Coronavirus infects fat tissue, could eventually infect humans

Written by By Dana Kaplan, CNN

How does a virus acquire the ability to survive in the body? Sometimes, we lose it. Sometimes, it takes a lot longer than we thought.

The coronavirus that has caused one of the worst infections to strike the UK in recent decades appears to exploit a class of cells in fat tissue called “fat bridges.”

Fat bridge cells play a pivotal role in immune response by activating a defense system called interleukin. When they are activated, they work as natural guards to defend against infection by other cells — including the World Health Organization’s designated coronavirus, known as NCoV.

Exposure to NCoV, however, may stimulate production of a protein within the cells called S3K. When S3K is activated, it causes additional cytokines to be produced, suggesting that S3K somehow influenced its recipients to respond in a “flooded way,” explains Anne Hanley, a virologist at the University of Birmingham, who studied the latest spike in NCoV infections in the UK.

“It’s a cat-and-mouse game,” says Don Smith, a virologist at the University of Oxford who was not involved in the work. “If you’re getting lots of cytokines, then that’s a nice signal that the host is responding to you.”

Increasing cytokine levels can provoke an immune response; they also keep cytokines coming for a longer period of time. “Once you’re starting to have these high numbers of cytokines circulating in the body, it’s easy to replicate, and therefore easier to cause infection,” Smith says.

Coronavirus-infected monkeys face a longer recovery period than HIV-infected monkeys

There is already some evidence that NCoV, if found to be a virus with innate immunity, could potentially affect the human immune system. This article, published in the journal Nature Medicine, suggests that rodents, like humans, may exhibit how their immune systems can be hijacked by a virus to become a carrier.

But the discovery that the virus is capable of proliferating and reproducing in fat tissue could throw the spotlight on the remarkable virulence of NCoV — or highlight the flaws in our medical system.

The virus is also showing a higher rate of survival among cases than we had previously predicted, says Richard Pebody, a virologist at the Royal Free Hospital, who was not involved in the research.

Worst cases of NCoV infection were largely confined to Scotland and the Northeastern United States. More recently, NCoV infections have appeared in the Middle East. And with the use of travel restrictions, there has even been a link between NCoV and a death in the UK as of last month.

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