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In total, more than four million people were found to be infected with the new coronavirus sars-cov-2, which was discovered in Chinese Wuhan in December, according to Johns Hopkins University.
It is still unclear how the immune system reacts when the coronavirus enters the body.
According to Anders Sönnerborg, professor of clinical virology at the Karolinska Institute, he is, as in Other infections: the body’s nonspecific immune system that responds most quickly to a crown attack. This part of the immune system is innate, quite primitive, and is made up, among other things, of so-called food cells that destroy foreign substances.
What is special about a SARS-cov-2 infection is that the body’s nonspecific immune system appears to be inferior to the production of interferon, the body’s own antiviral substances that kill virus particles. The researchers took different types of cells from the body, cultured them in test tubes, and exposed them to the virus to see how they react. Similar animal experiments have also been conducted. In addition, they have analyzed cells from an infected human, he says.
– Although it is not yet completely coated, most of all these attempts speak because they are poor in the production of interferon. One hypothesis is that the virus inhibits the formation of interferon, says Anders Sönnerborg, who is also head of the Karolinska Institute’s Department of Infectious Diseases and Skin, where his research team is working on the development of antiviral drugs for the disease.
The non-specific immune system Capacity is limited. When it fails to eliminate the virus on its own, the adaptive immune system is activated, which is directly aimed at attacking the specific virus. B cells, a type of white blood cell, form antibodies that bind to the virus so that they are destroyed. Then T cells, another type of white blood cell that belongs to the so-called cellular immune system, enter and destroy infected cells, Anders Sönnerborg describes.
What happens next is unclear.
In normal cases, both B cells and T cells can usually stop the infection. But in some people, the virus creeps down the windpipe into the lungs. That’s when the really troublesome one, the so-called cytokine storm, can come.
– Exactly what is happening is not really clear. What is really going to happen is that the cellular immune system kills the virus in the lower trachea, but for some reason it balances out, so there is a huge activation of this part of the immune system throughout the lungs, he says.
During cytokine storms, many inflammatory cytokines, a type of signaling molecule, form. It causes severe inflammation that further damages the lungs instead of removing the virus.
Anders Sönnerborg, professor of clinical virology at the Karolinska Institute.
Photo: Andreas Andersson / Karolinska Institute
If the patient can Cytokine storm and recover the issue of immunity remains.
The World Health Organization, WHO, recently said there is no evidence that people who have recovered from covid-19 and have antibodies are protected from a second infection. According to Anders Sönnerborg, it is not yet clear whether all individuals develop antibody-forming memory cells, which protect against the virus in the long term.
– The next time the sars-cov-2 virus enters the body, the hope is that memory cells will begin to make antibodies to make them immune to infection. With other viruses that cause common colds, immunity remains for two to three years, but it’s not clear what immunity looks like here, he says.
Follin Infection Protection Doctor At Smittskydd, Stockholm agrees that there are still questions about these three things. He believes that medical care would benefit from more knowledge.
“When it comes to interferon production, it is important to understand the mechanisms of the disease,” he writes in an email.
Infection protection physician Per Follin appreciates more insight into how the coronavirus affects the immune system.
Photo: Fredrik Persson / TT
More knowledge about cytokine storms is valuable in understanding the burden of intensive care and long care times, while immunity is interesting from the point of view of the spread of infection, he says.
“In short, we need to understand how infection spreads, immunity at the group and individual level, yes, in short, if you get protection after infection or if you can re-infect yourself,” he writes.
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