tetano
Editor, Senior Moderator
PLoS Pathog
. 2021 Jul 15;17(7):e1009705.
doi: 10.1371/journal.ppat.1009705. eCollection 2021 Jul.
SARS-CoV-2 infection in the Syrian hamster model causes inflammation as well as type I interferon dysregulation in both respiratory and non-respiratory tissues including the heart and kidney
Magen Ellen Francis[SUP] 1 2 [/SUP], Una Goncin[SUP] 3 [/SUP], Andrea Kroeker[SUP] 1 [/SUP], Cynthia Swan[SUP] 1 [/SUP], Robyn Ralph[SUP] 1 4 [/SUP], Yao Lu[SUP] 1 [/SUP], Athema Louise Etzioni[SUP] 5 [/SUP], Darryl Falzarano[SUP] 1 4 [/SUP], Volker Gerdts[SUP] 1 [/SUP], Steven Machtaler[SUP] 3 [/SUP], Jason Kindrachuk[SUP] 1 6 [/SUP], Alyson Ann Kelvin[SUP] 1 7 8 9 [/SUP]
Affiliations
Abstract
COVID-19 (coronavirus disease 2019) caused by SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) infection is a disease affecting several organ systems. A model that captures all clinical symptoms of COVID-19 as well as long-haulers disease is needed. We investigated the host responses associated with infection in several major organ systems including the respiratory tract, the heart, and the kidneys after SARS-CoV-2 infection in Syrian hamsters. We found significant increases in inflammatory cytokines (IL-6, IL-1beta, and TNF) and type II interferons whereas type I interferons were inhibited. Examination of extrapulmonary tissue indicated inflammation in the kidney, liver, and heart which also lacked type I interferon upregulation. Histologically, the heart had evidence of myocarditis and microthrombi while the kidney had tubular inflammation. These results give insight into the multiorgan disease experienced by people with COVID-19 and possibly the prolonged disease in people with post-acute sequelae of SARS-CoV-2 (PASC).
. 2021 Jul 15;17(7):e1009705.
doi: 10.1371/journal.ppat.1009705. eCollection 2021 Jul.
SARS-CoV-2 infection in the Syrian hamster model causes inflammation as well as type I interferon dysregulation in both respiratory and non-respiratory tissues including the heart and kidney
Magen Ellen Francis[SUP] 1 2 [/SUP], Una Goncin[SUP] 3 [/SUP], Andrea Kroeker[SUP] 1 [/SUP], Cynthia Swan[SUP] 1 [/SUP], Robyn Ralph[SUP] 1 4 [/SUP], Yao Lu[SUP] 1 [/SUP], Athema Louise Etzioni[SUP] 5 [/SUP], Darryl Falzarano[SUP] 1 4 [/SUP], Volker Gerdts[SUP] 1 [/SUP], Steven Machtaler[SUP] 3 [/SUP], Jason Kindrachuk[SUP] 1 6 [/SUP], Alyson Ann Kelvin[SUP] 1 7 8 9 [/SUP]
Affiliations
- PMID: 34265022
- DOI: 10.1371/journal.ppat.1009705
Abstract
COVID-19 (coronavirus disease 2019) caused by SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) infection is a disease affecting several organ systems. A model that captures all clinical symptoms of COVID-19 as well as long-haulers disease is needed. We investigated the host responses associated with infection in several major organ systems including the respiratory tract, the heart, and the kidneys after SARS-CoV-2 infection in Syrian hamsters. We found significant increases in inflammatory cytokines (IL-6, IL-1beta, and TNF) and type II interferons whereas type I interferons were inhibited. Examination of extrapulmonary tissue indicated inflammation in the kidney, liver, and heart which also lacked type I interferon upregulation. Histologically, the heart had evidence of myocarditis and microthrombi while the kidney had tubular inflammation. These results give insight into the multiorgan disease experienced by people with COVID-19 and possibly the prolonged disease in people with post-acute sequelae of SARS-CoV-2 (PASC).