Dr. Jawaher Alharthi, from the Westmead Institute and medical research, University of Sydney, Australia, and her colleagues have discovered how COVID-19 increases the risk of fatty liver disease and how the latter is increasing the severity of COVID-19, aiding the development of potential treatments for these patients.

Metabolic dysfunction associated fatty liver disease (MAFLD) affects one-in-four adults and nearly one-in-10 children worldwide. Globally, MAFLD is the most frequent kind of chronic liver disease.

Liver disease is a silent killer. Most people don't know they have a liver problem until it's advanced and they develop liver scarring, liver cirrhosis and, in severe cases, liver failure and deadly cancer. Its complications, however, are not limited to liver disease. It is strongly associated with several other cardiometabolic diseases such as Type 2 diabetes and cardiovascular diseases.

In response to COVID-19, the host (humans) mounts an immune response whose delicate balance determines the course of illness.

Severe COVID-19 is associated with exacerbated immune and hyperinflammatory responses and inflammatory macrophages can induce a cytokine storm leading to tissue damage.

A new study by researchers at the Westmead institute for medical research, University of Sydney, have discovered how COVID-19 increases the risk of fatty liver disease and how is the latter increasing the severity of COVID-19, aiding the development of potential treatments for these patients.

Dr. Jawaher Alharthi, the first author of this work said, "The relationship between fatty liver disease and COVID-19 considered a bit of a mystery, as we do not know how and why both diseases increases the risk of each other. Our research team led by professor Mohammed Eslam conducted a large and detailed genetic and molecular study and identified that gene called MBOAT7 associated with the severity of both MAFLD and COVID-19."

"This gene, plays an important role in the regulation of immune and inflammatory responses upon COVID-19. A disruption in the activity of the MBOAT7 gene could increase the chances of increase cytokines production and tissues damage and liver disease," Dr. Alharthi said.

The epigenome is a set of markers that determines not just gene expression, but genes themselves and influenced by environment, diet, and hormones.

"Interestingly, we also identified that disruption of MBOAT7 may 'preprogram' the cell epigenome and prime it to respond severely to even a weak stimulation upon COVID-19 that ultimately increases tissue damage."

The findings are published in the journal Nature Communications.