When COVID-19 or flu viruses kill they often have an accomplice — bacterial infections

Subject: Science and Technology

Section: Biotechnology

Context:

The 1918 influenza pandemic resulted in the loss of over 3 per cent of the world’s population — at least 50 million people But it wasn’t the flu virus that caused the majority of these deaths.
An analysis of lung samples collected during that flu pandemic indicated that most of the deaths were likely due to bacterial pneumonia, which ran rampant in the absence of antibiotics. Even in more recent history, like the 1957 H2N2 and 2009 H1N1 flu pandemics, nearly 18 per cent of patients with viral pneumonia had additional bacterial infections that increased their risk of death. And the COVID-19 pandemic is no different.

Viruses and bacteria team up

Multiple pathogens can cause multiple infections in different ways. Scientists distinguish each type based on the timing of when each infection occurs. Coinfection refers to two or more different pathogens causing infections at the same time. Secondary or superinfections, on the other hand, refer to sequential infections that occur after an initial infection. They’re often caused by pathogens resistant to antibiotics used to treat the primary infection.
Within our respiratory tract, the epithelial cells lining your airways and lungs serve as the first line of defense against inhaled pathogens and debris. However, viruses can kill these cells and disrupt this protective barrier, allowing inhaled bacteria to invade. They can also change the surface of epithelial cells to make them easier for bacteria to attach to.
Viruses can also alter the surface of epithelial and immune cells by reducing the number of receptors that help these cells recognize and mount a response against pathogens. This reduction means fewer immune cells report to the viral infection site, giving bacteria an opening to launch another infection.

Influenza, COVID-19 and bacterial infections

Interestingly, the two bacteria species most commonly involved in coinfections with the influenzavirus are Streptococcus pneumoniae and Staphylococcus aureus, which normally exist in the respiratory tract without causing disease. However, the influenza virus can damage the cell barrier of the lungs and disrupt immune function enough to make patients susceptible to infection by these otherwise benign bacteria.
Secondary bacterial infections are also exacerbating the COVID-19 pandemic. A 2021 review estimated that 16 per cent to 28 per cent of adults hospitalized for COVID-19 also had a bacterial infection. These patients stayed in the hospital for twice as long, were four times more likely to need mechanical ventilation and had three times greater odds of dying compared to patients with only COVID-19.
Researchers identified Z-DNA binding protein (ZBP1), a molecule already known to play a regulatory role in how the immune system responds to influenza. Specifically, ZBP1 detects influenza viruses within the lungs and signals infected epithelial and immune cells to self-destruct. This induced cell death eliminates the virus and promotes recruitment of additional immune cells to the infection site.