From Mild Cases to Critical Cases of COVID-19:  The Role of Genes in Inflammasome and Mitochondrial Dynamics

Azam Kia; Vahideh Hajhasan; Mona Nadi; Sadeq Azimzadeh Jamalkandi; Shahram Parvin; Ali Saffaie; Pedram Basirjafar; Jafar Salimian; Azam Samei

doi:10.18502/ijaai.v23i4.16213

Azam Kia Basic Science School, East Branch, Payame Noor University, Tehran, Iran
Vahideh Hajhasan Department of Cell and Molecular Biology, Faculty of Biological Sciences, North Tehran Branch, Islamic Azad University, Tehran, Iran
Mona Nadi Department of Cell and Molecular Biology, Faculty of Biological Sciences, North Tehran Branch, Islamic Azad University, Tehran, Iran
Sadeq Azimzadeh Jamalkandi Chemical Injuries Research Center, Systems Biology and Poisonings Institute, Baqiyatallah University of Medical Sciences, Tehran, Iran
Shahram Parvin Chemical Injuries Research Center, Systems Biology and Poisonings Institute, Baqiyatallah University of Medical Sciences, Tehran, Iran
Ali Saffaie Department of Clinical Pharmacy, School of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran
Pedram Basirjafar Department of Immunology, School of Medicine, Rafsanjan University of Medical Sciences, Rafsanjan, Iran
Jafar Salimian Applied Virology Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran
Azam Samei Allied Medical Science Faculty, Kashan University of Medical Science School, Kashan, Iran

DOI: https://doi.org/10.18502/ijaai.v23i4.16213

Keywords: Corona disease 2019 (COVID-19); Inflammasome; Mitochondria

Abstract

The coronavirus disease 2019 (CVOID-19) has varied clinical manifestations including mild to severe acute respiratory symptoms. Inflammasome complex and mitochondria play an important role in initiating inflammatory responses and could potentially be affected by this infection. To study the inflammasome and mitochondrial fission and fusion gene expression levels in COVID-19 patients, we designed this experiment.

The inflammasome and mitochondrial gene expression profiles were determined by real-time polymerase chain reaction in the peripheral blood of 70 hospitalized CVOID-19 patients with mild to moderate symptoms (HOSP) and 30 ICU patients with severe symptoms (ICU) compared to 20 healthy controls (HC).

The results indicated that the expression of the dynamin-related protein-1 was extremely suppressed in HOSP while it came back to the normal range in the ICU group. However, the expression of fission 1 protein had a non-significant increase in HOSP and a decrease in the ICU group. The mitofusin-1 and dominant optic atrophy genes showed high expression levels (10-fold) and (70-fold), respectively, in the HOSP group. However, mitofusin-2 significantly decreased in both groups. Although leucine-rich–containing family, pyrin domain–containing-3 (NLRP3) and apoptosis-associated speck-like protein containing a caspase activating and recruitment domain genes dramatically increased in both groups (10 and 4-fold), other inflammasome genes declined in both groups. Finally, Nuclear factor kappa-light-chain-enhancer of activate d B cells (NF-κB) extremely decreased, and Intreleukine-1 showed high expression in ICU patients (3-fold).

CVOID-19 infection suppresses the fission genes and elevates the fusion gene expression in mitochondria, and it can cause activation of the inflammasome via the NLRP3 pathway.