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).