Cytidine deamination-induced perpetual immunity to SAR-CoV-2 infection is a potential new therapeutic target

Abstract

As the world is racing to develop perpetual immunity to the SARS-CoV-2 virus. The emergence of new viral strains, together with vaccination and reinfections, are all contributing to a long-term immunity against the deadly virus that has taken over the world since its introduction to humans in late December 2019. The discovery that more than 95 percent of people who recovered from COVID-19 had long-lasting immunity and that asymptomatic people have a different immune response to SARS-CoV-2 than symptomatic people has shifted attention to how our immune system initiates such diverse responses. These findings have provided reason to believe that SARS-CoV-2 days are numbered. Hundreds of research papers have been published on the causes of long-lasting immune responses and variations in the numbers of different immune cell types in COVID 19 survivors, but the main reason of these differences has still not been adequately identified. In this article, we focus on the activation-induced cytidine deaminase (AID), which initiates molecular processes that allow our immune system to generate antibodies against SARS-CoV-2. To establish lasting immunity to SARS-CoV-2, we suggest that AID could be the key to unlocking it.

Nucleoside‐Based Drug Target with General Antimicrobial Screening and Specific Computational Studies against SARS‐CoV‐2 Main Protease

“…Furthermore, these derivatives interacted with similar residues on RdRp, suggesting that the high electron density associated with aromatic substituents could enhance the binding capabilities and antiviral potential of cytidine derivatives (Figure 13). [194] In this study, the stabilities of the complexes formed between RdRp and the compound of interest were assessed via a 200 ns molecular dynamics simulation (RMSD). Notably, the RMSD of the RdRp-compound 138 complex was somewhat greater than that of the other complexes (Figure 14).…”

“…Furthermore, these derivatives interacted with similar residues on RdRp, suggesting that the high electron density associated with aromatic substituents could enhance the binding capabilities and antiviral potential of cytidine derivatives (Figure 13). [194] …”

Host-mediated RNA editing in viruses

“…4). Among the APOBECs, AID is the key initiation factor of the host humoral immune response against SARS-CoV-2 [66], while APO-BEC1 and APOBEC3A, especially APOBEC3A, are likely to be responsible for C-to-U transformation and make a proviral effect by facilitating replication and propagation of SARS-CoV-2 [67]. Moreover, APOBEC-1 complementation factor (A1CF), a partner of APOBEC1, can interact with SARS-CoV-2 RNAs directly and specifically [68].…”

Methodologies to Isolate and Purify Clinical Grade Extracellular Vesicles for Medical Applications

“…miRNA-133a, miRNA-143/145, miRNA-150, miRNA-155, miRNA-214, miRNA-223, and miRNA320b in exosomes are considered as markers of arthrosclerosis (AS) [ 131 , 132 ]. Several proteins are suggested as biomarkers of AS, including integrins derived from exosomes secreted via macrophage foam cell [ 133 ], PSMA6 (prostate-specific membrane antigen), PSMA7, and annexin A2 in blood exosomes originated from innate immune system cells [ 21 , 134 ] and VCAM-1 (vascular cell adhesion molecule 1) and eNOS (endothelial constitutive nitric oxide synthase) identified in plasma endothelial cell-derived exosome [ 131 , 135 ].…”

“…Extracellular vesicles inherit their characteristics and content from their parent cells. Therefore, clarifying their characteristics can be used for the diagnosis and prognosis of various conditions [ 18 , 19 , 20 , 21 ].…”