Abstract
Influenza A virus (IAV) and respiratory syncytial virus (RSV) are leading causes of childhood infections. RSV and influenza are competitive in vitro. In this study, the in vivo effects of RSV and IAV co-infection were investigated. Mice were intranasally inoculated with RSV, with IAV, or with both viruses (RSV+IAV and IAV+RSV) administered sequentially, 24 h apart. On days 3 and 7 post-infection, lung tissues were processed for viral loads and immune cell populations. Lung functions were also evaluated. Mortality was observed only in the IAV+RSV group (50% of mice did not survive beyond 7 days). On day 3, the viral loads in single-infected and co-infected mice were not significantly different. However, on day 7, the IAV titer was much higher in the IAV+RSV group, and the RSV viral load was reduced. CD4 T cells were reduced in all groups on day 7 except in single-infected mice. CD8 T cells were higher in all experimental groups except the RSV-alone group. Increased airway resistance and reduced thoracic compliance were demonstrated in both co-infected groups. This model indicates that, among all the infection types we studied, infection with IAV followed by RSV is associated with the highest IAV viral loads and the most morbidity and mortality.
Highlights
Our results indicate that respiratory syncytial virus (RSV) inoculation 24 h before Influenza A virus (IAV) infection results in higher IAV viral loads than IAV infection alone on day 7 post-infection and leads to severe morbidity and mortality
Gonzalez and colleagues have shown that infection of mice with rhinovirus 2 days before IAV infection reduced the disease severity when using a low or medium, but not a high dose of IAV (PR8 strain) [18]
We demonstrated that IAV (PR8 strain) and RSV (A2 strain) co-infections always resulted in severe disease (increased morbidity and mortality (Figure 2)) compared to single infections
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Respiratory infections are major causes of both morbidity and mortality worldwide [1]. Diagnostic and surveillance studies have revealed that co-infections with more than one pathogen in the respiratory tract are common [2,3]. Pathogens involved in co-infections interact with the host and with themselves, thereby profoundly affecting replication of each pathogen, disease pathogenesis, immune responses and most notably the disease outcome [4,5]
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