The coronavirus disease has expanded rapidly across the globe, posing a threat to world health. Prior to COVID-19′s emergence from China, it was the cause of two pandemics: severe acute respiratory syndrome and Middle East respiratory syndrome. The virus spreads by direct contact transmission and is thought to have zoonotic origins. [1]. Several variants of severe acute respiratory syndrome (SARS-CoV-2) were described throughout the course of this pandemic, among which there are different levels of concern considered by the World Health Organization (WHO), given the global public health impact. Depending on the epidemiological update by the WHO, of December 11, 2021, since the beginning of the epidemic, five SARS-CoV-2 variants of concern (VOCs) have been discovered: Alpha: The initial form of the issue was reported in the United Kingdom in late December 2020. Beta: first noted in December 2020 in South Africa, early January 2021 saw the first reports of gamma, while December 2020 had the first reports of delta in India. Omicron was first noted in South Africa in November 2021 [2]. As COVID-19 spread throughout the world, countries reached the first, second, and third waves of the epidemic at different times. This is usually noticed by specific aspects of each area and its people [3].

The most prevalent clinical signs of SARS-CoV-2 infection are fever, fatigue, cough, sputum production, and shortness of breath. However, less prevalent signs involve muscle weakness, headache, breathlessness, pleuritic pain, and sore throat. Apart from the previous symptoms, nausea, vomiting, and chest tightness are the rare signs of COVID-19. With some peripheral nervous system (PNS) indicators including hypogeusia, hyposmia, and skeletal muscle injury, new COVID-19 symptoms such as dizziness, acute cerebrovascular disease, headaches, and unconsciousness have emerged. The main causes of COVID-19 death are respiratory failure, sepsis or multi-organ failure, cardiac failure, and renal failure [4], [5].

Due to the immune response, liver damage can result not just from hepatotropic viruses (hepatitis viruses) but also from systemic, respiratory infections (EBV, influenza, and SARS-CoV). [6]. Hepatocyte damage or hepatitis brought on by non-hepatotropic infections is mostly correlated with cytokine storm, liver CD8 + T cells, oxidative stress in hepatocytes, and hypoxemia. [7]. During the previous SARS epidemic, it was reported that around 60 % of patients developed different levels of liver damage. Hepatic dysfunction was observed in 14–53 % of COVID-19 cases during this pandemic, especially in those with severe illness. Acute liver damage cases have been documented and are linked to higher fatality rates. The direct cytopathic effect of COVID-19 on the liver, an uncontrolled immunological response, sepsis, or drug-induced liver damage are all possible causes of hepatic involvement. The host angiotensin-converting enzyme 2 (ACE2) receptors, which are widely distributed in type 2 alveolar cells, are the proposed route of viral entrance. It's interesting to note that ACE2 receptors are found in the liver's cholangiocytes, vascular endothelium, and gastrointestinal tract [8].

Elevated serum levels of the enzymes alanine aminotransferase (ALT) and aspartate aminotransferase (AST) are indicative of aberrant liver biochemistry in COVID-19. Hypoalbuminaemia is a non-specific marker of disease severity and acute phase reactant; it has been noted to be linked to a worse COVID-19 outcome. Elevation in serum bilirubin level was recorded rarely in cases infected with COVID-19 [9].

This study aimed to evaluate transaminase abnormalities in various waves of COVID-19 infection and detect their relation with disease severity or death.