Scientists find the cause of deadly inflammation in COVID-19

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A study from the University of Southern California (USC) has shed light on why COVID-19 can start with mild symptoms but become deadly for some patients later on.

The research reveals that the virus behaves differently in two types of cells, leading to a better understanding of the disease’s progression and how to combat it.

Initially, when SARS-CoV-2, the virus causing COVID-19, infects the lung cells, it triggers two opposite responses. One of its proteins activates the immune system to fight off the virus, while another protein blocks this activation, keeping inflammation low.

This balancing act explains why many people experience only mild symptoms at first.

However, the virus can take another route that leads to severe problems. It can enter immune cells through a different method, which not only hampers the virus’s ability to multiply but also stops the production of the anti-inflammatory protein.

As a result, the pro-inflammatory protein runs rampant, causing a surge in inflammation. This inflammation can lead to the severe symptoms associated with the later stages of COVID-19, including the life-threatening “cytokine storms.”

Researchers at USC have been probing into why some COVID-19 cases worsen after the initial week of infection. They discovered that certain viral proteins play key roles in regulating the body’s response.

One protein, NSP14, promotes inflammation, while another, ORF6, suppresses it. This dichotomy is crucial in the disease’s development.

In lung cells infected by the virus via the ACE2 protein, ORF6 effectively keeps NSP14 from causing inflammation.

It’s as if ORF6 locks the door, preventing NSP14 from delivering its inflammatory message to the cell’s control center. This mechanism keeps the initial phase of the disease relatively mild for many patients.

The USC team has also illuminated how SARS-CoV-2 affects immune cells, which usually don’t have the ACE2 entry point. Instead, the virus enters these cells through a different receptor, TLR1, leading to an unchecked inflammatory response. This response is a key player in the severe symptoms seen in advanced COVID-19 cases.

In an exciting development, the researchers identified a drug that reduces inflammation in human immune cells infected with SARS-CoV-2.

This treatment also improved survival rates in mice with COVID-19, highlighting a potential pathway for preventing the severe consequences of the disease.

This study not only deepens our understanding of how COVID-19 operates but also opens up new avenues for treating its later, more dangerous stages by focusing on controlling inflammation.

According to the researchers, managing inflammation could be crucial in fighting not just COVID-19 but many other diseases as well. The key lies in knowing when to boost the immune response and when to calm it down.

If you care about COVID, please read studies about vitamin D deficiency linked to severe COVID-19, death, and how diets could help manage post-COVID syndrome.

For more information about COVID, please see recent studies that low-sodium plant-based diets may prevent COVID-19 better, and results showing zinc could help reduce COVID-19 infection risk.

The research findings can be found in Nature Cell Biology.

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