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Interestingly, the two species of bacteria most involved in co-infections with the flu virus are Streptococcus pneumoniae and Staphylococcus aureus, which usually exist in the respiratory tract without causing illness. However, the flu virus can damage the cellular barrier of the lungs and alter immune serve as enough to make patients vulnerable to infection with benign bacteria in a different way.
Secondary bacterial infections are also exacerbating the COVID-19 pandemic. A 2021 review estimated that between 16% and 28% of adults hospitalized for COVID-19 also had a bacterial infection. These patients stayed in the hospital twice as long, were 4 times more likely to want mechanical ventilation, and were 3 times more likely to die than COVID-19 patients alone.
The immune formula reacts to viruses and bacteria. Antivirals do not act on bacteria and antibiotics do not act on viruses. A greater understanding of the pathways the framework uses to regulate antiviral and antibacterial infections is imperative for the treatment of secondary infections and co-infections.
Recent studies by my colleagues and myself could provide a clue. We sequenced the RNA of a type of immune cell, macrophages, in mice to identify which molecules were in cells that were or had died from a bacterial infection.
We know the Z-DNA binding protein (ZBP1), a molecule that is already known to play a regulatory role in how the immune formula responds to influenza. Specifically, ZBP1 detects influenza viruses in the lungs and signals inflamed epithelial and immune mobiles to self-destruct. This induced mobile death eliminates the virus and promotes the recruitment of more immune mobiles at the site of infection.
Based on this finding that ZBP1 is vital for fighting viral infection, we found that macrophages inflamed with Yersinia pseudotuberculosis, a type of bacteria that causes foodborne illness, also use this protein to initiate mobile death. This limits bacterial replication while sending inflammatory signals that assist bacteria.
These findings raise the option that ZBP1 possibly plays a dual role in how the system responds to viral and bacterial infections. Treatments that develop ZBP1 in certain mobile types could be useful in controlling bacterial and viral co-infections.
This article is republished from The Conversation, a nonprofit news site committed to sharing concepts from education experts. Written by: Hayley Muendlein, Tufts University.
Read more:
Antibiotic resistance is at a critical point: government for universities and Big Pharma to find new drugs could help defeat superbugs.
The COVID-19 flu season presents the risk of a “double epidemic,” making the need for vaccination even more urgent.
Hayley Muendlein does work, consults, owns shares or obtains investments from any company or organization that would benefit from this article, and has disclosed any pertinent partnerships beyond her educational position.