{"id":41396,"date":"2020-12-13T18:39:43","date_gmt":"2020-12-13T22:39:43","guid":{"rendered":"http:\/\/stateofthenation.co\/?p=41396"},"modified":"2020-12-13T18:43:23","modified_gmt":"2020-12-13T22:43:23","slug":"coronavirus-hijacks-immune-cells-to-create-cytokine-storms-says-new-study","status":"publish","type":"post","link":"https:\/\/stateofthenation.co\/?p=41396","title":{"rendered":"Coronavirus hijacks immune cells to create cytokine storms, says new study"},"content":{"rendered":"
\n\"\"<\/p>\n

By Ralph Flores
\nScience<\/p>\n

Scientists continue to be baffled by the Wuhan coronavirus (COVID-19), especially how it \u201chijacks\u201d certain cells of the body. A new study from the\u00a0Icahn School of Medicine at Mount Sinai<\/em><\/a>\u00a0suggests that SARS-CoV-2 \u2013 the\u00a0coronavirus strain behind the current pandemic \u2013 can inhibit one virus-fighting set of genes but allow another set to launch<\/a> \u2013 a pattern not seen\u00a0with other viruses.<\/p>\n

For Benjamin tenOever, a virus expert at Mount Sinai and the senior author of the study,\u00a0this behavior is something he has not seen in his 20 years of studying viruses. Other viruses, like the flu virus and the original SARS virus, interfere with two sets of genes in the body\u2019s immune response: The one that prevents viruses from replicating and the other that\u00a0recruits immune cells to the infection site to kill viruses.<\/p>\n

The first group of genes, which tenOever dubs\u00a0\u201ccall to arms genes,\u201d produces\u00a0interferons<\/strong>, which are proteins that interfere with the virus\u2019s ability to replicate. These proteins are important modulators of the immune response. Once interferons are released, they serve as a signal to nearby cells to activate their own genes. This slows down the virus\u2019s ability to make copies of itself if it invades them. According to tenOever, this process lasts anywhere between seven to 10 days, which is plenty of time for the second group of genes to do their job.<\/p>\n

The second group of genes produces chemokines<\/strong>, which are small proteins\u00a0that emit a biochemical \u201ccome here!\u201d alarm. TenOever calls these \u201ccall for reinforcement\u201d genes, on account that other immune cells \u2013 like the antibody-making B cells and the virus-killing T cells \u2013 rush to chemokine sources once they sense the alarm.<\/p>\n

\u201cMost other viruses interfere with some aspect of both the call to arms and the call for reinforcements,\u201d tenOever added. \u201cIf they didn\u2019t, no one would ever get a viral illness.\u201d<\/p>\n

SARS-CoV-2, however, behaves differently. It prevents the first group of genes from producing\u00a0interferons<\/a>\u00a0that can slow\u00a0its replication but allows\u00a0the second group of genes to secrete chemokines. This not only allows the virus to multiply unchecked, but it also causes immune cells to flood the lungs. The result is a storm of inflammatory molecules in the affected organ, which tenOever calls a unique and aberrant consequence of SARS-CoV-2.<\/p>\n

When your immunity turns against you<\/h2>\n

TenOever and his team examined healthy lung cells growing in lab dishes, ferrets\u00a0(which they called an appropriate animal model for SARS-CoV-2 infections) and lung cells from coronavirus patients. Within three days of infection, the team found a mild response from the \u201ccall to arms\u201d genes that inhibit replication and a large introduction of the \u201ccall for reinforcement\u201d genes.<\/p>\n

\u201cBasically people are contracting the disease, SARS-CoV-2 enters the lungs<\/a> and it begins to replicate and, at that site of replication, those cells that are infected, they don\u2019t do a good job of spreading the word about their infection which allows it to essentially fester in the lungs,\u201d tenOever explained.<\/p>\n

Without interferons, the virus is free to infect other cells<\/a> and replicate much faster, all while cells in the area continue to call for reinforcements. But by the time the reinforcements arrive, the virus has grown out of control.\u00a0The presence of large amounts of\u00a0immune cells, on the other hand,\u00a0triggers uncontrolled levels of inflammation, which does nothing\u00a0but induce more inflammation.<\/p>\n

This could explain why people with COVID-19 experience \u201ccytokine storms\u201d in which the body attacks its own cells and tissues instead of just the virus. (Related:\u00a0Study: Vitamin D deficiency found to increase the risk of fatal coronavirus infections and a deadly \u201ccytokine storm.\u201d<\/a>)<\/p>\n

According to tenOever, their findings point to two methods of treatment. For patients who have just started developing symptoms, he says that therapy should focus on inducing the missing \u201ccall to arms\u201d genes, so the virus can behave similarly to that of the flu. But for those with severe symptoms, he says that reducing inflammation and the risk of cytokine storms will be beneficial.<\/p>\n

TenOever and his team\u2019s findings\u00a0were published\u00a0last week in the journal\u00a0Cell<\/em>.<\/p>\n

Pandemic.news<\/a> has the latest on the ongoing coronavirus outbreak.<\/p>\n

Sources include:<\/strong><\/p>\n

StatNews.com<\/a><\/p>\n

Cell.com<\/a><\/p>\n

DailyMail.co.uk<\/a><\/p>\n

___
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