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10.1016/j.virusres.2020.198163

http://scihub22266oqcxt.onion/10.1016/j.virusres.2020.198163
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32918943!7480444!32918943
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suck abstract from ncbi

pmid32918943      Virus+Res 2020 ; 289 (?): 198163
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  • The role of host genetics in susceptibility to severe viral infections in humans and insights into host genetics of severe COVID-19: A systematic review #MMPMID32918943
  • Elhabyan A; Elyaacoub S; Sanad E; Abukhadra A; Elhabyan A; Dinu V
  • Virus Res 2020[Nov]; 289 (?): 198163 PMID32918943show ga
  • BACKGROUND: Susceptibility to severe viral infections was reported to be associated with genetic variants in immune response genes using case reports and GWAS studies. SARS-CoV-2 is an emergent viral disease that caused millions of COVID-19 cases all over the world. Around 15 % of cases are severe and some of them are accompanied by dysregulated immune system and cytokine storm. There is increasing evidence that severe manifestations of COVID-19 might be attributed to human genetic variants in genes related to immune deficiency and or inflammasome activation (cytokine storm). OBJECTIVE: Identify the candidate genes that are likely to aid in explaining severe COVID-19 and provide insights to understand the pathogenesis of severe COVID-19. METHODS: In this article, we systematically reviewed genes related to viral susceptibility that were reported in human genetic studies (Case-reports and GWAS) to understand the role of host viral interactions and to provide insights into the pathogenesis of severe COVID-19. RESULTS: We found 40 genes associated with viral susceptibility and 21 of them were associated with severe SARS-CoV disease and severe COVID-19. Some of those genes were implicated in TLR pathways, others in C-lectin pathways, and others were related to inflammasome activation (cytokine storm). CONCLUSION: This compilation represents a list of candidate genes that are likely to aid in explaining severe COVID-19 which are worthy of inclusion in gene panels and during meta-analysis of different variants in host genetics studies of COVID-19. In addition, we provide several hypotheses for severe COVID-19 and possible therapeutic targets.
  • |*Betacoronavirus[MESH]
  • |*Pandemics[MESH]
  • |Adolescent[MESH]
  • |Adult[MESH]
  • |Age Factors[MESH]
  • |Alleles[MESH]
  • |COVID-19[MESH]
  • |COVID-19 Drug Treatment[MESH]
  • |Coronavirus Infections/drug therapy/*genetics[MESH]
  • |Genetic Predisposition to Disease[MESH]
  • |Genome-Wide Association Study[MESH]
  • |Host-Pathogen Interactions/genetics[MESH]
  • |Humans[MESH]
  • |Inflammasomes/genetics[MESH]
  • |Lectins/genetics[MESH]
  • |Middle Aged[MESH]
  • |Models, Genetic[MESH]
  • |Molecular Targeted Therapy[MESH]
  • |Mutation[MESH]
  • |Pneumonia, Viral/*genetics[MESH]
  • |Polymorphism, Single Nucleotide[MESH]
  • |SARS-CoV-2[MESH]
  • |Severe Acute Respiratory Syndrome/genetics[MESH]
  • |Signal Transduction/genetics[MESH]
  • |Toll-Like Receptor 3/genetics[MESH]
  • |Toll-Like Receptors/genetics[MESH]
  • |Virus Diseases/genetics[MESH]


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