We declare no competing interests. Secondly, this is in keeping to our hypothesis that dysregulated hepatic innate immunity in patients with MAFLD contribute to the pathogenesis of COVID-19.
Apart from lung alveolar epithelial cells, the enterocytes of the small intestine also have abundant expression of ACE2 receptors and thus could be another portal of entry to COVID-19. In keeping with this, gastrointestinal manifestations, such as diarrhoea and abdominal pain occurred in up to one-quarter of the COVID-19 patients, without cough. Overall about half of the COVID-19 patients were tested positive for SARS-CoV-2 RNA in fecal and respiratory specimen concomitantly. 2 The liver is enriched with innate immune cells (such as macrophages, natural killer, natural killer T, and γδ T cells) 3 and due to its rich blood supply from the small bowel, circulation of the virus via the hepatic reticular system is expected. Hepatic innate immunity populations are potent cytokine producers and there are reports that obesity and NAFLD were associated with increased production of pro-inflammatory cytokines like TNF-α by adipose cells and Kupffer cells. 4, 5 This may lead to increased likelihood of symptomatic SARS-CoV-2 infections and the high prevalence of NAFLD in our study populations. Further studies are required to enhance our understanding