Is Gut Involvement a Cause or Effect of COVID-19?

Khairil Khuzaini Zulkifli,Yoen Young Chuah,Raman Muthukaruppan,Phei Oon Tan,Zheng Feei Ma,Nazri Mustaffa,Yeong Yeh Lee

doi:10.21315/mjms2021.28.6.14

Abstract

Digestive disorder symptoms in COVID-19 may be similar in form to post-infectious functional gastrointestinal disorder (PI-FGID). To cause clinical effects, SARS-CoV-2 must reach the bowels and gastric hypochlorhydria may facilitate such transit. Asian elderly are predisposed to greater infection rate and severity of COVID-19, and the high prevalence of gastric atrophy and intake of proton-pump inhibitor in this aged group might explain the risk. Persistence shedding of SARS-CoV-2 in stools indicates that faecal transmission should not be disregarded. Gut involvement in COVID-19 is mediated by angiotensin-converting enzyme 2 (ACE2) receptor, which serves as the entry point for SARS-CoV-2 in the small bowel. ACE2 dysregulation has an impact on the homeostasis of gut microbiota and altered inflammatory response. Liver injury is variable in COVID-19 and is likely a result of by-stander effects rather than actual viropathic process. Further research is needed to understand if gut involvement is a cause or effect of SARS-CoV-2.

Highlights

In the beginning, most have perceived the first outbreak of a novel coronavirus from Wuhan, China, in December 2019 as just another flu and some remained skeptical of its impact
Fast forward, as of December 2021, more than 160 million persons have been infected with a reported number of deaths already passed the three-million mark (WHO COVID-19 website: www.who.int/emergencies/diseases/novelcoronavirus-2019)
We propose that post-infectious functional gastrointestinal disorder (PI-FGID) may be an alternative explanation

Summary

Background

Most have perceived the first outbreak of a novel coronavirus from Wuhan, China, in December 2019 as just another flu and some remained skeptical of its impact. Two of the first five reported cases in Europe have positive stool samples for SARS-CoV-2 RNA despite not having any GID symptom [14]. Through gut ACE2, SARS-CoV-2 gains its footing in the bowels and results in dysregulation of gut microbiota and barrier function, leading to PI-FGID If this is the case, probiotics may work and this is based on our work among the flood victims who developed PIFGID [24]. A preprint paper has reported that SARS-CoV-2 preferably bind to ACE2-expressed cholangiocytes rather than hepatocytes indicating that the variable liver injury observed in COVID-19 is probably related to cholangiocyte dysfunction rather than hepatocellular [39]. Many trials are currently ongoing to repurpose drugs initially indicated for other RNA viruses to treat COVID-19, with some success [42]

Conclusion

Findings

Conflict of interest