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physiology related disease pathophysiology of pneumonia or pathophysiology of asthma. 6 pages. 32 Review Article International Journal of Research in H

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physiology related disease pathophysiology of pneumonia or pathophysiology of asthma.

6 pages. 32

Review Article

International Journal of Research in Health Sciences, Vol 8, Issue 4, Oct-Dec, 2020

INTERNATIONAL
JOURNAL OF
RESEARCH IN
HEALTH SCIENCES
e-ISSN: 2321-7251

Cite this Article: Nguyen JS, Osorio VM, Elias NH, Zayed T, Shahabbedin M, Khollesi K, et al. Insights on the Novel Coronavirus SARS-CoV-2
(COVID-19): Existing and Future Considerations. Int J Res Health Sci. 2020;8(4):32-40

Insights on the Novel Coronavirus SARS-
CoV-2 (COVID-19): Existing and Future
Considerations
Jennifer S. Nguyen1,#, Vivian M. Osorio1,#, Nora H. Elias1, Tala Zayed1, Majid Shahabbedin1,
Khalil Khollesi1,2, Ali Baroon1,3,4, Ali R. Jazirehi1,2,*

ABSTRACT
The recent outbreak of coronavirus disease 2019 (COVID-19) caused by severe acute
respiratory syndrome-coronavirus 2 (SARS-CoV-2), quickly progressed into a worldwide
pandemic. Coronavirus outbreaks in the past were related to Severe Acute Respiratory
Syndrome (SARS) and Middle East Respiratory Syndrome (MERS). SARS-CoV-2 consists
of a large genome structured as a spherical, single-stranded, positive sense (+) RNA. The
virus uses its spike glycoprotein to enter host cells via interaction with human angiotensin-
converting enzyme 2 (ACE2). COVID-19 is transmitted through droplets, indirect and
direct physical contact, possibly via aerosolized particles, and fecal-oral transmission.
Clinical manifestations of the disease display similarities to both SARS and MERS, including
symptoms such as fever, headache, shortness of breath, fatigue, dry cough, sore throat, and
muscle aches. Some patients develop other symptoms such as nausea, vomiting, and diarrhea.
Diagnosis of SARS-CoV-2 infection includes conducting real-time RT-PCR and serological
assays, with the former being the primary test of choice. Prevention of SARS-CoV-2 spread
includes effective implementation of self-isolation and increased healthy hygiene measures.
Treatment of COVID-19 remains to be supportive care, while clinical trials are being
conducted to test the efficacy of various pharmacological agents such as hydroxychloroquine/
chloroquine, remdesivir, lopinavir/ritonavir (LPVr), ivermectin, steroid therapy, targeting S
protein-HS interactions, and utilizing exogenous heparin as an inhibitory agent. While these
approaches have shown promise based on preliminary data, future studies are warranted to
ascertain the efficacy and safety of these treatment approaches and to identify novel targets
for therapeutic purposes. This review focuses on discussions on these topics.

©2020 Nguyen JS, et al. This is an open-access article
distributed under the terms of the Creative Commons
Attribution (CC-BY 4.0), which permits unrestricted use,
distribu-tion, and reproduction in any medium, provided the
original author and source are credited

Jennifer S. Nguyen1,#, Vivian M. Osorio1,#,
Nora H. Elias1, Tala Zayed1, Majid
Shahabbedin1, Khalil Khollesi1,2, Ali
Baroon1,3,4, Ali R. Jazirehi1,2,*
1Department of Biological Sciences, College of Natural
and Social Sciences, California State University, Los
Angeles (CSULA), Los Angeles, CA 90032, USA
2Los Angeles City College, Department of Life Science,
855 N. Vermont Ave., Los Angeles, CA, 90029, USA
3Westcoast University, Department of General education,
1477 Manchester Ave., Anaheim, CA 92802, USA
4Los Angeles Mission College, Department of Life
Science, 13356 Eldrige Ave., Sylmar, CA 91342, USA

Corresponding author:
Ali R. Jazirehi
CLS, Ph.D., Department of Biological Sciences, BS
134, California State University, Los Angeles, 5151 State
University Drive, Los Angeles, CA 90032, USA.
Tel: (323) 343-2050
E-mail: Ajazire@calstatela.edu

DOI: 10.5530/ijrhs.8.4.2

Received: 01-12-2020;
Accepted: 17-12-2020;
Published: 23-12-2020.

INTRODUCTION
Coronaviruses (CoVs) are very diverse
pathogens that belong to the order Nidovirales,
family Coronaviridae, and subfamily
Coronavirinae. The subfamily Coronavirinae
is composed of four genera: alphacoronavirus,
betacoronavirus, gammacoronavirus, and
deltacoronavirus.[1] Of the four genera,
alphacoronaviruses and betacoronaviruses more
commonly infect the human body.[2] Human
coronaviruses (HCoV) affect the respiratory
system. Mild HCoVs include: HCoV-OC43,
HCoV-229E, HCoV-HKU1, and HCoV-NL63.
In 2002, a betacoronavirus was discovered that
jumped species and caused a new disease,
called Severe Acute Respiratory Syndrome
(SARS). The disease caused pneumonia-
like symptoms including fever, cough,
dyspnea, and diarrhea.[2] In 2012, another
betacoronavirus was discovered that caused
middle east respiratory syndrome (MERS).
SARS and MERS affect the respiratory and
gastrointestinal (GI) systems and are predicted
to have originated from animals, specifically
bats. SARS-CoV and MERS-CoV are closely
related to other bat CoVs on the phylogenetic

tree.[1] Sequence analysis has revealed that these
RNA viruses have high mutation rates, which
may likely lead to host range expansion among
phylogenetically related species. Coronaviruses
are found in many animals. Wuhan Municipal
Health commission in China first reported
SARS-CoV-2, with the highest exposure rate
in Huanan Seafood Wholesale Market where
poultry, bats, snakes, and other animals are
being sold.[3] Coronavirus can affect a wide
array of animals such as swine, cattle, horses,
camels, cats, dogs, rodents, birds, bats, rabbits,
ferrets, mink, snakes, etc.[3]

The Avian infectious bronchitis virus was the
first CoV isolated in 1930.[4] All seven human
coronaviruses have a zoonotic origin and
reservoir hosts are dependent on evolution.[4]
The new SARS-CoV-2 has become the new
addition to the coronavirus family. Due to
mutation adaptation, the virus causes mild
diseases in the reservoir host. However, upon
entry into humans, SARS-CoV-2 starts a
new adaptation process and causes a severe
disease.[4] Bats are known to be reservoir hosts
of SARS-CoV-2 as well as other viruses such
as Ebola virus. Bats and other animals serve as

mailto:Ajazire@calstatela.edu

33

Nguyen, et al.: Insights on the Novel Coronavirus SARS-CoV-2 (COVID-19): Existing and Future Considerations

International Journal of Research in Health Sciences, Vol 8, Issue 4, Oct-Dec, 2020

SARS-CoV-2 transmission vectors which are potentially transmitted
to humans.[4] The potential of animal to human and human to human
transmission poses a major threat to public health.[5]

In December 2019, a betacoronavirus infection was observed in Wuhan,
China, that is predicted to have originated from bats and crossed to
humans.[1] The World Health Organization (WHO) named the novel
coronavirus 2019-nCoV, also referred to as coronavirus disease 2019
(COVID-19). The virus causing COVID-19 was identified as SARS-
CoV-2.[6] SARS-CoV-2 has a positive single-stranded RNA (+RNA)
genome with 5’-cap and 3’-poly-A tail. CoVs have crownlike spike
(S) glycoproteins on their envelope that target receptors in the human
body.[5] SARS-CoV and SARS-CoV-2 target the human angiotensin-
converting enzyme 2 (ACE2) which is found in many tissue and cell
types.[7] Apart from the oral and nasal mucosa, the ACE2 receptor is
also found in numerous human organs, such as bone marrow, brain,
colon, kidney, liver, lung, lymph nodes, nasopharynx, skin, small
intestine, spleen, stomach, and thymus.[8] Whereas, MERS-CoV
binds to dipeptidyl peptidase 4 (DPP4) found in the kidneys, lower
respiratory, and gastrointestinal tract.[2]

Similar to SARS-CoV and MERS-CoV, patients infected with SARS-
CoV-2 present with symptoms involving both the respiratory and
gastrointestinal systems.[2] In a study including 164 participants, 96%
of patients had 3 main symptoms including fever, cough or shortness
of breath.[7] Other SARS-CoV-2 symptoms include dyspnea, headache,
sore throat, diarrhea, nausea, vomiting, and abdominal discomfort.[7]
Although, not all individuals infected with coronavirus will present
signs and symptoms, making them asymptomatic carriers. The first case
of asymptomatic carriers of SARS-CoV-2 was observed when a family of
six traveled to Wuhan; only five were infected with SARS-CoV-2.[9] One
of the family members (a 10-year-old child) did not travel to Wuhan yet
had contact with infected family members. The child tested positive for
SARS-CoV-2, however, was an asymptomatic carrier.[9]

An individual’s status of the immune system is a determining factor in
combating the infection; immuno-compromised patients may develop
severe illness or die. SARS-CoV-2 affects immunocompromised older
males.[6]

As of December 9, 2020, there have been over 69 million confirmed
positive COVID-19 cases and over 1 million deaths.[10] Laboratory
testing is an important factor in diagnosing CoVs. Diagnostic testing
includes detection of the virus from nasal or oral samples using reverse
transcription polymerase chain reactions (RT-PCR) or using blood
samples in serology tests.[11] RT-PCR detects nucleic acid targets for
the novel coronavirus. Serology tests are not as reliable for diagnostic
purposes because the development of protective antibodies in response
to infection requires some time.[12] Thus, RT-PCR using respiratory
secretions is the preferred method for virus detection.[13]

Currently no specific antiviral therapies for CoVs exist. The coronavirus
evolving creates the need for vaccines and effective treatments.[5]
Current clinical trials aim to create vaccines by adapting SARS-CoV
and MERS-CoV approaches, amongst other diseases.[2] It is suggested
that mortality and complications due to infection or co-infection may
be reduced by providing patients with antibiotic treatments and steroids
early during the infection.[6] Moreover, early detection and treatment
are crucial to prevent further spread of coronavirus in severe cases.
Management of the virus includes providing supplemental oxygen and
other symptom relief methods.

The outbreak of the novel coronavirus addresses the importance of
preparedness for viral diseases.[5] With no potential cures yet available
for CoVs, prevention of the disease is very important to minimize the
spread of the infection. Public health officials have initiated prevention
practices based on previous zoonotic coronavirus outbreaks.[2] Best
practices for prevention include controlling the source of infection,
good hygiene, wearing a fitted face mask, and avoiding crowds.[1]

Isolation is recommended to further minimize contamination for
those exposed to the virus. Since HCoVs mainly spread from human to
human, social distancing and quarantine practices have been strongly
recommended to the public. Also, remaining at least 6 feet away from
another person minimizes the chance of spreading the virus through
respiratory droplets when not wearing protective equipment. Good
hygiene includes proper and frequent handwashing with soap and
water for a minimum of twenty seconds and frequent cleaning of
touched objects.[14] Furthermore, prevention of future diseases can be
put into practice by studying the evolution of the host range for CoVs.
Meanwhile, it has become clear that detailed understanding of the
pathogenesis of COVID-19 may provide more insight on identification
of the potential targets that may hinder or prevent the infection and
transmission of the virus.[15]

GENOME STRUCTURE
Coronavirus is the cause of SARS, MERS, and the novel coronavirus
2019 (COVID-19). Coronavirus is part of the coronaviridae family
which is commonly found in mammals and birds. The virus has single
stranded positive RNA and is the second largest RNA genome compared
to all other RNA viruses.[16] The genome includes 5’ cap and 3’ poly A
tails.[1] Virus RNA replicase gene is adjacent to the polyprotein la and
lab genes which code for proteins important for genome replication.[17]
Viral RNA encodes both structural and nonstructural proteins with
different functions on the 3’ end of the viral genome.[16] The genome
and subgenome contain at least six open reading frames (ORF); the
first ORF codes for nonstructural proteins.[16] The ORF at the 3’ end
encodes four main structural proteins such as spikes (S), membrane
(M), envelope (E) and nucleocapsid (N) proteins.[1] The other ORFs
contain small noncoding regions which cause some of the ORFs to
overlap. The end of the genome contains 5’ untranslated region (UTR),
also referred to as the leader sequence, with about 210-530 nucleotides
and 3’ contains about 270-500 nucleotides.[18] Due to the genome being
positive sense RNA, it is more infectious compared to viruses with
negative sense RNA genome. Positive sense RNA is more infectious
because the RNA genome could serve as messenger RNA (mRNA) to
produce virions and could be directly translated by the host.[19]

VIRAL ENTRY AND REPLICATION
Like other CoVs, SARS-CoV-2 utilizes its S protein to bind to host
(target) cell receptors and fuse into host cell plasma membranes
following priming by host cell proteases.[20] Specifically, SARS-CoV-2
utilizes the C-terminal domain on the S1 subunit (SARS-CoV-2-CTD
or otherwise referred to as SARS-CoV-2-RBD) to bind to human
ACE2 receptor and applies type II transmembrane serine protease,
TMPRSS2, for S protein priming and lysosomal cathepsins for cell
entry activation.[20-22] A recent study discovered SARS-CoV-2 entry
depends on the receptor binding domain (RBD) of the S protein to
interact with ACE2 and negatively charged cellular heparan sulfate
(HS), a copolymer.[15] The HS and ACE2 binding sites are adjacent to
one another and to the components of the host cell surface/extracellular
matrix. Consequently, HS acts as co-receptor/co-factor for SARS-
CoV-2, by initially binding to the S protein’s RBD subunit S1, thus,
priming the S protein by altering the structure of the RBD into an open
conformation. This change allows the RBD open conformation to bind
to the host cells’ ACE2 receptor.[15]

Comparison of the SARS-CoV-2-CTD and human ACE2 complex to
their homolog, SARS-CoV receptor binding domain (SARS-RBD),
shows increased intermolecular interactions and a 4-fold increase in
affinity towards human ACE2 by SARS-CoV-2-CTD.[20] However,
another study suggests that the overall binding strength of the SARS-
CoV-2 S protein is comparable to or even lower than that of the SARS-
CoV’s S protein.[22] These conflicting binding affinities were explained
by cryo-EM results revealing that the RBD of SARS-CoV-2 is primarily
displayed in a lying-down, rather than standing-up, state, whereas

34 International Journal of Research in Health Sciences, Vol 8, Issue 4, Oct-Dec, 2020

Nguyen, et al.: Insights on the Novel Coronavirus SARS-CoV-2 (COVID-19): Existing and Future Considerations

With seven HCoVs now identified, understanding the transmission
of coronaviruses is crucial. SARS-CoV-2 targets ACE2, which can be
found in the lungs, kidneys, GI tract, and liver. New studies found that
fecal-oral transmission of the virus is possible. Moreover, replication of
the virus can happen in the respiratory and digestive system.[35] SARS-
CoV and MERS-CoV can withstand various environmental conditions
and encourage fecal-oral transmission.[35] Also, traces of SARS-CoV
RNA can remain in the stool more than 10 weeks, leading to the
premise that SARS-CoV-2 potentially has the same characteristic. Stool
analysis is recommended for diagnosing patients who present with GI
symptoms.[35] The first confirmed patient in the United States presented
with GI symptoms for two days, and the nucleic acid analysis of stool
and respiratory samples revealed positive results for COVID-19.
Detection of viral RNA was likely due to its presence in enterocytes of
the ileum and colon.[28] It is believed that a person infected through fecal
transmission, can also spread the virus through respiratory droplets or
feces. Moreover, those with GI symptoms can still spread the virus after
respiratory symptoms have improved. Further studies are necessary to
determine the connection between fecal viral load and the presence of
GI symptoms as well as disease severity.[36]

There have been less reported cases of children of the age group of
0-17 years old affected by SARS-CoV-2 in the United States, likely
attributed to the closure of schools.[37] However, a study conducted in
Utah and Wisconsin on children infected with SARS-CoV-2 and their
household contacts, showed the transmission patterns in the household
and explained how children acquire SARS-CoV-2 by exposure to
household contacts.[38] Children have shown a high potential of being
asymptomatic carriers of SARS-CoV-2, with a notable 16% being
asymptomatic, which may play a role in transmitting the virus to others
including their household.[37]

PREVENTION OF COVID-19
Since the virus is spreading rapidly across the globe, specific measures
are recommended by the US Center of Disease Control and Prevention
(CDC). Virus spreads through droplets and through contact routes;
it is suggested that people should stay six feet apart to avoid infecting
others through droplet transmission. COVID-19 could spread via
asymptomatic carriers.[14] To prevent viral spread, individuals should
have healthy hygiene by frequently washing their hands with soap and
water for at least 20 seconds and use hand sanitizer. A person should
frequently wash their hands in their homes and out in public places
if they blow their nose, cough, or sneeze. People should also distance
themselves and avoid close contact with others. Individuals should
avoid crowded places and do not touch their face while conducting
errands. It is advised to wear a cloth face covering (surgical face mask)
in public. Cloth face coverings should not be placed on children under
2 years old and on individuals that have difficulty breathing.[14] People
should avoid using public transportation, limit traveling, and practice
self-isolation to help minimize/stop the spread of the virus.[39]

Surfaces such as doorknobs, toilets, light switches, countertops,
desks, phones, keyboards, and sinks should be decontaminated by
disinfectants.[14] Globally, the practice of isolation and containment
policy and whole countries’ quarantines have been enforced in Italy and
Iran, respectively[40] to stop the spread of COVID-19.

VIRAL PATHOGENESIS AND
PATHOLOGICAL FEATURES OF COVID-19
In order to enter the host cell, SARS-CoV-2 binds to HS and ACE2.
While HS is ubiquitously present in all cells, ACE2 is abundant in lung
and small intestine epithelia.[41,42] Combined with the virus’s route of
transmission, this would confer greater susceptibility of the pulmonary
system, explaining why the lungs can be considered as the classical
target organ in the setting of SARS-CoV-2 infection.

the opposite is seen in SARS-CoV. This leads to an overall lower RBD
accessibility, thus, explaining the comparable/lower binding strength of
the SARS-CoV-2 S protein.[22] Following the binding to human ACE2,
pre-activation of the S protein by proprotein convertase (PPC), furin
occurs. Subsequently, TMPRSS2 and cathepsins activate the S protein and
facilitate viral entry through fusion into the host cell membrane.[22] Viral
genome is then uncoated and released into the cytoplasm where viral
genome transcription protein translation will occur.[24] First, ORF1a
and ORF1b are transcribed from the genomic RNA and subsequently
translated to polypeptides 1a and 1ab (pp1a and pp1ab).[25] These proteins
are cleaved by viral proteases into nonstructural proteins which form
RNA-dependent RNA polymerase (RdRp). RdRp then uses the positive
sense RNA genomic RNA (gRNA) to synthesize negative-sense RNA
intermediates. These intermediates are then used as a template to form
gRNA as well as subgenomic RNA (sgRNA).[25] Transcriptome analysis
obtained via sequencing-by-synthesis (SBS) and nanopore-based direct
RNA sequencing (DRS) reveals transcription of 9 canonical sgRNAs:
S, 3a, E, M, 6, 7a, 7b, 8, and N.[25] Newly synthesized viral envelope
glycoproteins are inserted into the rough endoplasmic reticulum (ER)
or Golgi apparatus.[25] Assembled viral particles then enter the ER-Golgi
intermediate compartment (ERGIC) and are released out of the host
cell via exocytosis.[26,27]

MEANS OF COVID-19 TRANSMISSION
There are more than 69 million cases of COVID-19 as of December
9, 2020 globally and over 1 million deaths.[10] SARS (in 2003) and
MERS (in 2012) both shared the same modes of transmission through
droplets and direct contact.[28] Respiratory infection can be transmitted
through droplets. Inhaled droplets reside in the upper respiratory tract
which could be removed by mucus through the nose or move up the
mucociliary escalator.[29] SARS-CoV-2 is transmitted through droplets
and by direct and indirect physical contact.[30] Direct physical contact
occurs when an individual has contact with another individual who
either has the infection or is a carrier, such as shaking an infected
individual’s hand. Indirect physical contact occurs when touching
contaminated surfaces such as doorknobs. Droplet transmission
occurs when one person is close to another person that is coughing or
sneezing. Then an individual may become infected if their eyes, nose,
and mouth are exposed.[31] Many believe that COVID-19 is airborne,
however, the primary route of transmission is via droplets and contact.
The difference between the two types of transmission is that airborne
transmission contains aerosols that are much smaller than droplets,
which last longer in the air than droplets. However, it is also possible for
a person to be exposed to COVID-19 through airborne transmission by
treatment ventilators.[31]

Additionally, there were some cases where patients showed signs of
diarrhea, vomiting and stomach pain, raising the question whether
COVID-19 could be transmitted through fecal-oral transmission?
Two laboratories in China successfully isolated live COVID-19 from
infected patients’ stool samples,[28] suggesting that COVID-19 may
potentially be transmitted through fecal-oral transmission. Therefore,
the respiratory system and potentially the digestive system play a role
in transmitting the virus.

There is currently a controversy whether SAR-CoV-2 droplets can land
on exposed human eyes (ocular surface) and infect the host. A male
individual became infected by the virus for only wearing a mask and
not eye protection during an inspection at Wuhan.[32] A more recent
study also showed that human eyes may be susceptible to SARS-CoV-2
entry. SARS-CoV-2 uses the same receptor as SARS; both use ACE2.[33]
Immunohistochemical analysis showed that post-mortem eyes samples
express ACE2 and TMPRSS2 (surface protease that aids in viral entry)
on the conjunctiva, limbus, and cornea, with higher expression levels
on the surface of conjunctiva and corneal epithelium,[34] suggesting
that human eyes may serve as a port of entry for SAR-CoV-2 through
droplets transmission.

35

Nguyen, et al.: Insights on the Novel Coronavirus SARS-CoV-2 (COVID-19): Existing and Future Considerations

International Journal of Research in Health Sciences, Vol 8, Issue 4, Oct-Dec, 2020

ACE2 is present in many human organs and tissues, including the
brain, lungs, liver, kidneys, spleen, heart, blood vessels, GI tract,
skin, as well as arterial and venous endothelium,[42,43] leading to the
possibility of multiple organs and tissues being affected. SARS-CoV-2
infection and subsequent inflammatory changes affecting endothelial
cells can induce endotheliitis in several organs, which can ultimately
result in cell death.[44] Endothelial cell apoptosis and dysfunction
have also been reported in COVID-19 patients.[45] The endothelium
plays a role in preventing thrombosis by acting as a surface of which
prevents cell and clotting protein attachment.[46] As a result, endothelial
involvement in SARS-CoV-2 infection may increase the likelihood of
thromboembolism formation.

New studies suggest thromboembolism may play a key role in mortality
of COVID-19 patients.[47] In a study, autopsies were performed
on patients infected with SARS-CoV-2 in order to understand
the histopathological changes. Similar to SARS and MERS, it was
discovered that patients infected with SARS-CoV-2 show small vessel
thrombosis with alveolar hemorrhage postmortem.[43] Thrombosis was
present in many other organ systems due to immunothrombosis.[43]
When advanced, thrombosis can lead to multiple organ failure due to
disseminated intravascular coagulation (DIC). However, a very low
percentage of COVID-19 patients meet the criteria for DIC. Moreover,
pulmonary intravascular coagulopathy was coined to differentiate it
from DIC. Pulmonary intravascular coagulopathy suggests pulmonary
inflammation, vasculopathy and thrombosis.[47] Pathological changes
were observed in various organs.[43]

COVID-19 poses a threat to those with comorbidity or
immunocompromised individuals. There is a correlation between
mortality and a patient’s MuLBSTA score. MuLBSTA considers
multilobe infiltrate, absolute lymphocyte count, bacterial coinfection,
smoking history, hypertension history, and age in a scoring system. This
model is used to predict mortality in viral pneumonia patients but has
been used for COVID-19 patients. SARS-CoV-2 is more likely to infect
those with a weak immune response.[6]

CLINICAL SYMPTOMS OF COVID-19
In March 2003, an outbreak of SARS occurred in Hong Kong. It
presented as a respiratory illness that led to death. The symptoms for
SARS included fever, headache, fatigue, dry cough, and muscle aches.[48]
It was also common for individuals to have symptoms such as diarrhea
and nausea. Patients eventually developed pneumonia and had to be
placed under ventilation support. SARS was caused by coronavirus
which infects animals and spreads to humans.[48] MERS first occurred
in 2012 in Saudi Arabia and is associated with coronavirus as well. It is
known as a respiratory tract disease in which an infected patient shows
symptoms of fever, cough, difficulties in breathing, and development of
pneumonia.[48]

The first cases of COVID-19 were diagnosed in Wuhan, China and
patients experienced flu-like symptoms. In a study, 47 out of 99
patients who had a prior history of a chronic disease were exposed to
a Wuhan seafood market. The patients commonly exhibited symptoms
of pneumonia, fever, cough, and shortness of breath. Some also had
muscle ache, headache, confusion, chest pain, and diarrhea[6] at the
time of COVID-19 diagnosis. In general, COVID-19 symptoms are
similar to common “cold” symptoms. However, it is a severe illness that
leads to death. People who are at a higher risk include those who have
underlying diseases, are obese, immunocompromised, and those who
are 65 years and above.[14] After exposure to the virus, it takes 2-14 days
to develop symptoms such as fever, dry cough, and shortness of breath.[14]
Drastic signs of COVID-19 that require immediate medical attention
are when the patient has difficulty breathing, pain and pressure in the
chest, unable to lift their body, and if the patient’s face and lips turn
bluish due to the loss of oxygen.

COVID-19 has a wide variation of symptoms and many symptoms
are mistaken for the “common cold.”. In the United States, COVID-19
symptoms are limited and vary among patients. Between January
14-April 14, 2020, CDC conducted a questionnaire to better evaluate the
variations of symptoms in the United States.[7] 158 out of 164 patients
had three symptoms of fever, cough, and shortness of cough. Total of
57 adult patients were hospitalized and 39 of them had these three
symptoms, while 25 non-hospitalized patients commonly experienced
symptoms such as headache, abdominal pain, and diarrhea. Age and
sex were also are taken into consideration. The results showed that
the presentation of the three common symptoms of fever, cough, and
shortness of cough directly correlated with the age of patient.[7]

DIAGNOSIS OF COVID-19
Diagnosis of SARS-CoV-2 infection requires the detection of the
virus in a patient-derived sample, which can be done either through
real-time RT-PCR or serological assays. RT-PCR is currently the
main method for diagnosis, which uses a nasopharyngeal (NP) swab
obtained from the patient. The NP swab is processed and the RNA
(if present) is isolated and reverse-transcribed into DNA. The DNA
will undergo PCR amplification using SARS-CoV-2 specific primer.
The targeted sequences consist of genes that code for the viral RNA-
dependent RNA polymerase (RdRp), the viral envelope (E genes), and
the viral nucleocapsid (N genes).[13] Presence of the targeted sequences
constitutes a positive result. Another assay available is a rapid antigen
test, which is an option for point of care testing. Antigen tests are used
to detect antigens rather than antibodies or nucleic acid. Antigen tests
are used for those with an active infection. Rapid antigen tests can be
used for CoV patients and will produce results within minutes.[12] Faster
results are significant to help slow the spread of the virus. However,
antigen tests have a higher chance of missing an active infection and
may require a follow up test using RT-PCR.[12]

Serological assays involve detection of IgG/IgM antibodies being
generated by the host in response to a SARS-CoV-2 infection. Various
types of serological assays include rapid diagnostic tests (RDT), enzyme-
linked immunosorbent assay (ELISA), and neutralization assays.[49]
While RT-PCR and antigen test can only detect active infections with
detectable …

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