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In an isolated laboratory at the Icahn School of Medicine at Mount Sinai in East Harlem, virologist Benjamin tenOever managed to decode how the virus that causes COVID-19 attacks our immune system, wreaking havoc like no other virus he’s studied before.
According to The New Yorker, every cell of our body shares the same DNA and single-strand RNA, which acts like software, programming the cell to make proteins. SARS-CoV-2 disrupts the programming by replacing 60% of this software in each cell it infects. A typical virus replaces only 1% of the RNA in each cell.
“This is the highest I’ve ever seen,” said tenOever, who was born of Dutch parents. “Polio comes close.” He said that the novel coronavirus shuts down only one arm of our immune system — the one that signals other cells to defend themselves against viral spread — while leaving the other arm to run rampant. Unlike other viruses, SARS-CoV-2 does not modulate the second immune response that sends cytokines through the body to summon white blood cells.
Normally, according to The New Yorker, white blood cells help destroy the invaders selectively, but in COVID-19 victims, they are deployed too widely, creating inflammation and destruction throughout the body. According to the researchers, it is this response that causes the potentially deadly blood clots and so-called “cytokine storms” medical experts have reported in patients.
Their study, published in the journal Cell, summarizes that the “reduced innate antiviral defenses coupled with exuberant inflammatory cytokine production are the defining and driving features of COVID-19.” TenOever and his team also found in subsequent studies that the immune systems in older victims were less adaptive and therefore more prone to the destruction caused by the virus.
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