Surviving COVID-19 protects against severe forms of influenza.

More than 200 viruses can infect and cause disease in humans. Most people become infected with several viruses during their lifetime.

American scientists decided to test how an encounter with one virus affects the immune system’s response to another, reports the press service of Rockefeller University (USA).

By analyzing mice that were infected first with SARS-CoV-2 and then with the influenza A virus, scientists found that recovery from COVID has a protective effect against the worst effects of the flu, and that this memory response comes from an unexpected corner of the immune system. in the article.

Researchers found that epigenetic changes in macrophages—innate immune cells that are among the first to respond to a threat—developed a kind of “memory” after COVID that allowed these cells to better defend against an unrelated virus.

Immunological memory was long thought to be limited to adaptive immune cells, although recent research has challenged this dogma. What’s even more intriguing is that macrophage memory was not unique to any particular virus, the paper notes.

When the virus enters the body, the following reaction occurs:

• signaling molecules called cytokines instruct innate immune cells such as macrophages to pursue and engulf anything that alarms them;
• this universal approach is followed by a targeted attack by adaptive immune cells, such as T cells, identifying a virus-specific antigen, tailoring their attack to it and remembering it long-term to fight upcoming incursions of the same virus;
• however, discoveries over the past two decades indicate that innate immune responses can lead to cellular memory. For example, in multiple studies, scientists have found that in people who received the live attenuated Bacillus Calmette-Guérin vaccine, designed to protect against tuberculosis, months-long innate immune memory responses provided protection against non-TB infections.

But how this effective immune memory develops has been poorly understood to date. Scientists set out to study the long-term consequences of the SARS-CoV-2 coronavirus infection in the respiratory system:

• they focused their analysis on lung cells and found that alveolar macrophages located in the airways acquired a new epigenetic program after infection. In particular, the chromatin that packages genes became more accessible around antiviral genes, making them “ready to go” after recovery from COVID;
• Because macrophages in the lungs of post-COVID mice had acquired antiviral innate immune memory imprinted on their chromatin, they could more successfully fight off the disease caused by the new viral invader. Compared to mice that were not sick, they had fewer symptoms of influenza A, such as significant weight loss or abnormal inflammatory responses, and a lower mortality rate;
• these results are not limited to mice. By analyzing samples from people who had recovered from mild COVID, researchers found similar epigenetic changes in blood monocytes, macrophage precursor cells;
• The result of this epigenetic reprogramming is memory of previous infections and an altered immune response to future ones.

The fact that viral RNA itself is capable of triggering memory in macrophages lays the foundation that this memory is independent of antigen, the researchers note. “They recognize a pattern common to many viruses, as opposed to a virus-specific antigen.

Scientists confirmed this by exposing mice to a synthetic RNA virus mimic and found similar memory responses observed after SARS-CoV-2 infection.

However, when it came to fighting secondary influenza infections, memory-tuned macrophages outperformed adaptive T cells.

Macrophages are indeed the driving force behind this response, the scientists note.

Finally, to test how acute the macrophages’ memory was, the researchers extracted them from recovered mice, transplanted them into unaffected mice, and then infected those mice with influenza A virus.

If the restored macrophages were up to the task, the recipient mice should have developed less severe disease after infection with influenza A, the paper notes. – That’s what happened. Unsick mice implanted with reconstituted macrophages tolerated influenza better than mice implanted with untrained macrophages.

In the future, researchers want to determine what the critical factors are for the formation of innate immune memory in order to develop therapies that provide broad protection against many viruses. This approach could be especially useful in the context of a potential pandemic.

If, for example, there was a new pathogen on the horizon, it would be good to have a therapy that boosts overall antiviral immunity for the next month or so, the scientists note.

Source: Racurs

David

I am David Wyatt, a professional writer and journalist for Buna Times. I specialize in the world section of news coverage, where I bring to light stories and issues that affect us globally. As a graduate of Journalism, I have always had the passion to spread knowledge through writing.