tetano
Editor, Senior Moderator
Front Immunol
. 2020 Jun 30;11:1606.
doi: 10.3389/fimmu.2020.01606. eCollection 2020.
Deciphering the Role of Host Genetics in Susceptibility to Severe COVID-19
Madalina Elena Carter-Timofte[SUP] 1 2 [/SUP], Sofie Eg J?rgensen[SUP] 1 2 [/SUP], Mette Ratzer Freytag[SUP] 1 2 [/SUP], Michelle M?lgaard Thomsen[SUP] 1 2 [/SUP], Nanna-Sophie Brinck Andersen[SUP] 1 2 [/SUP], Ali Al-Mousawi[SUP] 1 2 [/SUP], Alon Schneider Hait[SUP] 1 2 [/SUP], Trine H Mogensen[SUP] 1 2 3 [/SUP]
Affiliations
Abstract
Coronavirus disease-19 (COVID-19) describes a set of symptoms that develop following infection by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Whilst COVID-19 disease is most serious in patients with significant co-morbidities, the reason for healthy individuals succumbing to fulminant infection is largely unexplained. In this review, we discuss the most recent findings in terms of clinical features and the host immune response, and suggest candidate immune pathways that may be compromised in otherwise healthy individuals with fulminating COVID-19. On the basis of this early knowledge we reason a potential genetic effect on host immune response pathways leading to increased susceptibility to SARS-CoV-2 infection. Understanding these pathways may help not only in unraveling disease pathogenesis, but also in suggesting targets for therapy and prophylaxis. Importantly such insight should instruct efforts to identify those at increased risk in order to institute preventative measures, such as prophylactic medication and/or vaccination, when such opportunities arise in the later phases of the current pandemic or during future similar pandemics.
Keywords: SARS-coronavirus 2; host immune defenses; immunopathology; innate immunity; primary immunodeficiency; whole exome sequencing.
. 2020 Jun 30;11:1606.
doi: 10.3389/fimmu.2020.01606. eCollection 2020.
Deciphering the Role of Host Genetics in Susceptibility to Severe COVID-19
Madalina Elena Carter-Timofte[SUP] 1 2 [/SUP], Sofie Eg J?rgensen[SUP] 1 2 [/SUP], Mette Ratzer Freytag[SUP] 1 2 [/SUP], Michelle M?lgaard Thomsen[SUP] 1 2 [/SUP], Nanna-Sophie Brinck Andersen[SUP] 1 2 [/SUP], Ali Al-Mousawi[SUP] 1 2 [/SUP], Alon Schneider Hait[SUP] 1 2 [/SUP], Trine H Mogensen[SUP] 1 2 3 [/SUP]
Affiliations
- PMID: 32695122
- PMCID: PMC7338588
- DOI: 10.3389/fimmu.2020.01606
Abstract
Coronavirus disease-19 (COVID-19) describes a set of symptoms that develop following infection by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Whilst COVID-19 disease is most serious in patients with significant co-morbidities, the reason for healthy individuals succumbing to fulminant infection is largely unexplained. In this review, we discuss the most recent findings in terms of clinical features and the host immune response, and suggest candidate immune pathways that may be compromised in otherwise healthy individuals with fulminating COVID-19. On the basis of this early knowledge we reason a potential genetic effect on host immune response pathways leading to increased susceptibility to SARS-CoV-2 infection. Understanding these pathways may help not only in unraveling disease pathogenesis, but also in suggesting targets for therapy and prophylaxis. Importantly such insight should instruct efforts to identify those at increased risk in order to institute preventative measures, such as prophylactic medication and/or vaccination, when such opportunities arise in the later phases of the current pandemic or during future similar pandemics.
Keywords: SARS-coronavirus 2; host immune defenses; immunopathology; innate immunity; primary immunodeficiency; whole exome sequencing.