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 / APOBEC s 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.
【저자키워드】 COVID-19, SARS-CoV-2, Germinal center, AID, APOBECs, APOBEC4, AID/APOBECs gene expression signature, lymphoid structures, 【초록키워드】 viruses, Structure, Coronaviruses, Antiviral, polymorphism, memory B cells, virus, mRNA, Apolipoprotein B, APOBEC, plasma, Germinal center, Cytidine deaminase, humoral immune response, expression, mechanism, APOBEC4, antiviral response, master regulator, antibody production, cell types, cell type, family members, focus, cytidine, cytosine, determinant, Reactions, subunit, enzyme, plethora, uracil, lymphoid, Dissection, driving, gene signature, Host, DNA and RNA, highlight, intrinsic, virus, the patient, anatomical, variety, catalytic, 【제목키워드】 LIGHT, concept,