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Time-Dependent Increase in Susceptibility and Severity of Secondary Bacterial Infection during SARS-CoV-2 Infection
Amanda P Smith1, Evan P Williams2, Taylor R Plunkett2
1Department of Pediatrics, University of Tennessee Health Science Center, Memphis, TN, USA.
Abstract:
Secondary bacterial infections can exacerbate SARS-CoV-2 infection, but their prevalence and impact remain poorly understood. Here, we established that a mild to moderate SARS-CoV-2 infection increased the risk of pneumococcal coinfection in a time-dependent, but sexindependent, manner in the transgenic K18-hACE mouse model of COVID-19. Bacterial coinfection was not established at 3 d post-virus, but increased lethality was observed when the bacteria was initiated at 5 or 7 d post-virus infection (pvi). Bacterial outgrowth was accompanied by neutrophilia in the groups coinfected at 7 d pvi and reductions in B cells, T cells, IL-6, IL-15, IL-18, and LIF were present in groups coinfected at 5 d pvi. However, viral burden, lung pathology, cytokines, chemokines, and immune cell activation were largely unchanged after bacterial coinfection. Examining surviving animals more than a week after infection resolution suggested that immune cell activation remained high and was exacerbated in the lungs of coinfected animals compared with SARS-CoV-2 infection alone. These data suggest that SARS-CoV-2 increases susceptibility and pathogenicity to bacterial coinfection, and further studies are needed to understand and combat disease associated with bacterial pneumonia in COVID-19 patients.
Insights
SARS-CoV-2 infection increases the risk of secondary pneumococcal coinfection in mice. This coinfection leads to increased lethality and altered immune responses, highlighting the need for further research into COVID-19 complications.
Area of Science:
- Infectious Diseases
- Immunology
- Virology
Background:
- Secondary bacterial infections complicate viral illnesses like SARS-CoV-2 (COVID-19).
- The prevalence and impact of bacterial coinfections in COVID-19 patients are not well understood.
- Understanding these coinfections is crucial for effective treatment strategies.
Approach:
- A transgenic K18-hACE mouse model of COVID-19 was used to study SARS-CoV-2 and *Streptococcus pneumoniae* coinfection.
- Bacterial challenge was initiated at different time points post-viral infection (3, 5, and 7 days).
- Morbidity, mortality, immune cell populations, and cytokine profiles were analyzed.
Key Points:
- SARS-CoV-2 infection increased susceptibility to pneumococcal coinfection in a time-dependent manner.
- Coinfection initiated at 5 or 7 days post-virus infection (pvi) resulted in increased lethality.
- Specific immune cell reductions (B cells, T cells) and cytokine changes were observed at 5 d pvi, while neutrophilia occurred at 7 d pvi.
- Viral load and lung pathology were not significantly altered by bacterial coinfection, but immune activation persisted post-resolution.
Conclusions:
- SARS-CoV-2 infection enhances susceptibility and pathogenicity to secondary bacterial coinfections.
- These findings underscore the clinical significance of bacterial pneumonia in COVID-19 patients.
- Further research is warranted to develop strategies to combat coinfections in COVID-19.
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