Abstract
Multiple respiratory viruses can concurrently or sequentially infect the respiratory tract and lead to virus‒virus interactions. Infection by a first virus could enhance or reduce infection and replication of a second virus, resulting in positive (additive or synergistic) or negative (antagonistic) interaction. The concept of viral interference has been demonstrated at the cellular, host, and population levels. The mechanisms involved in viral interference have been evaluated in differentiated airway epithelial cells and in animal models susceptible to the respiratory viruses of interest. A likely mechanism is the interferon response that could confer a temporary nonspecific immunity to the host. During the coronavirus disease pandemic, nonpharmacologic interventions have prevented the circulation of most respiratory viruses. Once the sanitary restrictions are lifted, circulation of seasonal respiratory viruses is expected to resume and will offer the opportunity to study their interactions, notably with severe acute respiratory syndrome coronavirus 2.
Highlights
Multiple respiratory viruses can concurrently or sequentially infect the respiratory tract and lead to virus‒virus interactions
Positive virus–virus interaction corresponds to a co-infection that might result in an increased disease severity and pathogenesis [1]
Factors that could predict an interference between respiratory viruses include the capacity of the interfering virus to induce a rapid IFN response; the degree of susceptibility of the second virus to immune mediators; the extent to which the different viruses counteract the induction and antiviral effects of IFN; and the differential innate immune response patterns triggered by each viruses in the upper and lower respiratory tracts
Summary
Multiple respiratory viruses can concurrently or sequentially infect the respiratory tract and lead to virus‒virus interactions. The type of virus–virus interaction (negative or positive) is probably dependent on the respiratory viruses involved, the timing of each infection, and the interplay between the response of the host to each virus In this perspective, we focus on viral interference. They can be infected by respiratory viruses and secrete IFNs and other immune mediators These ex vivo models are limited by the absence of some immune cells that could contribute to viral interference, they are convenient tools to characterize the mechanisms of virus–virus interaction at the mucosal level. Animal models that are susceptible to several human respiratory viruses, such as ferrets and golden Syrian hamsters, are valuable to evaluate the effects of concurrent and sequential viral infections on disease severity, immune response and the mechanisms of virus–virus interaction at the host level [16]. The mechanisms involved in viral interference were
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