Since the first emergence of the novel betacoronavirus in October 2019, severe acute respiratory coronavirus 2 (SAR-CoV-2) has been spread to 192 countries in the world. The infection of SARS-CoV-2 involves the binding of viral spike (S) protein to an ACE2 receptor on the surface of target cell. The subsequent cleavage of the S protein by a serine protease, TMPRSS2, primes the infection by allowing fusion of viral and lysosomal membranes. Clinical symptoms of SARS-CoV-2 induced COVID-19 include fever, cough, diarrhea, myalgias, and anosmia, and the severity of COVID-19 are variable, with mild COVID-19 patients typically not required for hospitalization and severe COVID-19 patients more likely to be hospitalized.
Genetic factors have been suggested to contribute to the variation in COVID-19 severity. Two genome-wide association studies (GWAS) of European populations have been conducted on severe COVID-19, however GWAS of severe/mild COVID-19 or asymptotic SARS-CoV2 infection among other populations are still lacking.
Recently identified risk single nucleotide polymorphisms (SNPs) associated with severe COVID-19 were derived from European populations, few of these genetic markers were found or replicated in other populations, including East Asian populations (ASN), African populations (AFR), and so on. Even worse, the biological mechanisms underlying these published COVID-19 association signals are not thoroughly investigated. Furthermore, as severe COVID-19 patients frequently have comorbidities, such as pulmonary diseases and other chronic disorders, many of which are also genetically influenced, it is hard to distinguish whether previously reported significant SNPs are specifically associated with severe COVID-19 or other comorbidities. In addition, SARS-CoV2 infection can induce at least three commonly recognized clinical phenotypes, including severe and mild COVID19, and asymptomatic SARS-CoV2 infection. There is an urgent need to investigate genetic factors that are protective or predispose to different phenotypes of COVID-19 among diverse populations. Our goal is to collect newly performed COVID-19 genetic studies to increase our understanding related to the pathogenicity of COVID-19, which may provide more options for COVID-19 treatment in the future.
(1) Pilot COVID-19 GWAS focused on different phenotypes of COVID-19 or SARS-CoV2 infection in European populations or other populations, including African, Asian and other populations.
(2) GWAS of severe/mild COVID-19 among vaccinated populations.
(3) Functional studies for candidate genes emerged from recently published COVID-19 GWAS of European populations or newly performed pilot COVID-19 GWAS in other populations.
(4) Trans-ancestry genetic studies of COVID-19 associated genes that reveal the common or population-specific biological mechanisms underlying the COVID-19 association.
(5) Investigations of gene associated with both COVID-19 and other comorbidities, including but not limit to pulmonary diseases, obesity, hypertension, neurological disorders, different cancer types, influenza, and tuberculosis.
(6) Integrative analyses of publicly available COVID-19 GWAS summary statistics from the COVID-19 Host Genetic Initiative (HGI) and the UK Biobank. Any novel methods or pipelines for analyzing these COVID-19 data or providing new insights into COVID-19 pathogenicity and treatment would be welcome.
Since the first emergence of the novel betacoronavirus in October 2019, severe acute respiratory coronavirus 2 (SAR-CoV-2) has been spread to 192 countries in the world. The infection of SARS-CoV-2 involves the binding of viral spike (S) protein to an ACE2 receptor on the surface of target cell. The subsequent cleavage of the S protein by a serine protease, TMPRSS2, primes the infection by allowing fusion of viral and lysosomal membranes. Clinical symptoms of SARS-CoV-2 induced COVID-19 include fever, cough, diarrhea, myalgias, and anosmia, and the severity of COVID-19 are variable, with mild COVID-19 patients typically not required for hospitalization and severe COVID-19 patients more likely to be hospitalized.
Genetic factors have been suggested to contribute to the variation in COVID-19 severity. Two genome-wide association studies (GWAS) of European populations have been conducted on severe COVID-19, however GWAS of severe/mild COVID-19 or asymptotic SARS-CoV2 infection among other populations are still lacking.
Recently identified risk single nucleotide polymorphisms (SNPs) associated with severe COVID-19 were derived from European populations, few of these genetic markers were found or replicated in other populations, including East Asian populations (ASN), African populations (AFR), and so on. Even worse, the biological mechanisms underlying these published COVID-19 association signals are not thoroughly investigated. Furthermore, as severe COVID-19 patients frequently have comorbidities, such as pulmonary diseases and other chronic disorders, many of which are also genetically influenced, it is hard to distinguish whether previously reported significant SNPs are specifically associated with severe COVID-19 or other comorbidities. In addition, SARS-CoV2 infection can induce at least three commonly recognized clinical phenotypes, including severe and mild COVID19, and asymptomatic SARS-CoV2 infection. There is an urgent need to investigate genetic factors that are protective or predispose to different phenotypes of COVID-19 among diverse populations. Our goal is to collect newly performed COVID-19 genetic studies to increase our understanding related to the pathogenicity of COVID-19, which may provide more options for COVID-19 treatment in the future.
(1) Pilot COVID-19 GWAS focused on different phenotypes of COVID-19 or SARS-CoV2 infection in European populations or other populations, including African, Asian and other populations.
(2) GWAS of severe/mild COVID-19 among vaccinated populations.
(3) Functional studies for candidate genes emerged from recently published COVID-19 GWAS of European populations or newly performed pilot COVID-19 GWAS in other populations.
(4) Trans-ancestry genetic studies of COVID-19 associated genes that reveal the common or population-specific biological mechanisms underlying the COVID-19 association.
(5) Investigations of gene associated with both COVID-19 and other comorbidities, including but not limit to pulmonary diseases, obesity, hypertension, neurological disorders, different cancer types, influenza, and tuberculosis.
(6) Integrative analyses of publicly available COVID-19 GWAS summary statistics from the COVID-19 Host Genetic Initiative (HGI) and the UK Biobank. Any novel methods or pipelines for analyzing these COVID-19 data or providing new insights into COVID-19 pathogenicity and treatment would be welcome.