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WASHINGTON: US researchers led by an Indian-origin scientist have identified a set of human genes that fight SARS-CoV-2, the virus which causes Covid-19, a study that could help in understanding the factors that affect disease severity and suggesting possible therapeutic options.
The study by scientists at Sanford Burnham Prebys Medical Discovery Institute in San Diego, California, was published in the journal Molecular Cell.
The genes in question are related to interferons, the body’s frontline virus fighters.
“We wanted to gain a better understanding of the cellular response to SARS-CoV-2, including what drives a strong or weak response to infection,” says Sumit K. Chanda, professor and director of the Immunity and Pathogenesis Program at Sanford Burnham Prebys and lead author of the study.
“We’ve gained new insights into how the virus exploits the human cells it invades, but we are still searching for its achilles’ heel so that we can develop optimal antivirals,” he said.
Knowing which genes help control viral infection can greatly assist researchers’ understanding of factors that affect disease severity and also suggest possible therapeutic options, the institute said in a press release.
Soon after the start of the pandemic, clinicians found that a weak interferon response to SARS-CoV-2 infection resulted in some of the more severe cases of Covid-19.
This knowledge led Chanda and his collaborators to search for the human genes that are triggered by interferons, known as interferon-stimulated genes (ISGs), which act to limit SARS-CoV-2 infection.
Based on knowledge gleaned from SARS-CoV-1, the virus that caused a deadly, but relatively brief, outbreak of disease from 2002 to 2004, and knowing that it was similar to SARS-CoV-2, the investigators were able to develop laboratory experiments to identify the ISGs that control viral replication in Covid-19, the statement said.
“We found that 65 ISGs controlled SARS-CoV-2 infection, including some that inhibited the virus’ ability to enter cells, some that suppressed manufacture of the RNA (Ribonucleic acid) that is the virus’s lifeblood, and a cluster of genes that inhibited assembly of the virus,” Chanda said.
“What was also of great interest was the fact that some of the ISGs exhibited control across unrelated viruses, such as seasonal flu, West Nile and HIV, which leads to AIDS”.
As a next step, the researchers will look at the biology of SARS-CoV-2 variants that continue to evolve and threaten vaccine efficacy.
The overall global Covid-19 caseload has topped 139.6 million, while the deaths have surged to more than 2.99 million, according to the Johns Hopkins University.
The study by scientists at Sanford Burnham Prebys Medical Discovery Institute in San Diego, California, was published in the journal Molecular Cell.
The genes in question are related to interferons, the body’s frontline virus fighters.
“We wanted to gain a better understanding of the cellular response to SARS-CoV-2, including what drives a strong or weak response to infection,” says Sumit K. Chanda, professor and director of the Immunity and Pathogenesis Program at Sanford Burnham Prebys and lead author of the study.
“We’ve gained new insights into how the virus exploits the human cells it invades, but we are still searching for its achilles’ heel so that we can develop optimal antivirals,” he said.
Knowing which genes help control viral infection can greatly assist researchers’ understanding of factors that affect disease severity and also suggest possible therapeutic options, the institute said in a press release.
Soon after the start of the pandemic, clinicians found that a weak interferon response to SARS-CoV-2 infection resulted in some of the more severe cases of Covid-19.
This knowledge led Chanda and his collaborators to search for the human genes that are triggered by interferons, known as interferon-stimulated genes (ISGs), which act to limit SARS-CoV-2 infection.
Based on knowledge gleaned from SARS-CoV-1, the virus that caused a deadly, but relatively brief, outbreak of disease from 2002 to 2004, and knowing that it was similar to SARS-CoV-2, the investigators were able to develop laboratory experiments to identify the ISGs that control viral replication in Covid-19, the statement said.
“We found that 65 ISGs controlled SARS-CoV-2 infection, including some that inhibited the virus’ ability to enter cells, some that suppressed manufacture of the RNA (Ribonucleic acid) that is the virus’s lifeblood, and a cluster of genes that inhibited assembly of the virus,” Chanda said.
“What was also of great interest was the fact that some of the ISGs exhibited control across unrelated viruses, such as seasonal flu, West Nile and HIV, which leads to AIDS”.
As a next step, the researchers will look at the biology of SARS-CoV-2 variants that continue to evolve and threaten vaccine efficacy.
The overall global Covid-19 caseload has topped 139.6 million, while the deaths have surged to more than 2.99 million, according to the Johns Hopkins University.
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