Human rhinovirus infection blocks SARS-CoV-2 replication within the respiratory epithelium

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Human rhinovirus infection blocks SARS-CoV-2 replication within the respiratory epithelium: implications for COVID-19 epidemiology


Abstract​

Virus-virus interactions influence the epidemiology of respiratory infections. However, the impact of viruses causing upper respiratory infections on SARS-CoV-2 replication and transmission is currently unknown. Human rhinoviruses cause the common cold and are the most prevalent respiratory viruses of humans. Interactions between rhinoviruses and co-circulating respiratory viruses have been shown to shape virus epidemiology at the individual host and population level. Here, we examined the replication kinetics of SARS-CoV-2 in the human respiratory epithelium in the presence or absence of rhinovirus. We show that human rhinovirus triggers an interferon response that blocks SARS-CoV-2 replication. Mathematical simulations show that this virus-virus interaction is likely to have a population-wide effect as an increasing prevalence of rhinovirus will reduce the number of new COVID-19 cases.

Acknowledgments. This work was supported by grants from the Medical Research Council of the United Kingdom (MC_UU_12014/9 to PRM, MR/N013166/1 to JH and MR/R502327/1 to DMG). MB is supported by centre funding from MRC under a concordat with the UK Department for International Development and the National Institute for Health Research Health Protection Research Unit in Modelling Methodology. VH was funded by the German Research Foundation (Deutsche Forschungsgemeinschaft; project number 406109949) and the Federal Ministry of Food and Agriculture (BMEL; Förderkennzeichen: 01KI1723G). JARA is supported by the University of Glasgow School of Veterinary Medicine VetFund. We thank Lynn Stevenson, Frazer Bell and Lynn Oxford for technical assistance. PRM owns shares of Astra Zeneca. The rest of the authors declare no conflicts of interest.

Rhinovirus jab anyone??
 

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