How the SARS-CoV-2 Virus Tricks the Human Cell

Viral infections start with the entry of viruses into the cells. This article describes how the SARS-CoV-2 tricks the human cells to let it in. This updated article was first published on April 23, 2020

The SARS-CoV-2 virus causes Covid-19. That virus has now infected almost 19 million and killed more than 700 thousand worldwide.

The Covid-19 virus has many ways to enter a human cell. A common strategy is to hook the Spike protein into a receptor on the surface of a human cell. The S proteins stick out of the virus and give it the appearance of a crown, and that’s why it is called coronavirus.

After the Spike protein attachment with the receptor, the Covid-19 virus enters the cell in a process called endocytosis.

800px-Viral_entry_(Endocytosis_and_lysis).svg — Viral endocytosis (entry) in a cell

Once inside, the virus can make copies of itself. As they increase, the host cells become overwhelmed and die. Those millions of viral copies are released and spread all over the body to cause infection and damage.

Why would a normal human cell let in a virus? The virus tricks the human cells into thinking that it is something valuable.

Cells need nutrients, and those nutrients float around in the fluid surrounding the cells in molecules. Those floating nutrients are similar to sushi moving around in a conveyor belt sushi bar. Once diners see something they like, they use their hands to get that tiny plate with sushi.

The cells use receptors on their surfaces instead of hands. Once a cell detects anything it can use, the cellular receptors grab hold of that molecule and allow it to get inside. In the case of the SARS-CoV-2, the receptors grab hold of the S protein.

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In short, SARS-Cov-2 tricks the cells’ receptors and enzymes into sensing that the virus is something that the cells can use. That is how the SARS-CoV-2 can get inside the cells and cause infection.

There are different cell receptors. So far, scientists have identified several of the host molecules that the SARS-CoV-2 uses. ACE2, TMPRSS2, CD147, GRP78, and FURIN receptors.

ACE2 is present in the lungs and the heart, and some have more than one, like ACE2 and TMPRSS2 in the lungs.

The discovery of the S proteins’ attachment to these receptors provides a treatment strategy. Inserting a drug between the receptor and the S protein can block viral entry and prevent infection. At least theoretically.

How does the Respiratory Tract Body Protect Itself Against Microbes?

Antibodies are one of the first-line defenses against attacking germs. There are specialized antibodies called immune globulin A or IgA in the lining of the respiratory passages, including the nose and throat down to the lungs.

The IgAs against COVID-19 are very effective in healthy people such that they can result in infected people having no symptoms or asymptomatic or very mild symptoms.

That study was featured here. The Total number of COVID-19 is much Higher. Research has shown that IgAs are so effective that the SARS-CoV-2 becomes undetected, and even if IgG and IgM antibody tests are done, they will come back negative.

That’s because the IgA did all the work. There is no need to activate the other antibodies like IgG and IgM.

That’s why COVID-19 cases could be much higher if the IgA is also tested among the asymptomatic and mild patients.

Strengthening the Immune System

Taking control of the blood pressure and blood sugar among hypertensive and diabetic people will help preserve the immune system.

Vitamin C and Zinc provide the necessary anti-oxidants to keep the immune system healthy.

This article talks about the drugs under research that block the S protein from attaching to cells.

The knowledge about Covid-19 is rapidly evolving, and information may update as discoveries are made. Stay current by subscribing.

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