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Coronavirus disease 2019 (COVID-19), a new, infectious, pneumonia-like disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has continued to spread rapidly worldwide, even in 2021. The COVID-19 outbreak has brought about some changes in influenza and respiratory syncytial virus (RSV) and rhinovirus infections, which were previously the main causes of viral pneumonia. This review discusses the epidemiology of these infectious diseases during the COVID-19 pandemic. Although influenza cases have been substantially decreasing worldwide, RSV infection cases, which had temporarily decreased initially, have started to increase again, and rhinovirus infection cases have been reported to be higher than usual. The authors reviewed the viral interferences among these infections in detail because they could exert considerable effect on epidemiological surveillance data. Based on experimental data, a recent study suggested that the influenza virus could promote SARS-CoV-2 infectivity. A previous study reported that influenza A virus inhibits RSV replication in an animal model. Another recent study revealed that although the replication of rhinovirus is not affected by SARS-CoV-2, the replication of SARS-CoV-2 is inhibited by rhinovirus, indicating that rhinovirus infection protects against SARS-CoV-2. Further studies are required to confirm these findings and evaluate the impact of SARS-CoV-2 on the activity of these viruses. [ABSTRACT FROM AUTHOR]

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 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. 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 [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 [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. Should read [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. [ABSTRACT FROM AUTHOR]

Seasonal influenza is an acute respiratory infection primarily caused by influenza A and B viruses, which circulate annually and cause substantial morbidity and mortality worldwide. Annual influenza vaccination is currently the most effective measure for preventing influenza and greatly reduces the risk of disease severity and the incidence of complications and death. Annual seasonal influenza vaccines are traditionally produced in Japan and many other countries using viruses propagated in embryonated chicken eggs. However, at present, the effectiveness of the seasonal influenza vaccines has some significant limitations, partly because of egg-adaptive mutations in the antigenic sites of the influenza virus haemagglutinin, which are caused by the continued evolution of seasonal influenza viruses. To overcome the limitations of egg-based influenza vaccine production, a mammalian cell culture-based influenza vaccine production system has been developed in Japan in the past decade as an alternative to the current production method. In this review, I have summarised the progress in the development of cell-based seasonal influenza vaccines and discussed the technological challenges encountered in the development of influenza vaccines., Competing Interests: The authors have no conflicts of interest to disclose., (2024, National Center for Global Health and Medicine.)

Some enveloped viruses such as influenza virus and human immunodeficiency virus type 1(HIV-1) enter cells via clathrin-mediated endocytosis and release their viral genome into the cytoplasm by fusion of the viral envelope with the cell membrane. However, the entry mechanisms of these viruses into cells are not fully understood. Until recently, entry of HIV-1 into CD4/CR expressing cells was believed to occur by fusion of viral envelope to the target cellular membrane at lipid rafts in a pH-independent manner. It has also been reported that HIV-1 entry into macrophages is mediated via lipid-raft dependent macropinocytosis. Recent studies demonstrate that HIV-1 enters cells via CD4/CR-mediated endocytosis and viral fusion with intracellular membrane compartments is enhanced by dynamin-dependent pathway.