Could interaction between Covid-19 and pre-existing bacteria explain severity in the obese?

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  • We already know that obesity increases the risk of severe Covid-19
  • While there is some research exploring the link, researchers are still investigating
  • Now, a new paper links pre-existing bacteria and inflammation to more severe Covid-19

Previous research has established that people with obesity and diabetes are more at risk for severe Covid-19 and a possibly fatal outcome.

Now, a new article published in eLife points towards the interaction of the body’s microbiota with Covid-19 in the lungs as a potential reason.

The researchers looked extensively at the mechanisms that link Covid-19, obesity and diabetes and cause those groups of people to experience more severe symptoms, often requiring hospitalisation and breathing assistance.

"There is rapidly emerging evidence highlighting obesity and type 2 diabetes as key risk factors linked to severity of Covid-19 infections in all ethnic groups, but the detailed underlying connections with these risk factors remain largely unknown," author Philipp Scherer, Professor at the Department of Internal Medicine, and Director of the Touchstone Diabetes Center, at the University of Texas Southwestern Medical Center, Dallas, US, stated in a news release.

"There is a paradox that people with obesity and diabetes are generally known to recover better from lung conditions than others. So, what is it about Covid-19 that makes this group of people more susceptible?"

The ACE2 receptor and existing bacterial conditions

To determine the link between diabetes, obesity and Covid-19, the authors specifically looked at two mechanism groups: those in whom the so-called ACE2 receptor is involved, and those where there is an interaction between Covid-19 and pre-existing bacterial conditions.

A previous Health24 article explained how ACE2 works to allow SARS-CoV-2 to adhere to human cells and infect them, causing illness.

This ACE2 receptor can be found on the surface of several cells of the body and is usually responsible for helping our blood vessels function and to regulate fluid volumes and blood pressure in the body.

It is believed that those with severe Covid-19 all fall in groups that have higher levels of ACE2 receptors on cells, thus offering more opportunity for the virus to grab hold and infect.

But besides the ACE2 receptors, the body’s microbiota can also play a role in how lung disease progresses.

The human body is known to carry more than 100 trillion bacteria, which is far more than the number of cells. According to the researchers, those with obesity or diabetes tend to have a body-wide dissemination of bacteria and substances they produce.

This then causes low-level ongoing inflammation in many tissues inside the body.

Impaired gut function barrier

"While all of these potential mechanisms can contribute to the severity of Covid-19, we believe that one of them plays the predominant role, and that this must be present not only in obese and diabetic patients, but also in other groups of increased risk in Covid-19," Scherer explains.

He then proposes that a deficiency in ACE2 caused by Covid-19, combined with diabetes or obesity, can lead to impaired gut barrier function which causes bacteria and toxins to leak into the rest of the body, including the lungs. These bacteria then cause even more inflammation and injury in the lungs than usual.

"Our theory is supported by experiments showing that the combination of bacterial and viral infection can lead to a 'cytokine storm' – an extreme inflammatory reaction – which is a hallmark of Covid-19", Scherer concludes. "Moreover, the involvement of viral-bacterial interactions can also explain the increased risk of severe Covid-19 seen in older people, those with heart disease and in some ethnic groups."

READ | Why can Covid-19 be so dangerous when patients are obese?

READ | Obesity ups the odds for severe Covid-19 in younger patients 

READ | Covid-19: Understanding the increased risk in people with diabetes 

Image credit: Getty Images

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