| Autor: |
Leventhal, Shanna S., Bisom, Thomas, Clift, Dean, Rao, Deepashri, Meade-White, Kimberly, Shaia, Carl, Murray, Justin, Mihalakakos, Evan A., Hinkley, Troy, Reynolds, Steven J., Best, Sonja M., Erasmus, Jesse H., James, Leo C., Feldmann, Heinz, Hawman, David W. |
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| Zdroj: |
Nature Communications; 10/25/2024, Vol. 15 Issue 1, p1-14, 14p |
| Abstrakt: |
Crimean-Congo Hemorrhagic Fever Virus (CCHFV) is a negative-sense RNA virus spread by Hyalomma genus ticks across Europe, Asia, and Africa. CCHF disease begins as a non-specific febrile illness which may progress into a severe hemorrhagic disease with no widely approved or highly efficacious interventions currently available. Recently, we reported a self-replicating, alphavirus-based RNA vaccine that expresses the CCHFV nucleoprotein and is protective against lethal CCHFV disease in mice. This vaccine induces high titers of non-neutralizing anti-NP antibodies and we show here that protection does not require Fc-gamma receptors or complement. Instead, vaccinated mice deficient in the intracellular Fc-receptor TRIM21 were unable to control the infection despite mounting robust CCHFV-specific immunity. We also show that passive transfer of NP-immune sera confers significant TRIM21-dependent protection against lethal CCHFV challenge. Together our data identifies TRIM21-mediated mechanisms as the Fc effector function of protective antibodies against the CCHFV NP and provides mechanistic insight into how vaccines against the CCHFV NP confer protection. Non-neutralizing antibodies against the nucleoprotein (NP) of Crimean-Congo hemorrhagic fever virus are protective against lethal challenge in mice. Here, the authors show that these anti-NP antibodies protect through the intracellular antibody receptor TRIM21 and that protection is independent of T cells. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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