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10.1096/fj.202001115R

http://scihub22266oqcxt.onion/10.1096/fj.202001115R
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suck abstract from ncbi


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pmid32525600      FASEB+J 2020 ; 34 (7): 8787-8795
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  • Genetic gateways to COVID-19 infection: Implications for risk, severity, and outcomes #MMPMID32525600
  • Debnath M; Banerjee M; Berk M
  • FASEB J 2020[Jul]; 34 (7): 8787-8795 PMID32525600show ga
  • The dynamics, such as transmission, spatial epidemiology, and clinical course of Coronavirus Disease-2019 (COVID-19) have emerged as the most intriguing features and remain incompletely understood. The genetic landscape of an individual in particular, and a population in general seems to play a pivotal role in shaping the above COVID-19 dynamics. Considering the implications of host genes in the entry and replication of SARS-CoV-2 and in mounting the host immune response, it appears that multiple genes might be crucially involved in the above processes. Herein, we propose three potentially important genetic gateways to COVID-19 infection; these could explain at least in part the discrepancies of its spread, severity, and mortality. The variations within Angiotensin-converting enzyme 2 (ACE2) gene might constitute the first genetic gateway, influencing the spatial transmission dynamics of COVID-19. The Human Leukocyte Antigen locus, a master regulator of immunity against infection seems to be crucial in influencing susceptibility and severity of COVID-19 and can be the second genetic gateway. The genes regulating Toll-like receptor and complement pathways and subsequently cytokine storm induced exaggerated inflammatory pathways seem to underlie the severity of COVID-19, and such genes might represent the third genetic gateway. Host-pathogen interaction is a complex event and some additional genes might also contribute to the dynamics of COVID-19. Overall, these three genetic gateways proposed here might be the critical host determinants governing the risk, severity, and outcome of COVID-19. Genetic variations within these gateways could be key in influencing geographical discrepancies of COVID-19.
  • |*Pandemics[MESH]
  • |Angiotensin-Converting Enzyme 2[MESH]
  • |Betacoronavirus/*physiology[MESH]
  • |COVID-19[MESH]
  • |Complement Activation/*genetics[MESH]
  • |Coronavirus Infections/complications/*genetics/immunology/transmission[MESH]
  • |Cytokine Release Syndrome/etiology/genetics[MESH]
  • |Disease Resistance/immunology[MESH]
  • |Genetic Predisposition to Disease[MESH]
  • |Genetic Variation[MESH]
  • |HLA Antigens/*genetics/immunology[MESH]
  • |Host-Pathogen Interactions/*genetics/immunology[MESH]
  • |Humans[MESH]
  • |Inflammation[MESH]
  • |Metagenomics[MESH]
  • |Mutation, Missense[MESH]
  • |Peptidyl-Dipeptidase A/*genetics/physiology[MESH]
  • |Pneumonia, Viral/complications/*genetics/immunology/transmission[MESH]
  • |Prognosis[MESH]
  • |Quantitative Trait Loci[MESH]
  • |Racial Groups/genetics[MESH]
  • |Receptors, Virus/*genetics/physiology[MESH]
  • |Risk[MESH]
  • |SARS-CoV-2[MESH]
  • |Toll-Like Receptors/*genetics/immunology[MESH]


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