Virus ja ihmisen antivirusjärjestelmien yhteissinfoniasta

https://pubmed.ncbi.nlm.nih.gov/34276680/

 

2021 Jul 1;12:690416.   doi: 10.3389/fimmu.2021.690416. eCollection 2021.

AID and APOBECs as Multifaceted Intrinsic Virus-Restricting Factors: Emerging Concepts in the Light of COVID-19

Anastasia Meshcheryakova  ¹ , Peter Pietschmann  ¹ , Philip Zimmermann  ² , Igor B Rogozin  ³ , Diana Mechtcheriakova  ¹

Affiliations

• PMID: 34276680
• PMCID: PMC8282206
• DOI: 10.3389/fimmu.2021.690416

Free PMC article

 Abstract

The AID (activation-induced cytidine deaminase)/APOBEC (apolipoprotein B mRNA editing enzyme catalytic subunit) family with its multifaceted mode of action emerges as potent intrinsic host antiviral system that acts against a variety of DNA and RNA viruses including coronaviruses. All family members are cytosine-to-uracil deaminases that either have a profound role in driving a strong and specific humoral immune response (AID) or restricting the virus itself by a plethora of mechanisms (APOBECs). In this article, we highlight some of the key aspects apparently linking the AID/APOBECs and SARS-CoV-2. Among those is our discovery that APOBEC4 shows high expression in cell types and anatomical parts targeted by SARS-CoV-2. Additional focus is given by us to the lymphoid structures and AID as the master regulator of germinal center reactions, which result in antibody production by plasma and memory B cells. We propose the dissection of the AID/APOBECs gene signature towards decisive determinants of the patient-specific and/or the patient group-specific antiviral response. Finally, the patient-specific mapping of the AID/APOBEC polymorphisms should be considered in the light of COVID-19.

Keywords: AID; AID/APOBECs gene expression signature; APOBEC4; APOBECs; COVID-19; SARS-CoV-2; germinal center; lymphoid structures. 

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