PMC:7307149 / 2845-6008 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7307149","sourcedb":"PMC","sourceid":"7307149","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7307149","text":"INTRODUCTION\nRecently, a new strain of betacoronavirus (severe acute respiratory syndrome coronavirus 2, or SARS-CoV-2) emerged as a global pathogen, prompting the World Health Organization in January 2020 to declare an international public health emergency (1). In the large coronavirus family, comprising enveloped positive-strand RNA viruses, SARS-CoV-2 is the seventh encountered strain that causes respiratory disease in humans (2) ranging from mild—the common cold—to severe—disease caused by the zoonotic Middle East respiratory syndrome coronavirus (MERS-CoV) and severe acute respiratory syndrome coronavirus (SARS-CoV). As of April 2020, there are over one million presumed or confirmed cases of coronavirus disease 19 (COVID-19) worldwide, with total deaths exceeding 50,000 (3). While age and many comorbidities, including cardiovascular and pulmonary disease, appear to increase the severity and mortality of COVID-19 (4–9), approximately 80% of infected individuals have mild symptoms (10). As with SARS-CoV (11, 12) and MERS-CoV (13, 14), children seem to have low susceptibility to the disease (15–17); despite infection rates similar to those seen with adults (18), only 5.9% of pediatric cases are severe or critical, possibly due to lower binding ability of the ACE2 receptor in children or generally higher levels of antiviral antibodies (19). Other similarities (20–22), including genomic (23, 24) and immune system response (25–33) similarities, between SARS-CoV-2 and other coronaviruses (34), especially SARS-CoV and MERS-CoV, are topics of ongoing active research, results of which may inform an understanding of the severity of infection (35) and improve the ongoing work of immune landscape profiling (36–40) and vaccine discovery (28, 37, 41–48).\nHuman leukocyte antigen (HLA) alleles, which are critical components of the viral antigen presentation pathway, have been shown in previous studies to confer differential viral susceptibility and severity of disease. For instance, disease caused by the closely related SARS-CoV (23, 24) shows increased severity among individuals with the HLA-B*46:01 genotype (49). Associations between HLA genotype and disease severity extend broadly to several other unrelated viruses. For example, in human immunodeficiency virus 1 (HIV-1), certain HLA types (e.g., HLA-A*02:05) may reduce risk of seroconversion (50), and in dengue virus, certain HLA alleles (e.g., HLA-A*02:07 and HLA-B*51) are associated with increased secondary disease severity among ethnic Thais (51).\nWhile the details of the clinical picture of the COVID-19 pandemic continue to emerge, there remain substantial unanswered questions regarding the role of individual genetic variability in the immune response against SARS-CoV-2 (51). We hypothesize that individual HLA genotypes may differentially induce the T-cell mediated antiviral response and could potentially alter the course of disease and its transmission. In this study, we performed a comprehensive in silico analysis of viral peptide-major histocompatibility complex (MHC) class I binding affinity across 145 different HLA types for the entire SARS-CoV-2 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