Immune Responses in SARS‑CoV‑2, SARS‑CoV, and MERS‑CoV Infections: A Comparative Review

Coronavirus, discovered in the 1960s, is able to infect human hosts and causes mild to serious respiratory problems. In the last two decades, the severe acute respiratory syndrome coronavirus (SARS‑CoV), Middle East respiratory syndrome coronavirus (MERS‑CoV) and severe acute respiratory syndrome coronavirus 2 (SARS‑CoV‑2) have been recognized. It has long been demonstrated that MERS‑CoV binds to dipeptidyl peptidase 4 and SARS‑CoV binds to angiotensin‑converting enzyme 2. A “cytokine storm” is the main pathophysiology of aforementioned viruses. Infiltration of neutrophils at the site of the infection is a risk factor for the development of acute respiratory distress syndrome and death. The new coronavirus, SARS‑CoV‑2, has infected more people than SARS‑Cov and MERS‑CoV as it can easily be transmitted from person to person. Epidemiological studies indicate that majority of individuals are asymptomatic; therefore, an effective and an efficient tool is required for rapid testing. Identification of various cytokine and inflammatory factor expression levels can help in outcome prediction. In this study we reviewed immune responses in SARS-CoV, Mers-CoV, and SARS-COV-2 infections and the role of inflammatory cells.