| Virus Name | Severe Acute Respiratory Syndrome Coronavirus 2 |
| Virus Short Name | SARS CoV-2 |
| Order | Nidovirales |
| Virus Family | Coronaviridae |
| Virus Subfamily | Coronavirinae |
| Genus | Betacoronavirus |
| Species | Betacoronavirus-1 |
| Host | Vertebrates |
| Cell Tropism | Epithelial cells of respiratory or enteric tracts, neurological tissues are also frequently infected |
| Associated Disease | Mainly respiratory diseases |
| Mode of Transmission | Sexual contact, blood, breast feeding |
| VIPR DB link | https://www.viprbrc.org/brc/vipr_search.do?species=Betacoronavirus |
| ICTV DB link | https://ictv.global/report/182/orthocoronavirinae |
| Virus Host DB link |
| Paper Title | SARS-CoV-2 hijacks host CD55, CD59 and factor H to impair antibody-dependent complement-mediated lysis |
| Author's Name | Laura Gebetsberger, Zahra Malekshahi, Aron Teutsch, Gabor Tajti, Frédéric Fontaine, Nara Marella, André Mueller, Lena Prantl, Hannes Stockinger, Heribert Stoiber, Anna Ohradanova-Repic |
| Journal Name | Emerging Microbes & Infections |
| Pubmed ID | 39435487 |
| Abstract | The complement system is a vital anti-microbial defence mechanism against circulating pathogens. Excessive complement activation can have deleterious outcomes for the host and is consequently tightly modulated by a set of membrane-associated and fluid-phase regulators of complement activation (RCAs). Here, we demonstrate that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) hijacks host cellular RCA members CD55 and CD59 and serum-derived Factor H (FH) to resist antibody-dependent complement-mediated lysis triggered by immunized human sera. Blockage of the biological functions of virion-associated CD55 and CD59 and competition of FH recruitment with functionally inactive recombinant FH-derived short consensus repeats SCR18-20 restore SARS-CoV-2 complement sensitivity in a synergistic manner. Moreover, complement-mediated virolysis is dependent on classical pathway activation and does not occur in the absence of virus-specific antibodies. Altogether, our findings present an intriguing immune escape mechanism that provides novel insights into the immunopathology observed in severe coronavirus disease 2019 (COVID-19) |
| Used Model | N/A. |
| DOI | 10.1080/22221751.2024.2417868 |