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Strategies to fight the Novel Coronavirus SARS HW jawaher final1

Jawaher Zaid Almarri
Strategies to fight the Novel Coronavirus SARS-CoV2
Background: The structure of SARS-CoV-2 determined from the genome information of the
virus. 2 3 SARS-CoV-2 is a positive single-stranded (+ssRNA) RNA virus, and RNA itself,
the viral genome, acts as a transcript. This gene encodes a number of structural proteins
including the four major proteins: Spike(S) glycoprotein, Nucleoprotein(N) protein,
Membrane(M) protein, and Envelope(E) protein. S protein is a protein located in the outer
shell of the corona virus and is involved in the penetration of the virus into the host cell
through interaction with the host cell's receptor. Protein N binds to the viral RNA to form the
nucleocapsid, a type of protein shell that protects the viral genome. In addition, it is an
important protein that plays a role in stabilizing and packaging the genome in virus particle
assembly, envelope formation, and RNA synthesis. Protein M plays a role of connecting this
capsid and membrane (phospholipid bilayer, a kind of membrane), and finally, protein E is
involved in the assembly and ejection of viruses and constitutes the outer shell.
Pathogenesis: Pathogenesis: Studies show that multi-organ infection of SARS-CoV-2 can
occur through the angiotensin-converting enzyme 2 (ACE2) receptor, which is found almost
everywhere in the body. Located on the surface of many immune and non-immune cells,
ACE2 is an enzyme that belongs to the system that regulates blood pressure, fluid and
electrolyte balance. It is also involved in regulating the cardiovascular system, the nervous
system, kidney function, and fertility. How does SARS infect humans? Coronavirus, as its
name suggests, is an important weapon for infecting people with spike proteins that protrude
like a crown from the outside. ACE2, a cousin of angiotensin-converting enzyme (ACE), is
said to play a role in SARS-CoV-2 receptors. Currently, SARS-CoV-2, the younger brother of
SARS, the nightmare of the whole world, is known to use the same ACE2 receptors to
invade our bodies. By drawing an easy-to-understand picture, a receptor protein, which locks
in our body called ACE2, opens the door to human cells by inserting a key called Spike
Protein for Coronavirus. The better the spike key binds to ACE2 lock, the more open the
human infiltration pathway, the greater the possibility of infection, and ACE2 is known before
ACE2, which acts as an invasion channel for Coronavirus. The angiotensin-converting
enzyme, acting on angiotensin and bradykinin, to narrow the blood vessels and cause
hypertension ..; ACE2 has a similarity of 42% with the ACE mineral catalytic domain. In
addition to converting angiotensin 2 (Ang II) to Angiotensin Ang- (1-7), ACE2 and
physiological or pathological changes are involved in the generation of Angiotensin and Ang(1-7). However, in ACE and ACE2, proteases degrade the peptides. They are found in
different locations and have different substrate properties.
Strategy to stop SARS-CoV 2: SARS-CoV-2 infection can be prevented in humans using
ACE2 inhibition by demonstrating its ability to fight viruses by synthesizing human proteins
associated with coronaviruses. By linking the coronavirus to the water-soluble ACE2 protein
that was placed in place of ACE2 in the host cell. The war between humans and viruses is
hidden. Coronavirus uses the ACE2 protein, which plays a role in preventing lung damage in
our bodies, as an invasion passage into the lungs. This therapeutic filter causes the
introduced virus to recognize and bind recombinant ACE2 as a true receptor. Viruses that
bind to the fake receptors die naturally. These protein fragments, called "nsp-nonstructural
proteins," also cause the virus to replicate in host cells. Non-structural proteins, such as
Lego blocks, must be split into 16 pieces to perform each task. Therefore, inhibiting this
mitosis process also limits virus growth. For example, Kaletra (a mixture of lopinavir and
ritonavir) was developed as a proteinase inhibitor of HIV. Kaletra is undergoing clinical trials
as a candidate for treatment of SAV-2, but it is not easy to expect a significant therapeutic
effect from the reports so far.
Jawaher Zaid Almarri
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Figure 2. The genotype and phylogenetic tree of
Figure 1. Imagination of an artificial synthetic protein (red) combining with
coronavirus instead of human cells to block infection
)Source = British Columbia, Canada(