1- Introduction
In the past two decades, there have been two major coronaviruses (CoV) outbreaks, namely the severe acute respiratory syndrome coronavirus (SARS-CoV) in 2002, and the middle east respiratory syndrome coronavirus (MERS-CoV) in 2012 (Cui, Li, & Shi, 2019; de Wit, van Doremalen, Falzarano, & Munster, 2016). The recent coronavirus outbreak which happened in Wuhan, China, is known as the 2019-nCoV outbreak, recently renamed as the SARS-CoV-2 outbreak or COVID-19 (Perlman, 2020; C. Wang, Horby, Hayden, & Gao, 2020).
The first case of SARS-CoV-2 infection was reported with the presentation of symptoms of atypical pneumonia. This case was further confirmed to be caused by the novel coronavirus, SARS-CoV-2 (”Coronavirus disease 2019 (COVID-19) Situation Report – 57,” 2020). The most potential risk for the spread of COVID-19 worldwide is related to traveling, which can lead to the regional and global spread of the disease (Q. Li et al., 2020). The origin of coronaviruses is primarily animal. The outbreaks occur when these viruses cross the species barrier and infect humans. SARS and COVID-19 viruses share many similarities in terms of their transmission and pathogenicity. All of them cause acute respiratory illness and follow human to human transmission. Although the coronavirus SARS-CoV-2, responsible for COVID-19, has been successfully isolated and the viral infectivity and pathogenicity have been understood, there is much room for the understanding of the viral antigenic structure, mode of action, and pathogenicity (Cui et al., 2019; de Wit et al., 2016).
SARS-CoV-2 is a novel emerging contagious agent that has found a way into human civilization. The prediction of Fan et. al (Fan, Zhao, Shi, & Zhou, 2019) that a future SARS or MERS-like CoVs epidemic would emerge in China with a probable bat source has turned into reality when the first case of concentrated viral pneumonia was reported in Wuhan. Later on, the novel coronavirus, designated as SARS-CoV-2, was found to be responsible for the viral outbreak of pneumonia in Wuhan (Rehman, Shafique, Ihsan, & Liu, 2020). Generally, emerging and re-emerging of viral infections is related to the RNA family of viruses, because these viruses are associated with high mutation rates, which leads to their eminent environmental adaptation through rapid evolution (E. K. Hui, 2006). To date, little knowledge is available about SARS-CoV-2.
A recently published report suggests that SARS-CoV-2 shares a 79% nucleotide identity with SARS-CoV and 51.8% nucleotide identity with MERS-CoV (Ren et al., 2020). These data are indicative of a high genetic homology among SARS-CoV-2, MERS-CoV, and SARS-CoV. In the SARS-CoV and MERS-CoV infected animal models, the marked inflammatory and immune responses may activate a “cytokine storm”, and apoptosis of epithelial and endothelial cells, thereby leading to subsequent vascular leakage, abnormal T cell and macrophage responses and finally lung injury/acute respiratory distress syndrome (ALI/ARDS) or even death (Channappanavar & Perlman, 2017).
However, the systemic landscape of immune responses in patients with COVID-19 is still unclear. Since the clinical features and immunopathogenesis of SARS-CoV-2 share similarities with SARS-CoV and MERS-CoV (J. Liu et al., 2020), the knowledge learned from SARS-CoV and MERS-CoV has important implications for understanding this new coronavirus (G. Zhou & Zhao, 2020).
To know the infection and develop effective management systems to handle viral infections in an outbreak scenario, we should understand the infection nature and the response of immune system to the novel virus and evaluate the similarities and dissimilarities of the novel virus with the viruses that have caused outbreaks in the past. In this review article, it is attempted to explore the similarities and dissimilarities of the response of the immune system against the SARS-CoV-2 with that in the case of other coronaviruses (SARS and MERS).