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10.1128/JVI.00985-20

http://scihub22266oqcxt.onion/10.1128/JVI.00985-20
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32699094!7495371!32699094
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suck abstract from ncbi


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pmid32699094      J+Virol 2020 ; 94 (19): ä
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  • Type I and Type III Interferons Restrict SARS-CoV-2 Infection of Human Airway Epithelial Cultures #MMPMID32699094
  • Vanderheiden A; Ralfs P; Chirkova T; Upadhyay AA; Zimmerman MG; Bedoya S; Aoued H; Tharp GM; Pellegrini KL; Manfredi C; Sorscher E; Mainou B; Lobby JL; Kohlmeier JE; Lowen AC; Shi PY; Menachery VD; Anderson LJ; Grakoui A; Bosinger SE; Suthar MS
  • J Virol 2020[Sep]; 94 (19): ä PMID32699094show ga
  • The newly emerged human coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has caused a pandemic of respiratory illness. Current evidence suggests that severe cases of SARS-CoV-2 are associated with a dysregulated immune response. However, little is known about how the innate immune system responds to SARS-CoV-2. In this study, we modeled SARS-CoV-2 infection using primary human airway epithelial (pHAE) cultures, which are maintained in an air-liquid interface. We found that SARS-CoV-2 infects and replicates in pHAE cultures and is directionally released on the apical, but not basolateral, surface. Transcriptional profiling studies found that infected pHAE cultures had a molecular signature dominated by proinflammatory cytokines and chemokine induction, including interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-alpha), and CXCL8, and identified NF-kappaB and ATF-4 as key drivers of this proinflammatory cytokine response. Surprisingly, we observed a complete lack of a type I or III interferon (IFN) response to SARS-CoV-2 infection. However, pretreatment and posttreatment with type I and III IFNs significantly reduced virus replication in pHAE cultures that correlated with upregulation of antiviral effector genes. Combined, our findings demonstrate that SARS-CoV-2 does not trigger an IFN response but is sensitive to the effects of type I and III IFNs. Our studies demonstrate the utility of pHAE cultures to model SARS-CoV-2 infection and that both type I and III IFNs can serve as therapeutic options to treat COVID-19 patients.IMPORTANCE The current pandemic of respiratory illness, COVID-19, is caused by a recently emerged coronavirus named SARS-CoV-2. This virus infects airway and lung cells causing fever, dry cough, and shortness of breath. Severe cases of COVID-19 can result in lung damage, low blood oxygen levels, and even death. As there are currently no vaccines approved for use in humans, studies of the mechanisms of SARS-CoV-2 infection are urgently needed. Our research identifies an excellent system to model SARS-CoV-2 infection of the human airways that can be used to test various treatments. Analysis of infection in this model system found that human airway epithelial cell cultures induce a strong proinflammatory cytokine response yet block the production of type I and III IFNs to SARS-CoV-2. However, treatment of airway cultures with the immune molecules type I or type III interferon (IFN) was able to inhibit SARS-CoV-2 infection. Thus, our model system identified type I or type III IFN as potential antiviral treatments for COVID-19 patients.
  • |Animals[MESH]
  • |Betacoronavirus/*immunology/physiology[MESH]
  • |Bronchi/cytology/immunology/virology[MESH]
  • |COVID-19[MESH]
  • |Cell Line[MESH]
  • |Cells, Cultured[MESH]
  • |Chemokines/immunology[MESH]
  • |Chlorocebus aethiops[MESH]
  • |Coronavirus Infections/*immunology/virology[MESH]
  • |Cytokines/immunology[MESH]
  • |Dogs[MESH]
  • |Epithelial Cells/*immunology/virology[MESH]
  • |Humans[MESH]
  • |Interferon Lambda[MESH]
  • |Interferon Type I/*immunology[MESH]
  • |Interferons/*immunology[MESH]
  • |Lung/cytology/immunology/virology[MESH]
  • |Madin Darby Canine Kidney Cells[MESH]
  • |Pandemics[MESH]
  • |Pneumonia, Viral/*immunology/virology[MESH]
  • |SARS-CoV-2[MESH]
  • |Vero Cells[MESH]


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