SARS-CoV2 (COVID-19) A Mutated Coronavirus that

Lethal and Dangerous to Human

(Chelsea 10B)

Introduction

A virus is a microscopic parasite, it is generally smaller than bacteria. They do not have the
capacity to thrive by themself and reproduce outside of a host body. Once, when they infect a susceptible
cell, the virus can direct the cell machinery to produce more viruses. Most viruses have either RNA or
DNA as their genetic material, they can not have both at the same time. The nucleic acid can be single or
double-stranded. The entire infectious virus particle is called a virion. The virion consists of nucleic acid
and an outer shell of protein. The simplest viruses contain only enough RNA or DNA to encode four
proteins. The most complex can encode 100-200 proteins. However, once viruses enter a host cell, the
viral nucleic acid becomes active and viral multiplication results. In this sense, viruses are alive when
they multiply in host cells they infect. From a clinical point of view, viruses can be considered alive
because they cause infection and disease, the same as pathogenic bacteria, fungi, and protozoa do.
Depending on one’s viewpoint, a virus may be regarded as an exceptionally complex aggregation of
nonliving chemicals, or as an exceptional sample living microorganism. ​(Aparna Vidyasagar et al., 2016)

Discussion
The first report of a covid-19 in Wuhan city, Hubei province, China in late December 2019 said
that the beginning starts from the Huanan seafood and wildlife market in Wuhan city where a variety of
mammalian species were available for purchase at the time of the outbreak. While this again suggests that
the market played an important role in virus emergence. After clinical cases began to appear, their
research team focused on a patient admitted to the Central Hospital of Wuhan in December 2019, six-day
after the onset of symptoms. This patient was experiencing fever, chest tightness, cough, pain, and
weakness, along with lung abnormalities indicative of pneumonia that appear to be commonplace in
Covid-19. Initial analysis revealed that the virus was closely related to those of SARS-like viruses. This
result was immediately reported to the relevant authorities, and an annotated version of the genome
sequence was submitted to NCBI/GenBank.​ (​http://creativecommons.org/licenses/by-nc-nd/4.0/)
Fig 1: The life cycle of SARS CoV2 in have cells starts its life cycle when S protein ties to the cellular
receptor ACE2. After receptors are authoritative, the compliance alters within the S protein encourages
viral envelope combination with the cell layer through the endosomal pathway. At that point SARS CoV2
discharges RNA into the have cell. Genome RNA is deciphered into viral replicase polyproteins pp1a and
1ab, which are at that point cleaved into little items by viral proteinases. The polymerase produces an
arrangement of subgenomic mRNAs by spasmodic translation and at last interpreted into proteins and
genome RNA are subsequently assembled into virions within the ER and Golgi and after that transported
through vesicles and discharged out of the cell. ACE2, angiotensin-converting chemical 2, ER
endoplasmic reticulum, ERGIC, ER Golgi middle of the road compartment. ​(M.A. Shereen et al., 2020)

This mechanism occurs because the virus has a rapid mutation process. The extremely high
mutation rates of viruses are not matched by any other organism in the kingdom of life. The high mutation
rates of viruses, coupled with short generation times and large population sizes, allow viruses to rapidly
evolve and adapt to the host environment. Virus mutation creates genetic diversity, which is subject to the
opposing action of selection and random genetic drift, both of which are directly affected by the size of
the virus population. Viruses possess mutation rates that are orders of magnitude higher than any other
replicating entity. These rates range from approximately 1.5 × 10−3 mut/nuc/rep in the RNA
bacteriophage Qβ to ∼10−8 mut/nuc/ rep in the DNA virus Herpes simplex. The rate at which mutation fix
in a population is termed the substitution rate, or evolutionary rate, which is measured by comparing the
genomes of different isolates of a virus collected at several different time points. RNA viruses possess
much higher substitution rates than DNA viruses, and covid has RNA inside it. This explains why viruses
mutation can not be avoided, and they mutate naturally and spontaneously. Moreover, DNA/RNA/protein
that contained in viruses are very easy to change because of the surrounding environment (UV, enzymes,
and any other chemicals). ​(Adi Stern, Raul Andino et al., 2018)
 If someone is already infected with a virus or disease, then there are several ways that can help
their bodies to produce antibodies to fight the disease or virus. One of them is by having vaccines.
Vaccines are like a training course for the immune system. They prepare the body to fight disease without
exposing it to disease symptoms. When bacteria or viruses enter the body, immune cells called
lymphocytes respond by producing antibodies, which are protein molecules. These antibodies fight the
invader known as an antigen and protect against further infection. Unfortunately, the first time the body
faces a particular invader, it can take several days to ramp up this antibody response. For antigens like the
measle virus or whooping cough bacteria, a few days is too long. The infection can spread and kill the
person before the immune system can fight back. That is where the vaccine comes in. Vaccines are made
of dead or weakened antigens. They can’t cause an infection, but the immune system still sees them as an
enemy and produces antibodies in response, After the threat has passed, many of the antibodies will break
down, but immune cells called memory cells remain in the body. When the body encounters that antigen
again, the memory cells produce antibodies fast and strike down the invader before it’s too late.
(Stephanie Pappas et al., 2010)

The vaccine might seem simple, we just add it to our body and there is no risk of catching the
disease for the rest of our life, but actually vaccines are not that simple. Some diseases are more resilient
than others. Over time, our body can lose the antibody effectiveness that was first provided by
vaccination, leaving it open to the disease once again. After initial vaccination, the body sometimes needs
a wake-up call to continue preventing a disease in the form of a booster. For many other vaccines though,
the need for a booster depends on other details. Booster shots may be needed if you were born before a
vaccine became a legal requirement or in a region of the world that did not provide immunization.
Booster vaccines may also be necessary to travel outside of the country. ​(Will Sowards et al., 2016).

Several major biotechnology companies have advanced nucleic acid platforms for COVID-19
vaccine development. The mRNA based vaccine prepared by the US National Institute of Allergy and
Infectious Diseases against SARS-CoV-2 is under phase 1 trial. INO-4800- deoxyribonucleic acid-based
mostly vaccinum are presently accessible for human testing. Chinese Centre for Disease Control and
Prevention (CDC) working on the development of an inactivated virus vaccine. Soon an mRNA based
vaccine sample will be available. GeoVax-BravoVax is working to develop a modified Vaccina Ankara
based vaccine. While Clover Biopharmaceuticals is developing a recombinant 2019-nCoV S - protein
subunit trimer based vaccine. ​(M.A. Shereen et al., 2020)

There is a lot of evidence that shows viruses that appear in this world are the result of natural
mutation and evolution processes and it is originating from previous viruses, and not from lab
experiments. From the Phylogenetic Tree, the protein structure or amino acid that found in RNA or DNA
of the viruses is having a mutation in the same ancestor, this is why they have similarities to each other.
We can take an incident in 2003 when the Chinese population was infected with a virus causing severe
Acute Syndrome (SARS) in Guangdong province. The virus was confirmed as a member of the Beta
coronavirus subgroup and was named SARS-CoV. The infected patients exhibited pneumonia symptoms
with a diffuse alveolar injury which lead to acute respiratory distress syndrome (ARDS). SARS initially
emerged in Guangdong, China, and then spread rapidly around the world with more than 8000 infected
persons and 776 deceased. Later in 2012, a couple of Arab Saudi Arabian nationals were diagnosed to be
infected with another coronavirus. The directed virus was confirmed as a member of coronaviruses and
named as the Middle East Respiratory Syndrome Coronavirus (MERS-CoV). The World health
organization reported that MERS-coronavirus infected more than 2428 individuals and 838 deaths.
MERS-CoV is a member of the betacoronavirus subgroup and is phylogenetically diverse from other
human CoV. Similar to SARS coronavirus, patients infected with MERS coronavirus suffer pneumonia
followed by ARDS and renal failure. Recently, by the end of 2019, WHO was informed by the Chinese
government about several cases of pneumonia with unfamiliar etiology. The outbreak was initiated from
the Hunan seafood market in Wuhan city, the virus was identified as a novel coronavirus. These
observations indicated a human spreading capability of this virus. It occurs due to close contact with an
infected person, exposed to coughing, sneezing, respiratory droplets or aerosols. For further, the diagrams
below explain and show that pas viruses have similarities to what is happening now. ​(M.A. Shereen et al.,
2020)

Fig 2​ : Phylogenetic tree of coronavirus.​(M.A. Shereen et al., 2020)

Fig 3: T​ he key supplies and mode of transmission of coronaviruses, as it were a and b coronaviruses have
the capacity to contaminate people, the utilization of contaminated creatures a source of creature to
human transmission of the virus and due to shut contact with a trained individual, the infection is assist
transmitted to sound people. Specked dark bolt appears the plausibility of viral exchange from bat though
the strong dark bolt speaks to the affirmed exchange. ​(M.A. Shereen et al., 2020)

Fig 4: Betacoronaviruses (SARS CoV2, SARS CoV, and MERS CoV) genome comprises of the 50
untranslated locales (50 UTR), open perusing outline (orf) 1 a/b (green box) encoding nonstructural
proteins (nsp) for replication, basic proteins counting spike (blue box), wrap (maroon box), layer (pink
box), and nucleocapsid (cyan box) proteins, extra proteins (light gray boxes) such as orf 3, 6, 71, 7b, 8,
and 9b within SARS CoV2 genome, and the 30 untranslated locales (30 UTR). The gushed underlined in
ruddy are the proteins which appear as a key variety between SARS CoV2 and SARS CoV. the length of
nsps and orfs are not drawn in scale. ​(M.A. Shereen et al., 2020)
 Through a genomic analysis, SARS-CoV2 has the commonplace of coronavirus structure with
spike protein conjointly, such as RNA polymerase, 3 chymotrypsin-like proteases, helicase, glycoprotein,
and extra protein that can be found in MERS coronavirus and SARS coronavirus. ​(M.A. Shereen et al.,
2020). ​Also, the genome sequence of the virus isolate from a pangolin (GX/P2V) which has high
similarities (99.83-99.92%) to the five sequence obtained through the metagenomic sequencing of the raw
samples, and all have similar genomic organization to SARS CoV2. ​(Lam et al., 2020)

Conclusion
From the evidence, there is a lot of similarity between SARS CoV2/Covid-19 with other
coronavirus species and it is reasonable to conclude that SARS CoV2/Covid-19 was not a biological
weapon and not deliberately lose but it is a virus that naturally occurs by a mutation and evolution process
in nature, and this mutation occur spontaneously and naturally and can not be avoided by humans. These
viruses may spread to the human body that occurs due to close contact with an infected person, exposed to
coughing, sneezing, and respiratory droplets. And vaccines are possibly one of the best options that
humans have to combat the virus, by injecting the vaccines to a human body, our body will produce an
antibody that has the ability to fight and eliminate the virus and to prevent the contagious and infectious
disease of COVID - 19. And also to prevent the higher severity impact of the spread of the virus in our
society and especially globally, the development of the COVID-19 vaccine should become the top priority
and the utmost concern for every stakeholder in every country so this put an end to this pandemic.

References​ :

Acevedo, A., Brodsky, L., and Andino, R. (2014). Mutational and fitness landscapes of an RNA virus revealed through
population sequencing. Nature 505, 686–690.

Annan A, Baldwin HJ, Corman VM, Klose SM, Owusu M, Nkrumah EE, et al. Human betacoronavirus 2c EMC/2012–related
viruses in bats, Ghana and Europe. Emerg Infect Dis 2013;19(3):456.

Boero, Ferdinando. “Faculty Opinions Recommendation of Identifying SARS-CoV-2 Related Coronaviruses in Malayan
Pangolins.” ​Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature,​ 2020,
doi:10.3410/f.737621625.793572849.

Batschelet, E., Domingo, E., and Weissmann, C. (1976). The proportion of revertant and mutant phage in a growing population,
as a function of mutation and growth rate. Gene 1, 27–32.

Centers for Disease Control and Prevention. Principles of vaccination. In: Hamborsky J, Kroger A, Wolfe S, eds. Epidemiology
and Prevention of Vaccine-preventable Diseases. 13th ed. Washington, DC: Public Health Foundation; 2015.

Daugherty, M.D., and Malik, H.S. (2012). Rules of engagement: molecular insights from host-virus arms races. Annu Rev Genet
46, 677–700.

Duffy, S., Shackelton, L.A., and Holmes, E.C. (2008). Rates of evolutionary change in viruses: patterns and determinants. Nat
Rev Genet 9, 267–276.

Holmes, E.C. (2008). Evolutionary history and phylogeography of human viruses. Annu Rev Microbiol 62, 307–328.
Huynh J, Li S, Yount B, Smith A, Sturges L, Olsen JC, et al. Evidence supporting a zoonotic origin of human coronavirus strain
NL63. J Virol 2012;8612816–25.

Lu R, Zhao X, Li J, Niu P, Yang B, Wu H, et al. Genomic characterisation and epidemiology of 2019 novel coronavirus:
implications for virus origins and receptor binding. The Lancet 2020.

Kan B, Wang M, Jing H, Xu H, Jiang X, Yan M, et al. Molecular evolution analysis and geographic investigation of severe acute
respiratory syndrome coronavirus-like virus in palm civets at an animal market and on farms. J Virol 2005;79(18):11892–900.

Memish ZA, Zumla AI, Al-Hakeem RF, Al-Rabeeah AA, Stephens GM. Family cluster of Middle East respiratory syndrome
coronavirus infections. N Engl J. Med 2013;368(26):2487–94.

Paden C, Yusof M, Al Hammadi Z, Queen K, Tao Y, Eltahir Y, et al. Zoonotic origin and transmission of Middle East
respiratory syndrome coronavirus in the UAE. Zoonoses Public Health 2018;65(3):322–33.

Pappas, Stephanie. “How Do Vaccines Work?” ​LiveScience,​ Purch, 1 June 2010,

www.livescience.com/32617-how-do-vaccines-work.html.

Sanjuan, R. (2012). From molecular genetics to phylodynamics: evolutionary relevance of mutation rates across viruses. PLoS
pathogens 8, e1002685.

Sanjuan, R., Nebot, M.R., Chirico, N., Mansky, L.M., and Belshaw, R. (2010). Viral mutation rates. Journal of virology 84,
9733–9748.

Shi Z, Hu Z. A review of studies on animal reservoirs of the SARS coronavirus. Virus Res 2008;133(1):74–87.

Zheng BJ, Guan Y, Wong KH, Zhou J, Wong KL, Young BWY, et al. SARS-related virus predating SARS outbreak, Hong
Kong. Emerg Infect Dis 2004;10(2):176.

Zhong N, Zheng B, Li Y, Poon L, Xie Z, Chan K, et al. Epidemiology and cause of severe acute respiratory syndrome (SARS) in
Guangdong, People’s Republic of China, in February 2003. The Lancet 2003;362(9393):1353–8.