A lab study published in the Journal of Infectious Diseases suggests that infection with human rhinovirus, the virus that causes the common cold, might provide some level of protection against COVID-19.
Prof Lawrence Young, Professor of Molecular Oncology, Warwick Medical School, said:
“This laboratory study clearly shows that infection with a human common cold virus (rhinovirus or HRVs) can block the growth of the SARS-CoV-2 virus, at least in cells in the lab. As HRVs are the most frequent cause of the common cold and are highly transmissible, this study suggests that this common infection could impact the burden of COVID-19 and influence the spread of SARS-CoV-2 particularly over the autumn and winter months when seasonal colds are more frequent.
“The study uses human bronchial cells infected with the viruses in tissue culture and shows that HRV infection significantly inhibits the replication of SARS-CoV-2. This effect was observed irrespective of whether the viruses are used as simultaneous co-infections or infections were staggered e.g. SARS-CoV-2 infection followed 24 hours later by HRV infection. The study also showed that this inhibitory effect was due to HRV inducing robust activation of the interferon-mediated innate immune response. The interferon response induced by SARS-CoV-2 infection is much lower and weaker.
“Finally, the study modelled the possible impact of this effect on COVID-19 cases in the population concluding that the number of new SARS-CoV-2 infections would decrease as the number of HRV infections increase – an effect that could restrict the spread of SARS-CoV-2.
“This is an interesting study that highlights the need for us to understand more about the biology of SARS-CoV-2 infections and how co-infections with other respiratory viruses (e.g. flu) might affect COVID-19. It also stresses the importance of the interferon response in controlling SARS-CoV-2 replication, supporting current clinical trials that are exploring the therapeutic benefits of interferon treatment in COVID0-19 patients.”
Prof Gary McLean, Professor in Molecular Immunology, London Metropolitan University, said:
“This is a good in vitro study using human airway epithelial cells in a culture system designed to mimic in vivo conditions. The authors show that rhinovirus infection can limit the infection of SARS-CoV-2 and suggest the mechanism is through induction by rhinovirus of innate mediators. Although the proof of this mechanism is somewhat limited.
“The major limitation of the study is that it is performed with just one strain of rhinovirus, there are at least 160, and there are no guarantees that each rhinovirus strain would have the same effect on SARS-CoV-2 infections. They also do not fully prove the induction by interferon is responsible here. Lastly, translating this to the situation in real life is very tricky. Although it is likely that a common cold virus such as rhinovirus would induce a strong innate immune response that could block SARS-CoV-2 infections, it would still require both infections to occur at a similar time. In addition, with all the non pharmaceutical interventions that have been in play over the past year it is not only limiting SARS-CoV-2 transmissions but any respiratory virus. Therefore, with reduced frequencies of circulating common colds in the community, as we know has happened, there would likely be less effect and chance of this innate protection inhibiting SARS-CoV-2.”
Prof Ian Jones, Professor of Virology, University of Reading, said:
“The seasonality of respiratory viruses is well known but even in the winter months of temperate climates, like the UK, different viruses peak at different times suggesting they jostle with each other for their slot in the human respiratory tract. This study formally shows that infection of human respiratory cells by the common cold virus releases interferon and sets up an antiviral state which then resists infection by SARS-CoV-2. Effectively, one virus pushes out another. The data support the limited trial data available for interferon nasal sprays which have shown some ability to improve Covid outcomes. However, the great problem for any prophylactic is when to give it and how long to give it for and although interesting the practical application of the data described is hard to see.”
Dr Julian Tang, Honorary Associate Professor/Clinical Virologist, University of Leicester, said:
“Interesting paper – which potentially touches on lots of phenomena.
“Virologists already know about the ‘viral interference’ between rhinoviruses and seasonal influenza – innate host immune responses (including interferon) induced by rhinoviruses can reduce the successful infection of influenza in humans.
“The fact that rhinoviruses may also ‘interfere’ with SARS-COV-2 infection is intriguing and needs further confirmation.
“One weakness of the study is that their in vitro viral culture system does not include the presence of cross-reactive, potentially cross-protective antibodies from other common cold coronaviruses (OC43, 229E, NL63, HKU1) – that may also inhibit successful SARS-COV-2 infection in humans.
“Also, the authors only examine the impact of one serotype of rhinovirus (A16), but there are over 100 serotypes of rhinoviruses, divided into rhinovirus species A, B, C: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3553670/ – and it is not clear from this study alone if all these different rhinovirus serotypes have the same degree of ‘viral interference’ effect on SARS-COV-2 infection.
“Some data on the dominance of rhinovirus amongst the seasonal respiratory viruses during the COVID-19 pandemic has been published already from Australia and New Zealand: https://www.nature.com/articles/s41467-021-21157-9 and https://www.eurosurveillance.org/content/10.2807/1560-7917.ES.2020.25.47.2001847?crawler=true and the UK PHE surveillance data shows something similar: https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/971212/Weekly_Flu_and_COVID-19_report_w11_v2.pdf
“Intriguingly, if you look at Figures 13 (showing SARS-COV-2 %positivity) and 14 (showing rhinovirus %positivity) over the same time period (weeks 35, 2020 to week 10, 2021), you might see a lower incidence of SARS-COV-2 at the peak rhinovirus incidence, which then increases during the Christmas/New Year surge, as the rhinovirus incidence starts falling. But a counter argument to this could also be that if rhinovirus was truly interfering with SARS-COV-2 infections, then there should not be a rise in SARS-COV-2 %positivity during weeks 39-43 when rhinovirus %positivity was also peaking.
“Further study is needed here as in real life situations the rhinovirus interference effect may have a more complex and multiphasic time-dependent impact on human (rather than in vitro) SARS-COV-2 infections.
“Finally, many of these seasonal coronaviruses and rhinoviruses will start to infect children from birth and may induce this innate immune ‘interference’ effect – to reduce/modify the SARS-COV-2 infection rates and severity of COVID-19 symptoms that we are seeing in children of different ages.”
‘Human rhinovirus infection blocks SARS-CoV-2 replication within the respiratory epithelium: implications for COVID-19 epidemiology’ by Kieran Dee et al. was published in the Journal of Infectious Diseases at 00:01 UK time on Tuesday 23 March 2021.
Prof Gary McLean: “No conflict of interest to declare.”
Prof Ian Jones: “No conflicts.”
None others received.