It may be as simple as inhibiting an immune system route to avoid COVID-19 infection and serious organ damage. 

In this colourized scanning electron micrograph, a cell (purple) is heavily infected with SARS-CoV-2 virus particles (yellow). According to a recent study, blocking a specific protein in a biological pathway may prevent SARS-CoV-2 infection and prevent the virus from misdirecting the immune system against healthy cells and organs.

While the world waits for a safe and effective vaccine to prevent infections caused by the coronavirus 2 that causes severe acute respiratory syndrome (SARS-CoV-2), researchers are focusing on learning more about how SARS-CoV-2 attacks the body in order to find new ways to limit the COVID-19 pandemic's devastation. A group of researchers discovered the key to one possibility in a new study: blocking a protein that allows the virus to turn the immune system against healthy cells. 

Based on their findings, the researchers believe that suppressing the protein known as factor D will also minimise the potentially lethal inflammatory reactions that many people have to the virus.The possibility that there are drugs in development for other illnesses that can conduct the necessary blocking adds to the thrill of the finding.Spike proteins on the surface of the SARS-CoV-2 virus, which resemble the spiny ball from a medieval mace, are known to be the pathogen's means of attaching to cells targeted for infection. The spikes do this by grabbing heparan sulfate, a huge, complicated sugar molecule located on the surface of cells in the lungs, blood arteries, and smooth muscle that makes up most organs. SARS-CoV-2 utilizes another cell-surface component, the protein known as an, after being aided by its first interaction with heparan sulfate. 

The researchers discovered that when SARS-CoV-2 binds to heparan sulfate, it prevents factor H from binding to cells with the sugar molecule.The primary function of Factor H is to prevent the immune system from harming healthy cells by controlling the chemical impulses that cause inflammation.Without this defense, cells in the lungs, heart, kidneys, and other organs could be destroyed by the natural defensive mechanism designed to protect them.  

"Previous research has suggested that, in addition to binding heparan sulphate, SARS-CoV-2 triggers a cascade of biological reactions — what we call the alternative pathway of complement, or APC — that, if misdirected, might result in inflammation and cell death." When bacteria or viruses attack the body, the APC is one of three chain reaction mechanisms that involves the breaking and combining of more than 20 different proteins (known as complement proteins). The last product of the complement cascade, known as membrane attack complex (MAC), forms on the invader's surface and destroys it, either by creating holes in bacterial membranes or shattering a virus' outer envelope.Healthy cells' membranes, on the other hand, can generate MACs. Humans, on the other hand, have a number of complement proteins, including factor H, that regulate the APC, keep it under control, and therefore protect normal cells from injury. The researchers employed normal human blood serum and three components of the SARS-CoV-2 spike protein in a series of tests to figure out how the virus activates the APC, hijacks the immune system, and puts normal cells at risk. They discovered that two of the subunits, S1 and S2, are the components that bind the virus to heparan sulfate, triggering the APC cascade and blocking factor H from connecting with the sugar, thereby disabling the complement regulation by which factor H prevents an immune response that is misdirected.  

The immune system's response to substances released by the lysis of dead cells, according to the researchers, could be to responsible for organ damage. They were able to halt the damaging chain of events caused by SARS-CoV-2 by blocking factor D, a complement protein that works directly upstream from factor H in the pathway. 

"When we injected a small molecule that suppresses the action of factor D, the APC was not triggered by the virus spike proteins." "We suspect that when the SARS-CoV-2 spike proteins bind to heparan sulphate, it increases complement-mediated death of normal cells because factor H, a key regulator of the APC, is unable to accomplish its task."

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To further understand what happens, think of the APC as a moving car.

"Without the brakes, the gas pedal can be floored without restraint, resulting in a collision and destruction." "Viral spike proteins impair the biological brakes, factor H, allowing the immune system's gas pedal, factor D, to accelerate and destroy cells, tissues, and organs." The brakes can be reapplied and the immune system reset if factor D is inhibited."  

Several complement-related human illnesses, including age-related macular degeneration, have already been linked to cell death and organ damage caused by a misdirected APC associated with factor H suppression. and atypical hemolytic uremic syndrome (aHUS), a rare condition in which blood clots impede renal blood flow.The researchers anticipate that their findings will spur greater research into the possible use of complement-inhibiting medicines already in development for other diseases against COVID-19. "Within the next two years, a lot of these medications will be FDA-approved and in clinical practice". "Perhaps one or more of these could be used in conjunction with vaccinations to help curb COVID-19 spread and prevent future viral pandemics."