Title:Gastrointestinal, Liver, Pancreas, Oral and Psychological Long-term
Symptoms of COVID-19 After Recovery: A Review
Volume: 23
Issue: 7
Author(s): Reza Afrisham, Yasaman Jadidi, Maryam Davoudi, Kiana Moayedi, Omid Soliemanifar, Chrysovalantou Eleni Xirouchaki, Damoon Ashtary-Larky, Shadisadat Seyyedebrahimi*Shaban Alizadeh*
Affiliation:
- Department of Clinical Biochemistry, Faculty of Medicine, Tehran University of Medical Sciences, Tehran,
Iran
- Department of Hematology,
School of Allied Medicine, Tehran University of Medical Sciences, Tehran, Iran
Keywords:
COVID-19, inflammation, long-term, mechanisms, liver, diabetes, SARS-CoV-2.
Abstract: Due to the importance of control and prevention of COVID-19-correlated long-term symptoms,
the present review article has summarized what has been currently known regarding the molecular
and cellular mechanisms linking COVID-19 to important long-term complications including
psychological complications, liver and gastrointestinal manifestations, oral signs as well as even
diabetes. COVID-19 can directly affect the body cells through their Angiotensin-converting enzyme 2
(ACE-2) to induce inflammatory responses and cytokine storm. The cytokines cause the release of
reactive oxygen species (ROS) and subsequently initiate and promote cell injuries. Another way,
COVID-19-associated dysbiosis may be involved in GI pathogenesis. In addition, SARS-CoV-2
reduces butyrate-secreting bacteria and leads to the induction of hyperinflammation. Moreover,
SARS-CoV-2-mediated endoplasmic reticulum stress induces de novo lipogenesis in hepatocytes,
which leads to hepatic steatosis and inhibits autophagy via increasing mTOR. In pancreas tissue, the
virus damages beta-cells and impairs insulin secretion. SARS-COV-2 may change the ACE2 activity
by modifying ANGII levels in taste buds which leads to gustatory dysfunction. SARS-CoV-2
infection and its resulting stress can lead to severe inflammation that can subsequently alter
neurotransmitter signals. This, in turn, negatively affects the structure of neurons and leads to mood
and anxiety disorders. In conclusion, all the pathways mentioned earlier can play a crucial role in the
disease's pathogenesis and related comorbidities. However, more studies are needed to clarify the underlying
mechanism of the pathogenesis of the new coming virus.
