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
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
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.