Review Article (Open access) |
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SSR Inst. Int. J. Life Sci., 6(2):
2509-2519,
March 2020
Review on Newly
Identified Coronavirus and its Genomic Organization
Keertana Rao1, Poonam
Verma2*, Krishan Kumar3, Manish Kr Verma4,
Areena Hoda Siddiqui5, Sunita Singh6, Jagmohan Singh
Dhakar7, Cansu Ilke Kuru8, Parshant Kumar Sharma9,
Navneet Omprakash Soni10, Sagar Aryal11
1A
B Shetty Memorial Institute of Dental Sciences, Mangalore, Karnataka, India
2Department of Biotechnology, IFTM
University, Moradabad, India
3Department of Medicine, Gajara Raja Medical College, Gwalior, Madhya Pradesh, India
4Department of Biochemistry, G.S.V.M.
Medical College Kanpur, India
5Department
of Lab Medicine, Sahara Hospital, Viraj Khand, Gomti Nagar, Lucknow, India
6Department
of Microbiology, KG Medical University, Lucknow,
India
7Department
of Community Medicine,
Santosh Medical College and Hospital, Ghaziabad, India
8Department of Biotechnology,
Graduate School of Natural and Applied Science, Ege University, Izmir, Turkey
9Department of Biotechnology, Dr. A.P.J. Abdul Kalam Technical University,
Lucknow, India
10Department
of Pharmacology, BLDE Deemed to be University, Karnataka, India
11Kathmandu Research Institute for Biological
Sciences (KRIBS), Lalitpur, Nepal
*Address for Correspondence: Dr. Poonam
Verma, Department of Biotechnology, IFTM University, Moradabad, India
E-mail: poonam.phdbiotech@gmail.com
ABSTRACT- Human Coronaviruses (HCoV) exhibit positive
single stranded RNA genome with enveloped nucleocaps id. Coronavirus belong to
the family Coronaviridae, originated
from avian and mammalian species causes upper respiratory tract infection in
humans by novel HCoVs viruses named as HCoV-HKU1, HCoV-NL63 but
predominant species is Middle East respiratory syndrome (MERS-CoV) across the
world. HCoV-HKU1 sp. is associated with chronic pulmonary disease, while
HCoV-NL63 causes upper and lower respiratory tract disease in both children and
adults, but most recent one was MERS-CoV, which caused acute pneumonia and
occasional renal failure. The novel coronavirus SARS-CoV-2 is a new strain that
causes the Coronavirus Disease 2019 (COVID-19) as named by the Word Heath
Organization. According to the recent world statistics report about the
COVID-19 cases approx. 101,500 confirmed cases and 3,500 death cases appeared.
And mostly, a case of infection with CoV was identified in Wuhan, China.
Structurally viral genome constitutes of 2/3rd of replicase gene
encoding ORFs regions and rest of the 1/3rd region of genome form
the structural proteins. The aim of the study was to understand the viral
genetic systems in order to facilitate the genetic manipulation of the viral
genome and to know the fundamental mechanism during the viral replication,
facilitating the development of antidotes against the virus. Keywords: Coronavirus, COVID-19, HCoV-HKU1, HCoV-NL63,
MERS-CoV, Respiratory tract infection, Structural protein
INTRODUCTION- CoVs
are enveloped viruses with (+) ss-RNA genome size of 22–32 kb in length [1].
CoV belong to the subfamily Orthocoronavirinae
under the family Corona viridae
inside the order Nidovirales,
and are categorized into four genera: Alpha-coronaviruses
(α), Beta-coronaviruses (β), Gamma-coronaviruses (γ), and Delta-coronaviruses (δ). Usually, CoV infect humans and
variety of avian and mammalian species worldwide [2,3]. Considering
the clamp of pneumonia cases are unknown etiology in Wuhan, Hubei Province,
China, was reported on 31 December 2019, diverse speedy epidemiological,
clinical and virological research around the world is working for the genomic
analysis [4,5]. The ingenious agent of the pneumonia is prompted to
be a novel coronavirus (COVID-19) of the same progeny (however genetically
specific) from the coronavirus leads to severe acute respiratory syndrome
(SARS) [4]. A recent study reports suggested that the CoVs
originated from bat, causing severe and fatal kind of pneumonia and
bronchiolitis especially in adult, children and immunological weak patients as
well. Actually, target site of this virus was respiratory and enteric tracts of
both animal and human [3,6,7]. Historically, it was proved the CoV
infection in humans have been associated with mild upper respiratory tract
sites, caused by the variety of HCoVs-HCoV-229E and HCoV-OC43 [8].
However, the HCOV identification in 2003 year, as novel life-threatening CoV
causing the severe acute respiratory syndrome (SARS-CoV) redefined its
historical existence [9]. Earlier reports investigated the three
novels HCoVs viruses and all three were associated with respiratory diseases,
the first one was HCoV-HKU1 which was associated with chronic pulmonary disease
[10], second one was HCoV-NL63 that causes upper and lower
respiratory tract disease in both children and adults across the world [11],
and the third and recent one (April-2012) arising in Middle East respiratory
syndrome CoV (MERS-CoV), and their symptoms is associated with acute pneumonia
and occasional renal failure [12]. These findings suggest that the
CoV exists in nature as potential human pathogen hence, it is necessary to
study their genetic systems to facilitate the genetic manipulation of the viral
genome to know the fundamental mechanism of viral replication, and take a
preventive action against this virus to develop antidotes.
Epidemiological
and Pathological Sense of Coronavirus
Epidemiological sense- Health
and Human Services (HHS) department of US declared the risk of novel CoV (nCoV)
in the year 2020. But jeopardy of nCoV is very low in US. In year 2019 [13],
World Health Organization (WHO) publicized a notice of the CoV [14].
The first case of CoV appeared in Chinese people in December 2019 diagnosis as
in the form of pneumonia. First 425 nCoV case report was published in “The New
England journal of medicine”, included characteristics and transmission of the
nCoV [15]. The journal concluded that nCoV also transmitted through
human to human, which are closely contact with infected peoples.
Here, in this report discussing about
the epidemiological and pathological study of HCoV classes summarized in Table
1.
Table
1: Epidemiological
and Pathological study of HCoV classes
Classes of HCoV |
Symptoms of HCoV |
Fatality Ratio (%) |
Incubation period
(Days) |
Median death Time
(Days) |
References |
229E |
Malaise
Headache, Nasal discharge, Sneezing, Sore throat, Fever and cough |
– |
2–7 days |
– |
Jones et al. [16]; Sharma et al. [55] |
OC43 |
Headache,
Malaise, Nasal discharge, Sneezing, Sore throat, Fever and Cough |
– |
2–7 days |
– |
Walsh et al. [17]; Lee et
al. [61] |
SARS-CoV |
Fever,
Headache Malaise, Chills, cough Dyspnea Respiratory distress, Diarrhea |
9% |
2–13 days |
24 days |
Mc-Bride et al. [9]; Gorse
et al. [18] |
NL63 |
Cough,
Rhinorrhea Tachypnea, Fever Hypoxia, Obstructive laryngitis |
– |
2–6 days |
– |
Graham et al. [19] |
HKU1 |
Fever,
Running nose Cough, Dyspnea |
– |
2–6 days |
– |
Liu
et al. [20]; Favreau et
al. [50] |
MERS-CoV |
Fever
Cough, Chills Sore throat, Myalgia Arthralgia, Dyspnea Pneumonia, Diarrhea
and vomiting |
36% |
2–11 days |
15 days |
Kim et al. [14]; Kvansakul and Hinds [39]; Schoggins and Rice
[74] |
The most prevalent classes existing
across the world are as follows: HCoV-229E, HCoV-OC43 and HCoV-NL63 and HCoV
occurrence usually during the winter season of temperate countries. The
worldwide statistics reported that the total number of cases of coronavirus was
101,500 appeared till date, while the total number of recovered cases count was
51,187 and rest 3,490 death cases appeared. A recent study reported that the
human coronavirus COVID-19 is affecting 89 countries and
territories around the world [21,22]. COVID-19 Real time data of top 10 affected worldwide graphical
representations with the country graph is presented in Fig. 1. Real time status
board of COVID-19 data in Table 2 was updated by the following source:
http://infographics.channelsnewasia.com/wuhan/gmap.html, https://wuhanvirus.kr/, WHO.
Fig.
1:
COVID-19 Real time worldwide
graphical representation with the country wise status
Table 2: Worldwide confirmed and death cases of Human
Coronavirus in 2020 year
Countries |
H-CoV Cases |
Death Cases |
China |
80,651 |
3,070 |
South Korea |
6,767 |
42 |
Iran |
4,747 |
124 |
Italy |
4,636 |
197 |
France |
613 |
9 |
Germany |
534 |
0 |
Spain |
365 |
8 |
Japan |
348 |
6 |
Switzerland |
181 |
1 |
United Kingdom |
163 |
2 |
United States |
148 |
12 |
Singapore |
130 |
0 |
Netherlands |
128 |
1 |
Hong Kong |
106 |
2 |
Malaysia |
83 |
0 |
Australia |
66 |
2 |
Kuwait |
58 |
0 |
Thailand |
48 |
1 |
Taiwan |
45 |
1 |
UAE |
42 |
0 |
Vietnam |
17 |
0 |
Pakistan |
5 |
0 |
Genomic organization of HCoV- Under
the electron microscopy, the CoV virions appear as a spherical or pleomorphic
in shape with distinct club like projections formed by the spike proteins [10,23-26].
Positive sense viral genomic m-RNA, comprising a 5’ terminal cap structure and
a 3’ poly-adenylate tail structure. This genomic m-RNA of HCoV has three
crucial capabilities during the viral replication cycle: (1) act as an initial
RNA of the infectious cycle; (2) acts as a template one for replication and
transcription events; and (3) acting as a substrate for viral packaging into
the progeny virus [27,28].
The
replicase-transcriptase system act as a protein that is translated from the
core region of the genome, while the rest of region of genome of all downstream
open reading frames of m-RNAs contributes viral products [29].
Structurally, all the varieties of CoVs have replicase genes, which makes up
approximately 5’-two-thirds region of the genome and it comprises of two
overlapping open reading frames (ORFs): ORF1a and ORF1b, encoding 16
non-structural proteins [30]. And rest of the3' structural and
nonessential accessory protein coding regions [31] comprises about
one-third region of the CoV genomic RNA has CoV sequential set of four
structural protein genes arranged in the order encoding spike (S) forming
proteins, viral envelope (E), outer membrane (M) and nucleocapsid (N) layer [32].
In addition, number of several accessory ORFs are also involved and interspersed
along the structural protein genes but their number and location vary among CoV
species. In most, CoV m-RNAs carry an identification number of 70-90 nts leader
sequences present at the 5’ ends [33-35]. And its upstream 3’ends of
the leader sequence region have regulatory regions controlling transcription
known as TRS-L regions and act as a cis-regulator of transcription [36].
Instead of this, all CoV TRS regions contain conserved 6-8 nucleotide core
sequences (CS) with variable 5’ and 3’ flanking sequences [37]. The
β form-CoVs carry a heptameric consensus sequence, 5’-UCUAAAC-3’,
additional contain SARS-CoV TRS a hexameric core sequences i.e. 5’-ACGAAC-3’ [38,39].
Starting of replication phase, after viral entry into the host cell, uncoating
of the viral particles with the incorporation of complete genetic material [15,40-42].
Virus sub-genomic region of m-RNAs through translation, form the assembly of
viral proteins. The replicated RNA genome of CoV is then encapsulated and
entered into the packaging phase of viral particles. A short sequence of 69-nts
length is responsible for packaging signals contained in MHV-ORF1-b of approx.
20kb in length from the 5’end of the genome, also responsible for incorporation
of RNA into virions [17,22,43,44]. The β form-CoVs packaging
signaling sequences exhibits 74% sequence similarity index to the MHV packaging
signal and localized in the same regions [45]. Similarly, the TGEV
packaging signal was originally mapped to the first 649 nts at the 5’ end of
the RNA genome; subsequently this position was further delimited to the first
598 nts [19,46].
Mechanism of action of HCoV
infection cycle- HCoVs act as an intracellular obligate
parasite; take over the host cell machinery for their viral copy makeup and
spread. Since, virus–host interactions actually form the basis of diseases,
knowledge about their interplaying reaction mechanism become a great research
interest of researchers. Here, in this study article the known contribution of
the cell’s during the CoV infection cycle: Completes into 4 steps: 1.
Attachment; entry into the host cell; 2. translation of the
replicase-transcriptase; 3. Replication of genome and transcription of mRNAs;
and 4. assembly and budding of newly packaged virions [47].
Receptor
Interaction, Fusion, and Entry- CoVs attach to specific
cellular receptors on the host cell membrane via the club like projection
formed by spike proteins (Table 1) [48,49]. The first of all
identified CoV receptor was CEACAM-1, utilized by MHV (141). As the Virus is
attached through spike proteins undergoes a conformational change ultimately
results into the fusion of viral and host cell membranes [50]. But
still no crystal structures are available for any CoV spike proteins and still
it assumes that these proteins follow the similar pattern of changes as other
type-1 fusion proteins of influenza virus hemagglutinin and human
immunodeficiency virus (HIV)-gp120, in order to facilitate the process of
fusion of viral and host membranous proteins. These CoV spike protein have
crucial role in viral entry into the host cell, cell-to-cell attachment and
spread, and determining the tissue tropism. After entering the cell cytoplasm
and un-coating, the viral particles releases, its genetic material i.e. RNA
genome, while CoV entry into host cells is, in general, not pH dependent, and
thus, it has been believed to occur directly on the plasma membrane and not
following an endosomal route [51]. However, some reports suggest
that some viruses follow an endosomal route [52,53] as well. But
there is some misconception about viral entry, directly attached with host cell
membrane and not via an endosomal route and this can be proven by suggesting
some explanation:
Entry
of SARS-CoV is retracted by lysosomotropic agents to follow an endosomal route
of entry (285, 349) into the host cell. Furthermore, their entry is restricted
by the application of protease treatment on virus already attached to the cell.
This, along with these observation, viral infection may be blocked by another
inhibitors, that is, pH-sensitive endosomal protease cathepsin L, (trypsin like
protease and trans-membranous protease, serine-2), suggesting that there is a
requirement ofS1/S2 cleavage of the SARS-CoV spike (S-proteins)while entering
through the non-endosomal entry [54,55] into host cell. Furthermore,
entry at the plasma membrane following protease treatment is more efficient
than entry by the endosomal pathway [53] during infection. Several
precursors of RNA are also involved: heterologous nuclear ribonucleoprotein
(hnRNA) family members (hnRNPA1, PTB, SYN-CRYP) have been found to be essential
for efficient RNA replication [44]. Other RNA-binding proteins such
as m-aconitase and poly-A-binding protein (PABP), DDX1, PCBP1/2 and zinc
finger, CCHC-type and RNA-binding motif 1 (MADP1) have also been suggested to
play an important role in CoV replication. After cell-cell fusion is takes
place, it forms giant, multinucleated cells, or syncytia, that has been
proposed as a strategy of viruses, to allow direct spreading of the virus
between the cells, subverting the virus-neutralizing antibodies [47-49].
In addition to this, some other accessory proteins are also involved, N
proteins its primary function to bind with CoV RNA genome and participate in
the nucleocapsid events [50]. Although, N protein is majorly
involved in the processes relating to the viral genome, CoV replication cycle
and the host cellular response against viral attack [51].
Interestingly, boundary localization of N-proteins to the endoplasmic reticulum
(ER)-Golgi region has been proposed to a function for it in assembly and
budding [52,53] of virus. However, transient expression of N
proteins was shown to substantially increase the production of virus-like
particles (VLPs) in some CoVs, suggesting that it might not be required for
viral-envelope formation, but it is necessary to complete virion formation
instead [43,44,54,55].
CoV: Viral assembly formation- The
viral accessible proteins such as (S, E and M proteins) are involved to make up
the virions (Fig. 2). This assembly process starts with the accumulation of new
genetic RNA material and structural components. During the viral infection
phase, helical shaped nucleocapsid containing the RNA genome combined with
other viral structural proteins.
This
viral assembly of CoV starts through the budding of the helical nucleocapsid
with the host cell membranes by following the secretory pathway from the
endoplasmic reticulum to the Golgi intermediate compartment. The contribution
of the host cells during the phase of the infection cycle doesn’t find any
evidence. Recent reports suggested that the known M protein orchestrates this
event of the entire assembly process, by selecting and organizing the viral
envelope called structural components at the assembly sites and also mediate
the interactions with the nucleocapsid to initiate the process of budding of
virions [48]. These membrane (M) proteins interact with other viral
structural proteins, such as the Envelope (E) protein, involved in assembling
of undeveloped viral state to mature state (Fig. 2). This interaction makes up
the scaffold of the virion envelope and induces the budding process and
ultimately release out the M protein-modified membrane and with the S protein
to assemble the projection made up of spike proteins into the viral envelope [48,49].
Following the assembly and budding event, the virions are transported into
vesicles and eventually released out by exocytosis mechanism. In a recent
report suggest that some viral load regulatory proteins such as
Valosin-containing protein (VCP/p97) is inhibited resulted in virus
accumulation in early endosome phase during the infection of bronchitis virus
(IBV), suggesting other investigator this VCP has an important role in the
maturation of virus-loaded in endosomes [50].
Fig. 2: Structural view of the Coronaviruses
The 2/3rd of viral genome
constitutes replicase gene encoding ORFs regions: ORF-1a and ORF-1b, and theses
ORFs region translated by frame shift mechanism (Fig. 3). Translated ORFs
regions generates the polyproteins, further processed into complex system of
replication-transcription component by the viral protease. and rest of 1/3rd
region of genome form the structural proteins known as S, E, M, and N, as well
as the genus specific proteins, which is the characteristics of several CoV
viruses expressed from bunch set of 3’ co-terminal sub genomic m-RNA [25,56,57].
Fig. 3: Genomic structure and transmission of Coronavirus
The
first ORFs sequences of DNA make up the 67% of the entire genome encodes 16
non-structural proteins (nsps), while the remaining ORFs sequences encode only
accessory proteins and structural proteins [58]. Some reports found
some differences between SARS-CoV and MERS-CoV, SARS-CoV have
angiotensin-converting enzyme 2 (ACE2), act as one of the main receptors
reported by Kawai and Akira [59] also known as CD-209L as a substitute
receptor [59], while MERS-CoV utilized dipeptidyl peptidase 4
(DPP4), also known as CD-26 act as the primary receptor. Phylogenetic analysis
study of 2019-nCoV had found a close evolutionary relationship with the
SARS-like bat coronaviruses. Here in this report, three of the newly identified
genomes of (2019-nCoV) with accession no. was represented, first one was
Wuhan/IVDC-HB-01/2019 (GISAID accession ID: EPI_ISL_402119) (HB01), second one
was Wuhan/IVDCHB-04/2019 (EPI_ISL_402120) (HB04), and third one was
Wuhan/IVDC-HB-05/2019 (EPI_ ISL_402121) (HB05) [1,11,60]. More
in-depth genome annotation, analysis of coronavirus was performed with a
comparison to related families of coronaviruses, including the count of 1,008
human SARS-CoV, 338 bat SARS-like CoV, and 3,131 human MERS-CoV, whose genomes
were already published in journal before January 12, 2020 (release date:
September 12, 2019) and source of data generated from the Virus Pathogen
Database and Analysis Resource (ViPR) and NCBI database.
CoV Virus Symptoms-
Cold or flu-like symptoms appear within two to fourteen days after exposure.
Common signs include respiratory symptoms, fever, and cough, shortness of
breath and breathing difficulties. In more severe cases; infection can cause
pneumonia, severe acute respiratory syndrome, kidney failure and death [61].
Preventive
measures- Middle-East Respiratory Syndrome (MERS) and Severe
Acute Respiratory Syndrome (SARS) are type of coronavirus. Coronavirus
transmitted human to human through droplets, contact and fomites, similar
pattern of transmission follows by 2019-nCov [62]. To diminish the
wide-ranging jeopardy of spreadof acute respiratory infections, Standard
recommendations to prevent infection spread include regular hand washing, covering mouth when coughing and sneezing,
thorough cooking of meat, avoiding vulnerable interaction with animals along
with improving the healthcare services in emerging sectors. No specific guidelines
given by WHO for explorers. If any symptoms of respiratory illness appeared
during or after the travel, traveler pursues the consultation from the medical
experts [63].
Vaccine development- Emerging
and reemerging of infectious viral diseases appears fatal for global health, economic
stability and national security. Vaccines
development are key strategies for reducing the load of coronaviral disease [64,65].
However, the utility of live-attenuated vaccines is limited in this sense
because of the risks of reversion or repair. Because of their history of
emergence events due to their prevalence in zoonotic pools, designing
live-attenuated coronavirus vaccines is an attractive and fruitful option for
human welfare that can be rapidly and broadly implemented is essential for outbreak
preparedness. Here in this report discuss about the coronaviruses with more
complex transcription regulatory networks (TRNs) acting as an effective vaccine
against the SARS-CoV [23,66,67]. By nature, TRN-complex containing
viruses are attenuated and protective against the lethal action of SARS-CoV.
Hence, the TRN complex utilization for vaccine development appears as a
feasible strategy for limiting reversion in an effective live-attenuated
coronavirus vaccine candidate and potential vaccine for all Nidovirales orders [68,69].
MERS is a deadly viral respiratory syndrome resulted due to MERS-CoV
infections. Unfortunately, still no treatment is available till date against
the MERS-coronavirus infection. In addition, no protective vaccine has been
developed to prevent MERS-CoV infection thus far [70]. Basis of
effective MERS vaccine development against MERS infection depends on the viral
spike (S) protein, has a significant role in the viral infectivity, although,
other studies intensively focused on other viral proteins such as the
nucleocapsid (N) protein, envelope (E) protein, and non-structural protein 16
(NSP16) has also been discussed [34,71,72].
Impact of CoV on Socioeconomics
status- China’s economic growth expected to slow to 4.5% in
the first quarter of 2020 year during the SARS-CoV outbreak, which is the
slowest pace since the financial crisis, according to a Reuter’s poll of
economists. In present scenario, the coronavirus and resulting measure
adversely reduces the global GDP rate by 0.4% in 2020 year [71,73].
On the other hand, if confinement measures against this virus begin to lift up
to Feb-10, the impact on the global GDP rate would be more limited resulting in
a 0.1% of reduction in global GDP rate [74,75]. Global
oil demand has been hit hard by the novel coronavirus, 2019-nCoV according to
the International Energy Agency (IEA) [76]. So, much impact on
factory shut downs are slowing, the flow of products and parts from China,
affecting the companies around the world, including Apple and Nissan. As the
world captured with the coronavirus attack, their economic impact is mounting
with the OECD warning the virus presents the biggest danger to the global
economy since the financial crisis [77]. There
are now more than 85,000 confirmed cases of COVID-19 globally arises
today, the new coronavirus that emerged in Wuhan, China in December 2019 and
was spreading around the world. Many businesses are adversely affected with
lost revenue and disrupted the supply chains due to almost China’s factories
were totally shutdowns, tens of millions of people were already lockdown in
dozens of cities and other countries extending travel restrictions across the
world [78].
CONCLUSIONS-
The study concluded about the
prevalence and genome organization of HCoV. For this purpose, study relevant to
the RNA structures, occasionally in the cis-acting region containing the MHV5’ untranslated region
(5’UTR) and this region is extending up to the N-terminal (nsp1) coding
sequence of trans-regulatory sequences (TRS), 3’UTR and poly(A) tail is
necessary to viral replication. A detailed understanding of the RNA structures
within the cis-acting sequences
of 5’UTR and 3’UTR region of m-RNAs. Understanding of these genetic material
interactions, helpful to define pathogenic coronaviruses, such as SARS-CoV and
MERS-CoV. The potential risk to public health posed by SARS-CoV and other CoVs,
and the lack of prevention agents, because of these two crucial matters a
global effort is needed to study about the molecular level of viruses in order
to develop effective strategies against the Coronavirus infections.
Corona
viruses like MERS-CoV have a property of emergence and reemergence from
Zoonotic sources: Bats and other small mammals and continue to transmit into
human population. Before emergence of novel species of coronaviruses, viral
surveillance studies of animal species including bats, rodents, and livestock,
are essential to understand the potential human pathogens exist in the
environment before they can spread in human populations.
CONTRIBUTION
OF AUTHORS
Research
concept-
Dr. Keertana Rao, Dr. Poonam Verma
Research
design- Dr. Keertana Rao
Supervision- Dr.
Poonam Verma
Materials- Dr.
Keertana Rao, Dr. Poonam Verma
Data
collection-Parshant Kumar Sharma
Data
analysis and Interpretation- Dr. Keertana Rao
Literature
search- Manish Kr Verma, Navneet Omprakash
Soni, Sagar Aryal
Writing
article-
Dr. Keertana Rao, Dr. Poonam Verma, Dr. Krishan
Kumar
Critical
review-
Dr. Sunita Singh, Dr. Areena Hoda Siddiqui
Article
editing-
Cansu Ilke Kuru, Jagmohan Singh Dhakar
Final approval- Dr. Sunita Singh, Dr. Areena Hoda Siddiqui
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