iStockHouston: The severity of COVID-19 in people with obesity and diabetes may be explained by the combined effects of the novel coronavirus and the body's natural community of bacteria - the microbiota - working together in the lungs, according to a new study.
The review research, published in the journal eLife, assessed mechanisms linking obesity and diabetes to COVID-19, and suggested that interactions between the novel coronavirus and existing bacterial conditions may explain why people with the co-morbid conditions may often require hospitalisation and ventilation.
"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," said study co-author Philipp Scherer from the University of Texas Southwestern Medical Center in the US.
"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," Scherer said.
In the research, the scientists revisited the factors and disease pathways that connect obesity and diabetes to the severity of COVID-19 infection.
They found that the mechanisms can be roughly divided into two groups - those connected with the human cells' ACE2 receptor, and those providing an interaction between COVID-19 and pre-existing bacterial conditions.
The scientists explained that the ACE2 receptor resides on the surface of many cells in the human body, and is involved in regulating blood pressure and the function of blood vessels, and is also used by the virus to enter human cells.
They hypothesised that increased amounts of ACE2 in people with obesity or diabetes makes it easier for the virus to enter cells and increases the viral load -- an important factor in determining disease severity.
Alternatively, the researchers said, an increased shedding of ACE2 in people with obesity causes it to move to the lungs, where the virus could use it.
They believe the body's own microbiota may also be influential in the progression of lung diseases.
According to the scientists, humans carry more than 100 trillion bacteria in the body - outnumbering the number of our own cells.
They said people with obesity and diabetes are thought to suffer from a body-wide dissemination of bacteria and the substances they produce, which in turn causes low-level continuous inflammation in different tissues.
They said one potential culprit could be the lipopolysaccharide (LPS) molecules that bacteria produce, which they said can cooperate with other coronaviruses to induce respiratory distress in pigs.
They noted in the study that the LPS molecules may likely join forces with COVID-19 in humans and trigger a chain of events that causes healthy tissue to transform into scarred tissue.
"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 explained.
The scientists said a combined deficiency in ACE2 caused by COVID-19, together with obesity or diabetes, may lead to impaired gut barrier function, allowing bacteria and their toxins to leak into the circulation.
They believe these bacteria and toxins may be working with the virus in the lungs to cause more severe injury than either would do alone.
"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 said.
"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," he added.
The review research, published in the journal eLife, assessed mechanisms linking obesity and diabetes to COVID-19, and suggested that interactions between the novel coronavirus and existing bacterial conditions may explain why people with the co-morbid conditions may often require hospitalisation and ventilation.
"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," said study co-author Philipp Scherer from the University of Texas Southwestern Medical Center in the US.
"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," Scherer said.
In the research, the scientists revisited the factors and disease pathways that connect obesity and diabetes to the severity of COVID-19 infection.
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They found that the mechanisms can be roughly divided into two groups - those connected with the human cells' ACE2 receptor, and those providing an interaction between COVID-19 and pre-existing bacterial conditions.
The scientists explained that the ACE2 receptor resides on the surface of many cells in the human body, and is involved in regulating blood pressure and the function of blood vessels, and is also used by the virus to enter human cells.
They hypothesised that increased amounts of ACE2 in people with obesity or diabetes makes it easier for the virus to enter cells and increases the viral load -- an important factor in determining disease severity.
Alternatively, the researchers said, an increased shedding of ACE2 in people with obesity causes it to move to the lungs, where the virus could use it.
They believe the body's own microbiota may also be influential in the progression of lung diseases.
According to the scientists, humans carry more than 100 trillion bacteria in the body - outnumbering the number of our own cells.
They said people with obesity and diabetes are thought to suffer from a body-wide dissemination of bacteria and the substances they produce, which in turn causes low-level continuous inflammation in different tissues.
The scientists are currently assessing how host bacteria might influence COVID-19 severity.
They said one potential culprit could be the lipopolysaccharide (LPS) molecules that bacteria produce, which they said can cooperate with other coronaviruses to induce respiratory distress in pigs.
They noted in the study that the LPS molecules may likely join forces with COVID-19 in humans and trigger a chain of events that causes healthy tissue to transform into scarred tissue.
"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 explained.
The scientists said a combined deficiency in ACE2 caused by COVID-19, together with obesity or diabetes, may lead to impaired gut barrier function, allowing bacteria and their toxins to leak into the circulation.
They believe these bacteria and toxins may be working with the virus in the lungs to cause more severe injury than either would do alone.
"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 said.
"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," he added.
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