Revealed: How SARS-CoV-2 evades our immune system

Editor’s note:  The statement is not accurate. at least not 100% accurate.  The bottom line is, eventually, a person’s normally functional immunity protects the person against covid 19 and help the patient to recover from the infection.
The message from the study seems to make you feel that you yourself could not do too much against the viral infection because the virus “could evade your immunity”.  This implies that you need drugs including vocid 19 gene therapy or so-called vaccines to help you.
The fact is that when it comes to Sars Cov 2 infection, healthy people are rarely at risk of any severe complications.  Some people die because either they are too frail or suffer chronic health conditions such as diabetes.

編者按:該聲明不準確。至少不是100%準確。 底線是,最終,一個人的正常功能免疫力可以保護該人免受covid 19的侵害,並幫助患者從感染中恢復過來。

該研究傳達的信息似乎讓您覺得您自己無法對病毒感染採取太多措施,因為病毒“可能會逃避您的免疫力”。 這意味著您需要藥物,包括 vocid 19 基因療法或所謂的疫苗來幫助您。

事實是,當涉及到SARS Cov 2 感染時,健康人很少有出現任何嚴重並發症的風險。 有些人死亡是因為他們太虛弱或患有糖尿病等慢性健康問題。

NEWS RELEASE 

Peer-Reviewed Publication

HOKKAIDO UNIVERSITY

Suppression of NLRC5 in SARS-CoV-2-infected cells
IMAGE: THE EXPRESSION OF THE IMMUNE RESPONSE GENE ​​NLRC5 (RED PURPLE) IS SUPPRESSED IN SARS-COV-2 (GREEN) INFECTED CELLS (PHOTO: KOICHI KOBAYASHI). view more 

CREDIT: KOICHI KOBAYASHI

Scientists at Hokkaido University and Texas A&M University have identified a key mechanism used by the SARS-CoV-2 virus to evade host immune systems.

Researchers in Japan and the United States have found SARS-CoV-2 can knock out an important molecular pathway linked to an immune complex called MHC class I. The finding should help scientists better understand how COVID-19 infection takes hold.

“Our discovery reveals how the virus can evade the human immune defense system and might help to explain why the pandemic has been so severe,” says Hokkaido University and Texas A&M University immunologist Koichi Kobayashi, who led the study. “The mechanisms we identify may provide new molecular targets for drug discovery.”

The scientists used a bioinformatics approach to look at how SARS-CoV-2, the virus that causes COVID-19, changes gene expression in the immune systems of COVID-19 patients compared to uninfected individuals. This is a useful way to look into the function of complicated cell signalling pathways that trigger immune responses to fight off harmful bacteria and viruses.

MHC (major histocompatibility complex) class I molecules are a central weapon in the immune response against viruses. When a virus infects a cell, the cell facilitates the expression of viral antigens on the surface of infected cells, drawing the attention of immune cells called cytotoxic T cells. These immune cells zero in on and destroy the infected cells, together with the invading virus inside them.

In addition to analysing gene expression in COVID-19 patients, the research team also infected human cell lines with the SARS-CoV-2 virus to validate their findings.

The results showed that a protein from the SARS-CoV-2 virus, called ORF 6, suppresses a host cell protein, called NLRC5, responsible for activating the MHC class I pathway.

The study showed this happens in two ways. ORF6 hampers cell signalling, which turns off the expression of NLRC5. ORF6 also blocks the function of NLRC5.

Other infectious viruses, including HIV and MERS, are known to also target the MHC class I pathway. Researchers believed that SARS-CoV-2 probably did as well, but this study is the first to unravel the mechanism.

“Without the activation of the MHC class I pathway, viruses in the infected cells are essentially hidden from the immune system. That helps to explain why SARS-CoV-2 virus persists in the body and why it keeps infecting others, leading to the pandemic,” Kobayashi says.

Further research could help find and test drugs that block the activity of the ORF6 viral protein, to restore host cell ability to activate the major histocompatibility complex. If successful, such drugs could encourage the host immune system to clear the virus itself, effectively boosting immune responses.


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