Influenza, RSV Coinfection May Provide Transient COVID-19 Resistance

Study results published in the Journal of Infectious Diseases showed that coinfection with influenza A virus or respiratory syncytial virus (RSV) may provide transient resistance against COVID-19 infection.

Researchers in the United Kingdom investigated interactions in the respiratory tract between SARS-CoV-2, influenza A virus, and RSV. Interactions between these viruses were evaluated via cultures obtained from human bronchial epithelial cells, and viral spread and replication were examined in both single infection and coinfection scenarios. The researchers also analyzed changes in virus replication kinetics, virus spread, and virus-induced lesions.

At infection onset, measurements of SARS-CoV-2 titers were similar in the single infection and coinfection with Influenza A scenarios. By 24 hours, SARS-CoV-2 titers were significantly lower in the coinfection scenario (P <.05). Decreases in SARS-CoV-2 titers were noted at 48 hours (P <.001), and titers were undetectable at 96 hours (P <.001).

For coinfection with RSV, the researchers noted SARS-CoV-2 titer levels were similar to those observed in the single infection assay at both infection onset and at 24 hours. Between 48 and 96 hours (both P <.001), RSV titer levels remained relatively stable. Of note, the occurrence of viral spread was inhibited by coinfection with both influenza A or RSV. Conversely, titers of IAV and RSV did not differ significantly at any time point during scenarios of single infection or coinfection with SARS-CoV-2.

In an antibody immunofluorescence experiment, single infection scenarios showed fluorescence patterns among all 3 viral antibodies. In coinfection scenarios, SARS-CoV-2-positive cells were rarely observed, whereas influenza A- and RSV-positive cells showed similar patterns to that of single infection scenarios.

Expression of interferon-stimulated genes with known antiviral activities were also observed to differ for SARS-CoV-2. Additionally, protein expression levels were lowest for SARS-CoV-2 when compared with influenza A virus or RSV in both single and coinfection scenarios. The researchers noted that the reduction in SARS-CoV-2 replication after 72 hours in coinfected cells was likely due to the innate immune response triggered by influenza A or RSV infection.

To test the effect of the timing of infection, the researchers infected cells with a single virus and waited for the occurrence of secondary infection. The largest reduction in SARS-CoV-2 was observed when cells were infected with influenza A virus 24 hours after primary SARS-CoV-2 infection. The researchers noted that a shorter time elapsed between infections resulted in a greater blockade on SARS-CoV-2 replication, regardless of which virus was the superinfecting virus. They also determined SARS-CoV-2 infection was significantly affected by influenza A and RSV coinfection in regard to transmission, immunity, and replication kinetics.

Study limitations include the inability to confirm results in animal models or a human population.

Based on these findings, SARS-CoV-2 appears to be susceptible to negative interference with other respiratory viral infections and stated. Moreover, “If this effect is translated at the epidemiological scale, it is feasible to speculate that the incidence of SARS-CoV-2 infections will decrease in future winter seasons as normal mixing resumes,” the researchers concluded.