Differential modulation of SARS-CoV-2 infection by complement factor H and properdin
These results imply that FH may function as a SARS-CoV-2 cell entry and binding inhibitor, reducing the inflammatory response linked to infection independently of complement activation. FP could aid cell viral entry and binding and aggravate hyperinflammation that might contribute to the severity of the infection.
Authors
- Taruna Madan (ORCID: https://orcid.org/0000-0003-2826-2443)
- Anthony G. Tsolaki (ORCID: https://orcid.org/0000-0003-1940-3144)
- Basel K. al-Ramadi (ORCID: https://orcid.org/0000-0002-1657-1938)
- Pretty Ponnachan (ORCID: https://orcid.org/0009-0004-2452-9539)
- Chandan Kumar (ORCID: https://orcid.org/0000-0003-1212-8418)
- Susan Idicula‐Thomas (ORCID: https://orcid.org/0000-0003-3766-6757)
- Khaled Masmoudi (ORCID: https://orcid.org/0000-0002-4408-1207)
- Manu Vatish (ORCID: https://orcid.org/0000-0002-6012-2574)
- Martin Mayora Neto (ORCID: https://orcid.org/0000-0002-5331-5554)
- Uday Kishore (ORCID: https://orcid.org/0000-0002-6033-6759)
- Nigel James Temperton (ORCID: https://orcid.org/0000-0002-7978-3815)
- Nazar Beirag
- Praveen M. Varghese (ORCID: https://orcid.org/0000-0001-9502-378X)
Institutions
- National Institute for Research in Reproductive Health (IN)
- Medway School of Pharmacy (GB)
- United Arab Emirates University (AE)
- University of Oxford (GB)
- Brunel University of London (GB)
- Umeå University (SE)
- Zayed University (AE)
Publication Details
- Journal
- Frontiers in Immunology
- Published
- 2025-08-15
- DOI
- https://doi.org/10.3389/fimmu.2025.1620229
- Primary Topic
- COVID-19 Clinical Research Studies
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- Wellcome Trust
- United Arab Emirates University