New studies explain how the coronavirus bypasses the immune system; paying off

Two new papers reveal the mechanisms by which coronaviruses evade the immune response. Viruses use enzymes known as proteases to evade the innate defenses of the immune system. These enzymes “turn off” a molecular signal that helps recognize areas on the surface of the virus where the defense cells are activated.

The results of the research were published last Tuesday (2) in the specialized journal Science Signaling from the Science Group. Coronaviruses are a group of viruses in the Coronaviridae family, the best known currently being Sars-CoV-2, the causative agent of the Covid pandemic. But there are six other coronaviruses known to infect humans, including SARS, MERS, and four coronaviruses that cause the common cold.

In general, the effects of coronavirus infection vary from asymptomatic cases with mild cold symptoms to a severe inflammatory condition that can lead to the need for hospitalization and assistance with mechanical ventilation.

What will determine the effects of coronavirus infection is the amount of virus replicating in the body, the type of variant (some variants of Sars-CoV-2 cause more or less symptoms, as we have seen during the pandemic) and the immune response of our organism. In the latter case, since the immune response is mainly against entry into cells, viruses are always mutating and looking for ways to evade this defense. One such method is to “mask” the area of ​​the virus that is recognized by the defense cells and that would help trigger the immune response.

In the first experiment, conducted by scientists at Peking University, researchers identified enzymes known as PLPs (papain-like proteases) on the surface of several types of coronavirus. These PLPs had varying effects on the immune response against, for example, the cold coronavirus, where it was milder, and Sars-CoV-2, where the proteases were more potent and produced greater evasion of the immune response.

The mechanism involved in the action of the protease is known as Sting (or interferon gene inducer). In general, interferons are molecular markers that are released in the face of an inflammatory process, as well as cytokines, which help the organism recognize where the invader — a virus, bacteria, or cancer cell — is and attack it. Because the coronavirus protease inhibits this molecular signal, the interferon is not activated, and the immune response fails, allowing the virus to multiply.

The ensuing experiment sought to assess whether using a sting-like molecule (called an agonist) in conjunction with a viral protease inhibitor prevents SARS-CoV-2 virus replication. When testing human lung cells with the two compounds, researchers at Third People’s Hospital in Shenzhen, China, saw that this molecular structure inhibited virus replication.

According to the researchers, this molecule may be a target in the search for new antivirals that have a more effective effect in preventing the virus from multiplying in cells and reducing infection. Exhaust mechanism changes between variants? As in the first experiment, the scientists saw that different types of coronavirus have a different response with regard to the action of proteases, and the researchers also tested whether different variants of Covid present the same process of “disabling” the Sting mechanism.

The researchers also note that in Sars-CoV-2, the proteases show small differences in their amino acid sequences. The Covid alpha, beta, gamma, and delta variants had different mutations in this region, but all were involved in the process of stopping Sting, thus slowing down the immune response against the virus. Since many of the body’s defense mechanisms aim, initially, to recognize the pathogen in the body through proteins on the surface of the virus (called antigens), an antiviral that contains different types of mutations found in the variants may be more effective. In preventing the multiplication of the virus and ending the infection.

The authors conclude that the study is the first to reveal this complex cellular mechanism involved in recognizing and repelling coronavirus, which, when deactivated, can end up favoring so-called immune escape. Sting inactivation mechanism [sistema de interferons e citocinas molecular] It seems to be the way in which human coronaviruses evade antibodies.” (ANA BOTTALLO/Folhapress)

–

the time Promotes commitment to quality professional journalism from the state of Minas Gerais. Our newsroom produces responsible information on a daily basis that you can trust.

He follows the time In the FacebookIn the Twitter no Instagram. Help grow our community.