1. Introduction:<\/p>\n
In human history, there are many cases of viral pandemic infections including polio [1], ebola [2], smallpox [3], chicken pox [4], HIV-AIDS [5], which had put human life on serious risk [3]. Nevertheless, owing to efforts taken by medical sectors across the globe, such diseases were controlled by either vaccine [6] or\u00a0 treatments [7] or some of them are reduced by
\nprevention only [8]. The diseases mentioned above were life threatening and caused a potential biological loss in\u00a0 the world [9,10,11]. Of them, airborne and contagious diseases [12] are more challenging to humankind since they are challenging to control. It is true, especially in those countries where the population is high, and awareness among people is less. Like other
\nbiological species, viruses are capable of altering their
\ngenetic makeup [13,14] and get chances of
\nreappearances [13,14,15], hence making them more
\ninfectious than their parents [16]. The variation in
\ngenes results in altered protein sequence leading to
\nchanged functions of proteins [17]. The antiviral drugs
\navailable against these infections are not as
\nproductive as those were made to recognize only
\nspecific target sites [18]. As a result, the infectious
\nparticles go on infecting people continuously resulting
\nin international health concern and panic with
\nuncontrolled deaths.
\nAccording to Prajapat, M. et al. [19], there is only
\none Protein Data Bank (PDB ID:6LU7) on the 2019-
\nnCoV, which forms a complex with the N3 inhibitor.
\nHowever, the genome sequence shows that there is
\n95% similarity with the bat -SL-CoVZC45 and 88% to SIRS CoV-ZSc [19]. This study suggests that the
\nchanges have occurred in the amount of
\nrecombination process in 2019-nCoV and the protein
\nstructural and functional levels.
\nIn this review, we analyzed the evolution of corona
\nvirus family (Coronaviridae) [20] to know the genetic
\nsimilarity and variation patterns in relation with newly
\narrived Severe Acute Respiratory Syndrome (SARS\u0002CoV2)virus, which infected 2,078,605 people from 213
\nareas, countries and territories with 139,515deaths
\n(table 1) till April 17,2020.Till date, there is no vaccine
\nor effective measure to stop its spread [16]. Apart
\nfrom analyzing the evolutionary aspect, the article
\nalso discusses the probable genetic variation leading
\nto substantial uncontrolled health risk to human life
\n[13, 14] causing a higher uncontrolled health risk to
\nhumans.
\n2. Evolution and future reappearance:
\nThe viruses which contain RNA as their genetic
\nmaterial have potential to get evolved [21] and
\ncoronaviridae family has RNA as genetic material [22],
\nwhich can evolve. In sequence, the viral genetic
\nevolution has occurred in SARS-CoV that spreads
\nthrough human to human contact [12] and this idea
\nhas been supported by [23]. They stated that SARS\u0002CoV and SARS-CoV2 belong to a beta group of corona
\nvirus. They have 70% similarity at a genetic level
\nshowing DNA level differences among them (figure 1).
\nThis indicates that both viruses are 30% different in
\ntheir genetic structure that is a result of mutations
\nsuch as genetic recombination, gene deletion or
\ninsertion creating the probability of outbreak in future
\nlike its ancestors created in the past [16]. Likewise,
\ngenome level gene exchange, recombination [24],
\ngene deletion or insertion may create a probability of
\noutbreak in future, like past incidences [25] (figure 1)
\nsuch as SARS CoV epidemics.
\nAdditionally, SARS-CoV2 is considerably similar with
\nSARS-CoV helping for predictions on occurred
\nepidemic health disaster, and corona viruses may be
\nresponsible for outbreaks with variant mutations like
\nprevious one in upcoming years [13, 14, 25] (Figure 1).
\nThis suggests that both types of corona viruses are
\ngenetic variants. Besides, SARS-CoV and SARS-CoV2 are similar for
\ntheir severity. This idea was supported by Huang, C.,
\net al., Chen, N., et al., Wang, D., et al., [27, 28, 29]
\nwho proposed that SARS-CoV2 severity mimicked with
\npreviously spread SARS-CoV and they also share same
\nclinical features [30]. Chaolin Huang et al. [31] supported our concept and
\nstated that corona viruses might lead to substantially
\nmore novel as well as severe zoonotic incidences.
\nMoreover, clinical characters of 2019-nCoV showed
\nsimilarity with previously studied beta coronavirus
\ninfections [31]. Features showed by 2019-nCoV
\ninfections revealed some resemblance with SARS-CoV
\nas well as MERS-CoV infections [32, 33].This strongly
\nsuggests that the novel coronavirus (SARS-V2) has
\nevolved from previously observed SARS-CoV, a
\nmember of the betacorona virus group.
\nAdditionally, there is a difference between SARS
\nand 2019-nCoV regarding immunogenicity as former
\ncauses pulmonary inflammation with high level lung
\ndamage whereas the second causes raised production
\nof Th2 cytokines retarding inflammation [34]. This
\neffect might be due to 17% genetic variation caused
\nby 2019-nCoV in PL pro sequences. As a result, the
\ninternational crisis has occurred and there is no
\nproper vaccine or drug against it till writing this
\narticle.
\nIn spite of 83% similarity in the PLpro sequences of
\nSARS-CoV and SARS-CoV-2, both of them share active
\nsites which are similar [35]. According to Huang, C. et
\nal. [27], infections by SARS-CoV-2 and earlier
\nbetacoronavirus showed similarities in clinical
\ncharacteristics. To add, sequence identity between
\nSARS-CoV2 and betacoronavirus members regarding
\ndomains of conserved replicase is lower than 90% [36]
\nsuggesting the relationship between both entities.\u00a0 SARS-CoV-2 is considerably homologous to CoV that
\ncaused SARS (Severe Acute Respiratory Syndrome)
\nduring 2003. Also, SARS-CoV2 pathogen is more
\nsimilar in relation with genetic makeup to SARS-CoV
\nas compared with MERS-CoV [37, 38, 39]. As well,
\nboth have a common factor, i.e. human ACE2 receptor
\n[39], which indicated that the genetic modifications in
\nnewly arrived pathogen do not affect human cell
\nreceptor recognition. With the exception, the COVID\u000219 pathogen binds human ACE2 more weakly with
\nhelp of its S protein than SARS-CoV, causing less
\npotential infection than SARS-CoV [37]. Furthermore,
\nit was observed that death rate due to COVID-19 was
\nfound as 2% [40] while that of SARS spread in 2002, it
\nwas 10% [41] and in case of MERS, it was 37% [42]. It
\nmay be because of genetic modifications. Moreover,
\nSARS-CoV has same size as SARS-CoV-2 [43], and both
\nhave high homology [44] supporting morphological
\nsimilarity among them. Interestingly, over 95% sequences show a similarity
\nbetween SARS-CoV2 3CLpro and RdRp protease with
\nthat of SARS-CoV, and both viruses have 79% genetic
\nsimilarity in their sequences [39]. Besides, they share
\npotentially conserved Receptor Binding Domain (RBD)
\nalong with S protein domain [35,37,45] which is due
\nto recombination\/mutation acquisition in SARS-CoV-2
\n[16]. To add, novel viral host cell entry and replication
\nproteins are similar with that of SARS-CoV with
\nrespect to their structure [46]. Additionally, it is found that SARS-CoV2 is one of
\nthe seven coronaviruses that infect human beings and
\nothers are MERS-CoV, SARS-CoV (cause severe
\ninfection), 229E, OC43, NL63, HKU1 (cause mild
\nsymptoms) [49]. In future, genetic variations may
\noccur in the last four types (figure 2). Since the COVID\u000219 pathogen has similarity with SARS-CoV along with
\nsome symptoms, there is sense of its upcoming arrival
\n[13, 14].
\nOut of six genera (ending with suffix \u2018virus\u2019) of
\nfamily coronaviridae, i.e. alpha, beta, gamma delta toro and bafini [20], betacoronaviruses include
\nSARS-CoV, MERS, SARS-CoV-2 [46] and SARS-CoV-2
\nis a novel coronavirus in the genus that is
\nbelonging to MERS-CoV and SARS-CoV (figure 1).
\nLike MERS-CoV and SARS-CoV, SARS-CoV2 targets
\nlower part of the respiratory system leading to
\npneumonia and it also infects heart, kidney,
\ngastrointenstinal system, liver as well as central
\nnervous system [47, 48] showing pathological
\nsimilarity. It means that the virus family
\nunderstudy is genetically changeable and in
\nupcoming decade, the same virus or other viruses
\nof the same family will reappear [13, 14] with their
\ngenetic variants (figure 1).
\n3. Conclusion:
\nThe coronavirus family is highly changing and its
\ngenetic variants may appear. In this sequence,
\ngenetic mutants of SARS-CoV2 may be detected in
\nfuture.<\/p>\n","protected":false},"excerpt":{"rendered":"
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