Image copyright Getty Images Image caption Researchers have identified the proteins which they say can cause a severe acute respiratory syndrome
Fat tissue in people who have the fatal coronavirus infection differs from the fat tissue of healthy people, a study says.
Researchers found the differences were “mostly anatomical” in a new analysis of laboratory experiments and animal models.
It raises the possibility that the E.coli bacteria – which causes the respiratory illness – may be able to damage fat tissue and cause severe respiratory symptoms.
The findings were published in the journal Nature Microbiology.
The coronavirus that has been the focus of recent international concern is linked to severe pneumonia and kidney failure and so far has killed at least 36 people.
Coronavirus can be spread by person-to-person spread. It is the result of an E.coli infection passed on through food and water – in the form of tomatoes, lettuce and water lilies.
However, the cause of those syndromes in the current outbreak is not clear.
Currently, there is no vaccine or treatment for the disease.
Image copyright Getty Images Image caption People who suffer from severe respiratory illness are being told to seek medical advice if they are suffering from fever and respiratory problems
Researchers from Britain, Canada and the United States used macrophages, cells in the body’s immune system, and found fat tissue tissue was more resilient to the virus than normal tissue.
More than 80% of macrophages were able to survive an E.coli infection, and even 16 days later, two thirds were still alive.
Meanwhile, the fat tissue was barely damaged.
This suggests macrophages are more able to help the body clean up the deadly microbes.
It also suggests the fat tissue is more able to produce compounds which could cut the bacteria’s staying power, according to research led by Dr John Treacy from University College London (UCL).
Image copyright David Hill / Alamy Stock Photo Image caption The number of people in the UK suffering from the virus has dropped since it was first identified
Senior author Professor Geoffrey Vella of the University of British Columbia said this might be why the first people to catch the virus looked and felt less unwell.
He added: “The people who develop serious complications may have lost the ability to divide – at least enough of it to be able to fight off their infection.”
Previous studies found that fat cells shed bits of DNA in fat tissue with different levels of potential damage.
Scientists had also shown that fat tissue had fewer genes in it than human blood cells, suggesting the cells were “super-effective at diffusing fat cells”.
Other research has found that fat cells from people who have been infected with E.coli can contain snippets of RNA (ribonucleic acid), which turn out to be a molecule of specific RNA.
Many groups of these RNA sequences are made in the liver, suggesting their function is to dispose of fat cells.
Molecules from HIV and rubella also contain a small RNA molecule.
Dr Nicola Masters, an immunologist at Barts and the London NHS Trust who was not involved in the work, said the findings were “particularly exciting”.
“This is part of the evolution of resistance to pathogens and there is no question that certain bacteria are becoming increasingly adept at infecting and potentially damaging our cells.
“These studies highlight a previously under-studied aspect of the disease and appear to shed light on the mechanism at play.”
An investigation by BBC News last year found there had been a 400% increase in cases of hospital admissions for people with the coronavirus over the past two years.