AN ASIGNMENT

ON

COMMUNICABLE DISEASES 1 (CHO 215)

WRITTEN BY

NWANKWO CHIOMA PEACE

FCAI/HND/HRE/2019/2020/0114

SUBMITTED TO

DR. NWOSU E.C

IN PARTIAL FULFILMENT OF THE REQUIREMENTS FOR THE

AWARD OF HIGHER NATIONAL DIPLOMA IN HOME AND RURAL
ECONOMICS, FEDERAL COLLEGE OF AGRICULTURE ISHIAGU,
EBONYI STATE.

NOVEMBER, 2020

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Introduction

Coronaviruses are a group of related RNA viruses that cause diseases in mammals
and birds. In humans and birds, they cause respiratory tract infections that can
range from mild to lethal. Mild illnesses in humans include some cases of the
common cold (which is also caused by other viruses, predominantly rhinoviruses),
while more lethal varieties can cause SARS, MERS, and COVID-19. In cows and
pigs they cause diarrhea, while in mice they cause hepatitis and encephalomyelitis.
There are as yet no vaccines or antiviral drugs to prevent or treat human
coronavirus infections.

Coronaviruses constitute the subfamily Orthocoronavirinae, in the family

Coronaviridae, order Nidovirales, and realm Riboviria. They are enveloped viruses
with a positive-sense single-stranded RNA genome and a nucleocapsid of helical
symmetry. The genome size of coronaviruses ranges from approximately 26 to 32
kilobases, one of the largest among RNA viruses. They have characteristic club-
shaped spikes that project from their surface, which in electron micrographs create
an image reminiscent of the solar corona, from which their name derives.

Coronaviruses are large, roughly spherical particles with unique surface

projections. Their size is highly variable and generally is an average diameter of
120 nm. Extreme sizes are known from 50 to 200 nm in diameter. The total
molecular weight is on average 40,000 kDa. They are enclosed in an envelope
embedded with a number of protein molecules. The lipid bilayer envelope,
membrane proteins, and nucleocapsid protect the virus when it is outside the host
cell.

The viral envelope is made up of a lipid bilayer, in which the membrane (M),
envelope (E) and spike (S) structural proteins are anchored. The ratio of E:S:M in

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the lipid bilayer is approximately 1:20:300. The E and M protein are the structural
proteins that combined with the lipid bilayer shape the viral envelope and maintain
its size. S proteins are needed for interaction with the host cells. But human
coronavirus NL63 is peculiar in that its M protein has the binding site for the host
cell, and not its S protein. The diameter of the envelope is 85 nm. The envelope of
the virus in electron micrographs appears as a distinct pair of electron-dense shells
(shells that are relatively opaque to the electron beam used to scan the virus
particle).

Causative Organism

The recent outbreak began in Wuhan, a city in the Hubei province of China.
Reports of the first COVID-19 cases started in December 2019.

Coronaviruses are common in certain species of animals, such as cattle and camels.
Although the transmission of coronaviruses from animals to humans is rare, this
new strain likely came from bats, though one study suggests pangolins may be the
origin.

However, it remains unclear exactly how the virus first spread to humans.

Some reports trace the earliest cases back to a seafood and animal market in
Wuhan. It may have been from here that SARS-CoV-2 started to spread to humans.

Methods of Transmission

Researchers believe that the viruses transmit via fluids in the respiratory system,
such as mucus.

For example, a coronavirus can spread when a person:

 coughs or sneezes without covering their mouth, dispersing droplets into the
air
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  has physical contact with someone who has the infection
 touches a surface that contains the virus, then touches their nose, eyes, or
mouth

Also, while some animal coronaviruses may spread to humans through contact
with feces, it is unclear whether human coronaviruses can spread in the same way.

Coronaviruses infect most people at some point.

To prevent transmission, people with symptoms should stay at home, rest, and
avoid coming into close contact with others.

Covering the mouth and nose with a tissue or handkerchief while coughing or
sneezing can also help prevent transmission. It is important to dispose of used
tissues right away and maintain high levels of hygiene, especially around the
home.

Symptoms of Corona virus

According to the CDC, people may start to experience COVID-19 symptoms 2–14
days after exposure to SARS-CoV-2. Symptoms may include:

i. a fever
ii. chills
iii. a cough
iv. shortness of breath or difficulty breathing
v. a sore throat
vi. congestion or a runny nose
vii. fatigue
viii. a headache
ix. muscle pain

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 x. a new loss of taste or smell
xi. nausea, vomiting, or both
xii. diarrhea

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Pathology

SARS-CoV-2 primarily targets the lungs, the vasculatures, and the immune
system. The initial step of the viral multiplication is the binding to the surface of
respiratory cells mediated by the spike (S) viral protein. It had been speculated that
SARS-CoV-2 likely utilize angiotensin- converting enzyme 2 (ACE2, EC
3.4.17.23) of various mammals, except murines and a few birds, such as pigeon.
The affinity of SARS-CoV-2 for ACE2 is 10–20-higher than that of SARS- CoV.

ACE2 is a metalloproteinase and shares about 60% homology with the

carboxypeptidase angiotensin- converting enzyme (ACE, EC 3.4.15.1). ACE2,
which is made up of 805 amino acids, is type I transmembrane glycoprotein having
a single extracellular catalytic domain. Its expression is reported in the lungs,
cardiovascular system, gut, kidneys, CNS and adipose tissue. It is the key active
peptide of the renin-angiotensin system (RAS) or renin–angiotensin–aldosterone
system (RAAS).

The pathogenesis involves two interconnected processes: lung inflammation and

immune deficiency, both of which are related to an improper immunologic
response and over-production of proinflammatory cytokines, Additionally, altered
redox balance in infected cells through alteration of NAD+ biosynthesis, poly
(ADP-ribose) polymerase (PARP) function along with changeing proteasome and
mitochondrial function further exacerbate inflammation and lipid peroxidation
resulting in cell damage. Furthermore, SARS-CoV-2 induced activation of
apoptosis and p53 signaling pathway in lymphocytes causes lymphopenia in such
patients.

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Prevention

Infection can spead only in the existence of contact. Nosocomial spread is usually
controlled through preliminary infection control measures, including wearing of
face masks, respiratory etiquette, hand and environmental hygiene. Personal
protective equipment (PPE) is a vital element; but it is just one component of a
shielding system from COVID-19 infection. Quarantine or physical segregation is
vital to confirm effectiveness, including short- to medium-term lockdowns,
voluntary home curfew, curb on the gathering of people, cessation of social and
public events and closure of mass transit systems.

Control

As extracorporeal membrane oxygenation (ECMO) is considered as an efficient

remedy in the treatment of severe COVID-19.

No valdated medicine is available till date against COVID-19. Some drugs that are
indicated for other afflictions are being tested, although without unambiguous
evidence. Lipophilic antibiotics tetracyclines (e.g. tetracycline, doxycycline, and
minocycline) can chelate zinc (Zn) compounds on matrix metalloproteinases
(MMPs). Coronaviruses are believed to depend on host MMPs for survival, cell
infiltration, cell to cell adhesion, and replication; many of those have Zn as a part
of their MMP complex. It is possible that the Zn-chelating characteristic of
tetracyclines may be responsible to inhibit SARS-CoV-2 infection in humans, and
controlling their capacity to multiply within the host. Ivermectin, an FDA-
approved anti-parasitic drug that was previously shown as broad-spectrum anti-
viral activity in vitro, was reported as an inhibitor of the causative virus (SARS-
CoV-2) in Vero-hSLAM cells.

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The spike (S) protein on the viral envelope, is believed as a major intention of
vaccine development for the prevention of coronavirus infection. The choices to
block viral ingress include the employment of natural neutralizing antibodies from
convalescent plasma (discussed elsewhere within the manuscript) and engineered
antibodies. Engineered antibodies or neutralizing fragments are often utilised in
various formats. The antibody/Fc-receptor complex imitates viral receptor to
intervene viral entry. Antibody-dependent enhancement (ADE) of viral entrance
has been observed for several viruses. In such cases, antibodies mark one serotype
of viruses and subneutralize another, causing to ADE of the second virus. A unique
mechanism for the ADE is that a neutralizing antibody attaches to the S protein of
coronaviruses like a viral receptor, triggers a conformational change of the spike,
and mediates viral entry into IgG Fc receptor-conveying cells through canonical
viral-receptor-dependent pathways.