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S100A8 and S100A9, biomarkers of SARS-Cov2-infected patients, suppress HIV replication in primary macrophages

Raphael M. Oguariri, Terrence W. Brann, Joseph W. Adelsberger, Qian Chen, Suranjana Goswami, Anthony R. Mele, Tomozumi Imamichi
doi: https://doi.org/10.1101/2021.10.20.464686
Raphael M. Oguariri
1Laboratory of Human Retrovirology and Immunoinformatics, Frederick National Laboratory for Cancer Research, Frederick MD, 21702, USA
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Terrence W. Brann
1Laboratory of Human Retrovirology and Immunoinformatics, Frederick National Laboratory for Cancer Research, Frederick MD, 21702, USA
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Joseph W. Adelsberger
2AIDS monitoring Laboratory, Frederick National Laboratory for Cancer Research, Frederick MD, 21702, USA
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Qian Chen
1Laboratory of Human Retrovirology and Immunoinformatics, Frederick National Laboratory for Cancer Research, Frederick MD, 21702, USA
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Suranjana Goswami
1Laboratory of Human Retrovirology and Immunoinformatics, Frederick National Laboratory for Cancer Research, Frederick MD, 21702, USA
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Anthony R. Mele
1Laboratory of Human Retrovirology and Immunoinformatics, Frederick National Laboratory for Cancer Research, Frederick MD, 21702, USA
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Tomozumi Imamichi
1Laboratory of Human Retrovirology and Immunoinformatics, Frederick National Laboratory for Cancer Research, Frederick MD, 21702, USA
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  • For correspondence: timamichi@mail.nih.gov
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Abstract

S100A8 and S100A9 are members of the Alarmin family; these proteins are abundantly expressed in neutrophils and form a heterodimer complex. Recently, both proteins were identified as novel biomarkers of SARS-CoV-2 infection and were shown to play key roles in inducing an aggressive inflammatory response by mediating the release of large amounts of pro-inflammatory cytokines, called the “cytokine storm.” Although co-infection with SARS-CoV-2 in people living with HIV-1 may result in an immunocompromised status, the role of the S100A8/A9 complex in HIV-1 replication in primary T cells and macrophages is still unclear. Here, we evaluated the roles of the proteins in HIV replication to elucidate their functions. We found that the complex had no impact on virus replication in both cell types; however, the subunits of S100A8 and S100A9 inhibits HIV in macrophages. These findings provide important insights into the regulation of HIV viral loads in SARS-CoV2 co-infection.

Competing Interest Statement

The authors have declared no competing interest.

Copyright 
The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY 4.0 International license.
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Posted October 21, 2021.
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S100A8 and S100A9, biomarkers of SARS-Cov2-infected patients, suppress HIV replication in primary macrophages
Raphael M. Oguariri, Terrence W. Brann, Joseph W. Adelsberger, Qian Chen, Suranjana Goswami, Anthony R. Mele, Tomozumi Imamichi
bioRxiv 2021.10.20.464686; doi: https://doi.org/10.1101/2021.10.20.464686
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S100A8 and S100A9, biomarkers of SARS-Cov2-infected patients, suppress HIV replication in primary macrophages
Raphael M. Oguariri, Terrence W. Brann, Joseph W. Adelsberger, Qian Chen, Suranjana Goswami, Anthony R. Mele, Tomozumi Imamichi
bioRxiv 2021.10.20.464686; doi: https://doi.org/10.1101/2021.10.20.464686

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