tetano
Editor, Senior Moderator
mSphere
. 2026 Apr 20:e0012526.
doi: 10.1128/msphere.00125-26. Online ahead of print.
Bacterial alteration of redox stressors impacts environmental stability of influenza A virus
Matthew R Williams[SUP] 1 [/SUP], Hannah M Rowe[SUP] 1 [/SUP]
Affiliations
Influenza A virus (IAV) causes annual morbidity and mortality and remains a constant pandemic threat due to the emergence of novel strains. Therefore, understanding the factors important in host-to-host transmission of IAV is a key control point for protecting individual and public health. Transmission is highly heterogeneous with viral factors and host inflammatory and immune factors being implicated. Also implicated is the upper respiratory microbiome. While typically thought to act indirectly on viral pathogenesis, in an immunomodulatory capacity to enhance or reduce susceptibility to viral infection, recent studies on the pathogenesis of IAV have identified direct interactions between the virus and upper respiratory pathobiont bacteria. We hypothesize that the bacterial cells and their metabolites co-shed into respiratory droplets with IAV particles alter the viability of the IAV particles in the environment, therefore altering the capacity for host-to-host transmission. In this investigation, we utilize a simplified model of fomite transmission in the absence of confounding host factors and demonstrate how oxidative stress from both the environment and the metabolic activity of Streptococcus pneumoniae contributes to the killing of IAV, while catalase or the metabolic activity of Staphylococcus aureus can protect IAV from environmental or pneumococcally produced reactive oxygen species. These findings support a mechanism for bacterial modulation of viral transmission where bacterial metabolic products present in the respiratory droplet are capable of stabilizing and destabilizing viral particles during environmental transit and therefore modulating viral transmissibility.IMPORTANCEInfluenza A virus is a major cause of illness and death every year. A key knowledge gap exists in understanding what factors modulate viral transmission. One potential mediator of viral transmission is the bacteria that are found in the human nasopharynx. However, the mechanisms responsible for bacterial modulation of viral transmission are unclear. Here, we utilize a simplified model of environmental survival where we expose viral particles to indoor environmental conditions in the presence of bacterial cells. We demonstrate that hydrogen peroxide produced by Streptococcus pneumoniae reduces viral environmental survival, while incubation with catalase or viable Staphylococcus aureus cells can protect viral particles from S. pneumoniae-mediated viability loss. This supports a model of trans-kingdom bacterial-viral interactions where bacterial metabolites produced in the respiratory droplet are capable of modulating viral environmental survival and therefore transmission.
Keywords: Streptococcus pneumoniae; catalase; influenza; transmission.
. 2026 Apr 20:e0012526.
doi: 10.1128/msphere.00125-26. Online ahead of print.
Bacterial alteration of redox stressors impacts environmental stability of influenza A virus
Matthew R Williams[SUP] 1 [/SUP], Hannah M Rowe[SUP] 1 [/SUP]
Affiliations
- PMID: 42003595
- DOI: 10.1128/msphere.00125-26
Influenza A virus (IAV) causes annual morbidity and mortality and remains a constant pandemic threat due to the emergence of novel strains. Therefore, understanding the factors important in host-to-host transmission of IAV is a key control point for protecting individual and public health. Transmission is highly heterogeneous with viral factors and host inflammatory and immune factors being implicated. Also implicated is the upper respiratory microbiome. While typically thought to act indirectly on viral pathogenesis, in an immunomodulatory capacity to enhance or reduce susceptibility to viral infection, recent studies on the pathogenesis of IAV have identified direct interactions between the virus and upper respiratory pathobiont bacteria. We hypothesize that the bacterial cells and their metabolites co-shed into respiratory droplets with IAV particles alter the viability of the IAV particles in the environment, therefore altering the capacity for host-to-host transmission. In this investigation, we utilize a simplified model of fomite transmission in the absence of confounding host factors and demonstrate how oxidative stress from both the environment and the metabolic activity of Streptococcus pneumoniae contributes to the killing of IAV, while catalase or the metabolic activity of Staphylococcus aureus can protect IAV from environmental or pneumococcally produced reactive oxygen species. These findings support a mechanism for bacterial modulation of viral transmission where bacterial metabolic products present in the respiratory droplet are capable of stabilizing and destabilizing viral particles during environmental transit and therefore modulating viral transmissibility.IMPORTANCEInfluenza A virus is a major cause of illness and death every year. A key knowledge gap exists in understanding what factors modulate viral transmission. One potential mediator of viral transmission is the bacteria that are found in the human nasopharynx. However, the mechanisms responsible for bacterial modulation of viral transmission are unclear. Here, we utilize a simplified model of environmental survival where we expose viral particles to indoor environmental conditions in the presence of bacterial cells. We demonstrate that hydrogen peroxide produced by Streptococcus pneumoniae reduces viral environmental survival, while incubation with catalase or viable Staphylococcus aureus cells can protect viral particles from S. pneumoniae-mediated viability loss. This supports a model of trans-kingdom bacterial-viral interactions where bacterial metabolites produced in the respiratory droplet are capable of modulating viral environmental survival and therefore transmission.
Keywords: Streptococcus pneumoniae; catalase; influenza; transmission.