"}). Various blood and biochemical abnormalities have been witnessed in patients with COVID-19. The most commonly found irregularities include leucocytosis, leukopenia, lymphopenia, increased CRP, lactate dehydrogenase (LDH), and erythrocyte sedimentation rate (ESR) ([@ref12]). Other observed discrepancies include abnormal procalcitonin, and albumin and liver enzyme levels. On viral entry into the body, the virus attacks the throat, causing the initial symptoms of COVID-19, further progresses to the lungs, and causes distress, following which it reaches the bloodstream ([@ref13]), resulting in the progression of the condition. In healthy individuals, white blood cells (WBCs) circulate in the blood and are attacked by foreign particles, such as bacteria and viruses. Leukocytosis occurs when there is an abnormal increase in WBCs above the normal range (3,400 to 9,600 cells/μL). This is a common sign of inflammation induced by viral entry. Similarly, leukopenia is the anomalous decrease of WBCs (less than 4,000 cells/μL) in the blood and can also result from various viral infections in which the WBCs are used more quickly than they are made. Likewise, lymphocytes are cells produced by the bone marrow involved with immunity; a dynamic balance is maintained in the number of lymphocytes in healthy individuals. Lymphopenia or reduction of lymphocytes (less than 1,000 lymphocytes/μL) is another abnormality commonly observed in COVID-19 patients. Lymphopenia is a factor that is positively correlated with disease severity ([@ref14]) and may be caused by the surge in cytokines mediated by COVID-19 or by direct inactivation by SARS-CoV-2. Correspondingly, the inflammatory response triggered by SARS-CoV-2 results in the modification of levels of CRP and ESR in the blood. In COVID-19, CRP concentration rises following IL-6 secretion caused by the cytokine storm after infection. It binds to markers present on dying cells and consequently activates the complement system to mediate phagocytosis of the dead cells. As a result, 