Abstract
Recently, several studies have highlighted a skewed prevalence of infectious diseases within the African continent. Furthermore, a growing number of studies have demonstrated unique genetic variants found within the African genome are one of the contributing factors to the disease severity of infectious diseases within Africa. Understanding the host genetic mechanisms that offer protection against infectious diseases provides an opportunity to develop unique therapeutic interventions. Over the past two decades, several studies have linked the 2'-5'-oligoadenylate synthetase (OAS) family with a range of infectious diseases. More recently, the OAS-1 gene has also been associated with disease severity caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which led to a global pandemic. The OAS family serves as an antiviral factor through the interaction with Ribonuclease-Latent (RNase-L). This review explores the genetic variants observed within the OAS genes and the associations with various viral infections and how previously reported ethnic-specific polymorphisms drive clinical significance. This review provides an overview of OAS genetic association studies with a particular focus on viral diseases affecting individuals of African descent.
Keywords:
OAS; SARS-CoV-2; human genetics; infectious diseases; polymorphisms; viral disease.
Publication types
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Systematic Review
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Review
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Research Support, Non-U.S. Gov't
MeSH terms
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Adenine Nucleotides
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COVID-19*
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Humans
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Oligoribonucleotides
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SARS-CoV-2*
Substances
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2',5'-oligoadenylate
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Adenine Nucleotides
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Oligoribonucleotides
Grants and funding
VR was funded as a FLAIR Research Fellow (the Future Leader in African Independent Research (FLAIR) Fellowship Programme was a partnership between the African Academy of Sciences (AAS) and the Royal Society that was funded by the United Kingdom Government as part of the Global Challenge Research Fund (GCRF) (Grant No. FLAIR-FLR\R1\190204); supported by the South African Medical Research Council (SAMRC) with funds from the Department of Science and Technology (DST). Funding was also provided in part through the Sub-Saharan African Network for TB/HIV Research Excellence (SANTHE), a DELTAS Africa Initiative (Grant No. DEL-15-006) by the AAS. Support was also provided by the Grants, Innovation, and Product Development unit of the South African Medical Research Council with funds received from Novartis and GSK R&D (Grant No. GSKNVS2/202101/005). AG was funded by The Poliomyelitis Research Foundation (PRF) [Grant No. PRF22/77] and CHS Funding, College of Health Science, University of KwaZulu-Natal. TA is funded by South African Medical Research Council Sir Grant and L’ORÉAL UNESCO Women in Science South African Young Talent fellow. The authors declare that this study received funding from Novartis and GSK R&D. The funder was not involved in the study design, collection, analysis, interpretation of data, the writing of this article, or the decision to submit it for publication.