Version 1
: Received: 17 June 2024 / Approved: 17 June 2024 / Online: 18 June 2024 (13:30:58 CEST)
How to cite:
Begum, M. M.; Bokani, A.; Rajib, S. A.; Soleimanpour, M.; Maeda, Y.; Yoshimura, K.; Satou, Y.; Ebrahimi, D.; Ikeda, T. Potential Role of APOBEC3 Family Proteins in SARS-CoV-2 Replication. Preprints2024, 2024061182. https://doi.org/10.20944/preprints202406.1182.v1
Begum, M. M.; Bokani, A.; Rajib, S. A.; Soleimanpour, M.; Maeda, Y.; Yoshimura, K.; Satou, Y.; Ebrahimi, D.; Ikeda, T. Potential Role of APOBEC3 Family Proteins in SARS-CoV-2 Replication. Preprints 2024, 2024061182. https://doi.org/10.20944/preprints202406.1182.v1
Begum, M. M.; Bokani, A.; Rajib, S. A.; Soleimanpour, M.; Maeda, Y.; Yoshimura, K.; Satou, Y.; Ebrahimi, D.; Ikeda, T. Potential Role of APOBEC3 Family Proteins in SARS-CoV-2 Replication. Preprints2024, 2024061182. https://doi.org/10.20944/preprints202406.1182.v1
APA Style
Begum, M. M., Bokani, A., Rajib, S. A., Soleimanpour, M., Maeda, Y., Yoshimura, K., Satou, Y., Ebrahimi, D., & Ikeda, T. (2024). Potential Role of APOBEC3 Family Proteins in SARS-CoV-2 Replication. Preprints. https://doi.org/10.20944/preprints202406.1182.v1
Chicago/Turabian Style
Begum, M. M., Diako Ebrahimi and Terumasa Ikeda. 2024 "Potential Role of APOBEC3 Family Proteins in SARS-CoV-2 Replication" Preprints. https://doi.org/10.20944/preprints202406.1182.v1
Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has acquired multiple mutations since its emergence. Analyses of the SARS-CoV-2 genomes from infected patients exhibit a bias toward C-to-U mutations, which are suggested to be caused by the apolipoprotein B mRNA editing enzyme polypeptide-like 3 (APOBEC3, A3) cytosine deaminase proteins. However, the role of A3 enzymes in SARS-CoV-2 replication remains unclear. To address this question, we investigated the effect of A3 family proteins on SARS-CoV-2 replication in THP-1 cells lacking A3A to A3G genes. The Wuhan, BA.1, and BA.5 variants had comparable viral replication in parent and A3A-to-A3G-null THP-1-ACE2 cells. On the other hand, the replication and infectivity of these variants were abolished in A3A-to-A3G-null THP-1-ACE2 cells in a series of passage experiments over 20 days. In contrast to previous reports, we observed no evidence for A3-induced SARS-CoV-2 mutagenesis in the passage experiments. Furthermore, our analysis of a large number of publicly available SARS-CoV-2 genomes did not reveal conclusive evidence for A3-induced mutagenesis. Taken together, our studies suggest that A3 family proteins can positively contribute to SARS-CoV-2 replication, however this effect is deaminase-independent.
Keywords
APOBEC3 family proteins; SARS-CoV-2; Deaminase-independent mechanism
Subject
Biology and Life Sciences, Virology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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