How Covid-19 triggers massive inflammation

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<strong>US researchers have identified the reason why Covid-19 causes severe inflammation in some people, leading to acute respiratory distress and multi-organ damage.</strong></p>
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The study, led by researchers at Boston Children's Hospital, also finds that antibodies that people develop when they contract Covid-19 can sometimes lead to more inflammation, while antibodies generated by mRNA Covid-19 vaccines seem not to.<br />
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These findings, detailed in the journal Nature, may have implications for using monoclonal antibodies to treat Covid-19, helping to explain why the treatment works only when given early.<br />
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"It may be that later on, antibodies may help enhance inflammation. We may need to look at the properties of the antibodies," said Judy Lieberman from Boston Children's Programme in Cellular and Molecular Medicine.<br />
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In the study, the team analysed blood samples from patients with Covid and compared these with samples from healthy people and patients with other respiratory conditions.<br />
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They found that SARS-CoV-2 can infect monocytes – immune cells in the blood that act as "sentinels" or early responders to infection – as well as macrophages, similar immune cells in the lungs. Once infected, both types of cells die a fiery death (called pyroptosis) that releases an explosion of powerful inflammatory alarm signals.<br />
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"In the infected patients, about 6 per cent of blood monocytes were dying an inflammatory death," Lieberman said. "That's a large number to find, because dying cells are rapidly eliminated from the body."<br />
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The team also examined the lung tissue from people who died from Covid, and found that about a quarter of the macrophages in the tissue were dying.<br />
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When the researchers studied the cells for signs of SARS-CoV-2, they found that about 10 per cent of monocytes and 8 per cent of lung macrophages were infected.<br />
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The fact that monocytes and macrophages can be infected with SARS-CoV-2 was a surprise, since monocytes don't carry ACE2 receptors, the classic entry portal for the virus, and macrophages have low amounts of ACE2.<br />
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Lieberman thinks SARS-CoV-2 infection of monocytes might have previously been missed in part because researchers often study frozen blood samples, in which dead cells do not show up.<br />
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While SARS-CoV-2 was able to infect monocytes and macrophages, it wasn't able to produce new infectious viruses. ItA may be because the cells died quickly from pyroptosis before new viruses could fully form, the researchers said.</p>
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