Errata:
Erratum for “The Importance of Monitoring Viral Respiratory Infections During the COVID-19 Crisis” (Vol.17, pp. 73-81, 2022)
Itsuki Hamamoto* and Noriko Shimasaki**
*Influenza and Respiratory Virus Research Center, National Institute of Infectious Diseases (NIID)
4-7-1 Gakuen, Musashimurayama, Tokyo 208-0011, Japan
**Department of Virology III, National Institute of Infectious Diseases (NIID), Tokyo, Japan
Due to an authors' error, the original version of this article contained errors in in-text citations under Section 4.4 and the corresponding references. Reference [55] should be listed as [56] and the following paper should be listed as [55].
K. P. Tao, M. Chong, J. C. S. Pun, J. G. S. Tsun, S. M. W. Chow, C. S. H. Ng, M. H. T. Wang, Z. Chan, P. K. S. Chan, A. M. Li, and R. W. Y. Chan, “Suppression of influenza virus infection by rhinovirus interference at the population, individual and cellular levels,” medRxiv, doi: 10.1101/2021.08.09.21256656, 2021.
The two paragraphs in Section 4.4 (pp. 79–80) should be corrected as follows:
Now reads | Should read |
---|---|
Co-infections of the influenza virus and rhinovirus are relatively common, especially in young children. Previous infection with rhinovirus inhibits subsequent influenza A virus infection by the IFN-mediated innate immune system in differentiated human airway epithelium (Fig. 17) [7]. In other words, rhinovirus induces an IFN response that suppresses subsequent influenza virus infection [7]. A recent study revealed that the replication of rhinovirus is not affected by SARS-CoV-2, although the replication of SARS-CoV-2 is inhibited by rhinovirus, indicating that rhinovirus infection protects against SARS-CoV-2 [55]. SARS-CoV-2, similar to the influenza virus and many other viruses, is inhibited by IFNs [55]. Therefore, the number of COVID-19 cases may be reduced due to the inhibitory effects of rhinovirus-induced IFN response. |
Co-infections of the influenza virus and rhinovirus are relatively common, especially in young children. Previous infection with rhinovirus inhibits subsequent influenza A virus infection by the IFN-mediated innate immune system in differentiated human airway epithelium [7]. An another study also reported similar phenomenon (Fig. 17) [55]. In other words, rhinovirus induces an IFN response that suppresses subsequent influenza virus infection [7]. A recent study revealed that the replication of rhinovirus is not affected by SARS-CoV-2, although the replication of SARS-CoV-2 is inhibited by rhinovirus, indicating that rhinovirus infection protects against SARS-CoV-2 [56]. SARS-CoV-2, similar to the influenza virus and many other viruses, is inhibited by IFNs [56]. Therefore, the number of COVID-19 cases may be reduced due to the inhibitory effects of rhinovirus-induced IFN response. |
In the Reference list (p. 81), references [55] to [56] should be corrected as follows:
Now reads | Should read |
---|---|
[55] K. Dee, D. M. Goldfarb, J. Haney, J. A. R. Amat, V. Herder, M. Stewart, A. M. Szemiel, M. Baguelin, and P. R. Murcia, “Human rhinovirus infection blocks severe acute respiratory syndrome coronavirus 2 replication within the respiratory epithelium: Implications for COVID-19 epidemiology,” J. Infect. Dis., Vol.224, No.1, pp. 31-38, 2021. |
[55] K. P. Tao, M. Chong, J. C. S. Pun, J. G. S. Tsun, S. M. W. Chow, C. S. H. Ng, M. H. T. Wang, Z. Chan, P. K. S. Chan, A. M. Li, and R. W. Y. Chan, “Suppression of influenza virus infection by rhinovirus interference at the population, individual and cellular levels,” medRxiv, doi: 10.1101/ 2021.08.09.21256656, 2021. [56] K. Dee, D. M. Goldfarb, J. Haney, J. A. R. Amat, V. Herder, M. Stewart, A. M. Szemiel, M. Baguelin, and P. R. Murcia, “Human rhinovirus infection blocks severe acute respiratory syndrome coronavirus 2 replication within the respiratory epithelium: Implications for COVID-19 epidemiology,” J. Infect. Dis., Vol.224, No.1, pp. 31-38, 2021. |
The authors regret these errors, and these errors have now been corrected in the PDF version of the article.
This article is published under a Creative Commons Attribution-NoDerivatives 4.0 Internationa License.