Non-alcoholic fatty liver disease does not raise the risk of COVID-19, gene study shows

Keith Alcorn
Published:
26 May 2020
Image: Bru-nO/Pixabay

People with a genetic profile that strongly predicts non-alcoholic or metabolic-associated fatty liver disease were not at higher risk of being hospitalised with COVID-19 in the United Kingdom, an analysis of the UK Biobank has found.

The study calls into question Chinese findings which suggest that people with non-alcoholic fatty liver disease (NAFLD), also known as metabolic-associated fatty liver disease (MAFLD), were at higher risk of severe COVID-19. A separate study in China also found a higher risk of severe COVID-19 illness in people under 60 years old who had metabolic-associated fatty liver disease.

The findings, published in the Journal of Hepatology, come from an analysis of anonymised patient data made available by the UK Biobank UKBB cohort study. The cohort of 502,640 people aged 40-69 provides medical history, biological samples and genetic data to address research questions about life-threatening diseases.

Researchers in Italy and Sweden analysed data on 1460 white British cohort members who had been tested for SARS-CoV-2 infection (526 positive and 934 negative). Fifty-seven per cent of the entire sample were hospitalised and the researchers used hospitalisation in the positive cases as a surrogate for a severe COVID-19 outcome.

They looked for people with a high genetic risk score for MAFLD, looking for genes previously validated as predictive for the accumulation of fat in the liver and concomitant liver damage. In the absence of systematic testing for MAFLD, genetic markers that are highly predictive of liver fat accumulation in the age group studied are a surrogate for a diagnosis of MAFLD using laboratory and biopsy measures.

The researchers found no association between a high genetic risk score for MAFLD and higher risk of severe COVID-19 outcome. They say that much larger studies are needed to examine the impact of obesity, metabolic disorders and cardiovascular disease on the risk of severe COVID-19 outcomes.

In a second study, French researchers investigated whether MAFLD increased the potential for infection of liver cells by SARS-CoV-2. They looked at the expression in liver cells of four human proteins essential for SARS-CoV-2 entry into cells. Higher levels of expression would predict greater vulnerability of cells to infection, they hypothesised.

Looking at previously published data on liver gene expression in 12 lean people without NAFLD, 16 obese people without NAFLD and 17 people with biopsy-proven NASH, they found no evidence of increased expression of the genes for proteins associated with SARS-CoV-2 cell entry in people with NASH or obese people. Data from mouse studies similarly showed no increase in expression of the relevant genes in mice fed on a fattening diet.

References

Valnet L, Jamialahmadi O, Romeo S. Lack of genetic evidence that fatty liver disease predisposes to COVID-19. Journal of Hepatology, advance online publication, 20 May 2020. https://doi.org/10.1016/j.jhep.2020.05.015

Biquard L, Valla D, Rautou PE. No evidence for an increased liver uptake of SARS-CoV-2 in metabolic associated fatty liver disease. Journal of Hepatology, advance online publication, 30 April 2020.

Zhou YJ et al. Younger patients with MAFLD are at increased risk of severe COVID-19 illness: A multicenter preliminary analysis. Journal of Hepatology, advance online publication, 26 April 2020. https://doi.org/10.1016/j.jhep.2020.04.027

doi: https://doi.org/10.1016/j.jhep.2020.04.035.

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