Influenza A virus – commonly known as the flu – causes pandemic and seasonal outbreaks. In some cases, patients with the flu acquire additional secondary Streptococcus pneumoniae infections that can cause severe illness and even death. The study “Secondary infection with Streptococcus pneumoniae decreases influenza virus replication and is linked to severe disease” published in FEMS Microbes explores the relationship between the two pathogens within a ferret model. First authors Karina Mueller Brown and Valerie Le Sage explain for the #FEMSmicroBlog how the collaboration between pneumococcus and influenza can make us even sicker. #FascinatingMicrobes
Two pathogens meet in a common host
Global pandemics caused by influenza virus have devastating effects on health systems. This is famously illustrated by the 1918 Spanish flu pandemic, often referred to as the most devastating epidemic in recorded history. More recently, one may recall the 2009 Swine flu pandemic.
Some patients can get additionally infected with the bacterial pathogen Streptococcus pneumoniae – also known as pneumococcus. In this case, infections with both pathogens lead to worse outcomes when compared to infections with one of them individually. Such a relationship is often referred to as synergistic.
Logically, one can assume that the virus and bacterium collaborate with each other when making us sick. Consistent with this assumption, the bacterial partner does indeed spread and transmit more efficiently when the influenza virus is present.
It seems that pneumococcus and influenza collaborate to make us even sicker.
The research article “Secondary infection with Streptococcus pneumoniae decreases influenza virus replication and is linked to severe disease” published in FEMS Microbes reveals another facet of this relationship: the pneumococcus bacterium has a negative influence on the influenza virus.
Pneumococcus and influenza – are they friend or foe?
This study focuses on understanding the interaction between these two pathogens in a mammalian host from the viral perspective. Specifically, how does pneumococcus affect influenza virus replication in the host and how efficiently can the virus transmit to a susceptible individual through the air?
The work uses the ferret model to explore the interaction between virus and bacteria, their airborne transmission and the consequences to the mammalian host in isolation and during co-infections. Surprisingly, the study provides evidence that synergy is not always at play. Indeed, in some cases, pneumococcus can either have a negative effect on the virus or no effect at all. This suggests an asymmetry in the viral-bacterial relationship.
When pneumococcus is present in the animal, the amount of virus in the upper respiratory tract is lower. Moreover, viral transmission efficacy inversely correlates with symptom severity. Hence, the sicker the host, the less likely they are to spread the virus. This implies that airborne transmission of influenza is driven by healthier hosts and not those with severe symptoms.
Finally, severe disease outcomes rely on influenza virus infecting the host first, followed by pneumococcus. Animals colonized with the bacterial pathogen and that are then exposed to influenza virus become no sicker than when they acquired the virus alone. Therefore, the consequences of the co-infected mammalian host likely depend on when each pathogen was acquired. That is, a secondary bacterial infection may provoke severe disease. On the other hand, infections where the bacterium precedes the virus may be much less virulent.
Why is it so important to understand co-infection scenarios?
Studying co-infections with pneumococcus and influenza highlights how symptoms, mortality and transmission of a single pathogen can change depending on what other microbes are present. Also, it becomes clear that we need to look beyond pathogens in isolation.
To better understand pathogenic disease, we need to look beyond the single pathogen.
Specifically, this study sets the stage to unravel pathogenic co-infections in hosts. We now better comprehend how bacteria negatively influence influenza viruses and how this asymmetrical relationship impacts the epidemiology of influenza viruses. The better we understand these microbial relationships; the more possibilities we have to tackle devastating pathogenic diseases!
- Read the paper “Secondary infection with Streptococcus pneumoniae decreases influenza virus replication and is linked to severe disease” by et al. (2022).
About the authors of this blog
Karina Mueller Brown is a Ph.D. candidate at Carnegie Mellon University in Pittsburgh (USA) in Dr. N. Luisa Hiller’s Lab. Her research focuses on host-microbial interactions.
Dr. Valerie Le Sage is a Research Assistant Professor at the University of Pittsburgh (USA) in Dr. Seema Lakdawala’s Lab. Her research focuses on examining the airborne transmission of influenza virus.
About this blog section
The section #FascinatingMicrobes for the #FEMSmicroBlog explains the science behind a paper and highlights the significance and broader context of a recent finding. One of the main goals is to share the fascinating spectrum of microbes across all fields of microbiology.
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