We often talk about the tens of millions of deaths caused by the Spanish flu pandemic of 1918: but are we sure that it was really the H1N1 virus that killed the sick? According to an article in The Conversation written by immunologist Hayley Muendlein, often the cause of deaths of those infected by a virus is not the virus itself, but a concomitant bacterial infection. This was the case not only with the Spanish flu, as the analysis of lung tissue samples from the deceased (mostly bacterial pneumonia deaths) showed, but also with the 1957 H2N2 and 2009 H1N1 pandemics. when almost a fifth of infected patients were also affected by bacterial infections which increased their risk of death.
Covid too. Covid appears to behave in the same way: according to a systematic review carried out in 2021, between 16% and 28% of adults admitted to the ICU due to covid also had a bacterial infection. “Compared to those who were just infected with the coronavirus, these patients stayed in hospital twice as much, were four times more at risk of needing mechanical ventilation and three times more at risk of dying,” explains Muendlein.
Having seasonal flu and contracting a bacterial infection at the same time increases the risk of hospitalization: the two bacteria that normally cause co-infections are the Streptococcus pneumoniae and it Staphylococcus aureuswhich usually live silently in our respiratory tract.
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Deadly collaboration. But how do viruses and bacteria interact, debilitating the infected host’s body? They work as a team: viruses are in fact able to kill the epithelial cells that cover the lungs and act as a barrier against inhaled pathogens, leaving the bacteria free. Viruses can also alter the surface of epithelial and immune cells by reducing the number of receptors that allow them to recognize pathogens and prepare the body for a response. ‘infection.
How to fight viruses and bacteria? Given that antivirals don’t work against bacteria and antibiotics don’t work against viruses, is there a drug that can fight both pathogens at the same time? A study in which Muendlein participated presents a possible solution: the molecule ZBP1, which plays a fundamental role in the body’s immune response to influenza, appears to be able to detect influenza viruses in the lungs, and it forces infected immune and epithelial cells to commit suicide. In this way, infected cells are eliminated, and new healthy immune cells are “recruited” to fight the infection. “It is possible that treatments that increase ZBP1 in some cell types may serve to better manage bacterial and viral co-infections,” concludes Muendlein.