The SARS virus likes to eat your muscle

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That the virus takes a liking to tissue with fat is one of the best known facets of how the SARS coronavirus has spread across the globe since 2002. Since then, SARS had also been found to cause severe breathing difficulties in animals like mice, bats and dogs, and it has killed 867 people out of 8,880 people infected with the virus.

Now scientists with the Scripps Research Institute in Florida and researchers at Fort Collins, Colorado, think they have finally been able to pin down exactly what SARS does. In a new paper in the journal Science Advances, the research team report how a protein the virus uses to infect the cells it infects also goes after muscle. While people have been aware that the SARS virus likes to infect fat, their data suggests that the virus also targets muscle, and that that flexibility probably makes it easier for it to spread.

“We found that when you get to the core of the virus, the core core of the virus is much more complex,” lead author Reshma Jagsi, an assistant professor at Scripps Research Institute in La Jolla, California, said in a press release.

Jagsi and her colleagues investigated how the SARS virus spreads in murine cells, laying the groundwork for the research they are about to do in human cells. The protein the virus uses to infect cells is called Type 7, a ligand that not only is secreted from the virus, but also increases the cellular energy available to the virus in the cell. Since Type 7 has a lower energy value when it’s secreted from SARS virus, which has a much higher energy value, this ligand can only affect the core of the virus—it can’t go further into the virus like the many other properties of SARS viruses have allowed them to do.

“When we isolated [Type 7] in the virus, what we found was that the core of the virus was very rare in the virus, but when we looked at its identity, it looked so similar to muscle that it was almost like a super strain,” said Jagsi.

Jagsi and her colleagues created two different strains of Type 7 ligand, the only ones they’ve encountered in the SARS virus, which allow Type 7 to bind much more strongly to the host cells of those human SARS corrobacteriaceae. Their hope is that as these mutations become more and more widely-performed, humans with cases of Type 7 ligand-infected SARS will become more resistant to it.

Jagsi, along with the researchers from the University of Colorado, partnered with the National Institutes of Health and the University of Texas Medical Branch in Galveston on the experiments which allowed them to figure out how Type 7 binds. Both findings give hope that even if people catch the SARS virus in the future, they might not develop devastating symptoms like coughing, vomiting and kidney failure, which are the primary warning signs of SARS infection.

“If we just isolated a smaller part of [Type 7], it would be harder for us to spot when somebody is sick,” said Jagsi. “Now it’s much more likely that if somebody is sick with SARS, they might have an acute infection and not have to be a very high risk, high-hazard infection to make it into the [study] in the first place.”

While Type 7 is proving to be an extremely helpful component of the SARS virus, it may also have other effects. It’s certainly not a bad look to be able to name your own genetic signatures.

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