count)
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75Number of works referenced by this work
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-
10Other works algorithmically related by OpenAlex
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