Coronaviruses can cause respiratory illnesses and are transmitted between humans and other mammals. COVID-19 is caused by SARS-CoV-2, a new coronavirus that emerged in 2019 and caused a global pandemic. Approved COVID vaccines work by introducing genetic material that teaches the immune system to recognize and fight the virus. Common side effects are short-term and mean the immune system is responding as intended. Histopathological examination of COVID-19 patient lungs typically shows diffuse alveolar damage, hyaline membrane formation, and inflammation. Additional organ involvement can occur, such as acute kidney injury seen on renal histopathology.

1. BY
Lecturer Dr. Mohammed Jassim
Lecturer Assistant Iyman Jewad
Lecturer Assistant Hesnaa Saeed

2. Coronaviruses

Coronaviruses are enveloped non-segmented
positive-sense RNA viruses belonging to the
family Coronaviridae and the order
Nidovirales and broadly distributed in
humans and other mammals.

the epidemics of the two betacoronaviruses,
severe acute respiratory syndrome
coronavirus (SARS-CoV) and Middle East
respiratory syndrome coronavirus (MERS-
CoV), and the third is pandemeic corona
virus COVID19

4. vaccination

Currently approved COVID-19 vaccines are considered to be safe and effective

Most side effects occur within 6 weeks of someone getting the vaccine. FDA has
required 8 weeks of safety monitoring.

Current studies have 30,000 to 50,000 participants. § This demonstrates how
safety is a top priority for the FDA and the healthcare community.

Side effect

Short-term discomfort: headache, muscle pains, fatigue, chills, fever, pain at
injection site. These side effects are normal and common. They last 1-2 days.

It means your body is doing its job and making antibodies (IT IS A GOOD
THING)

Side effects could be more pronounced with the second dose.

More serious reactions may include shortness of breath, cough, fever, sore
throat, runny nose, loss of taste or smell. If these or other reactions occur, consult
your healthcare provider right away.

5. How to work(Pfizer)

First, COVID-19 mRNA vaccines are given in the upper arm muscle.
Once the instructions (mRNA) are inside the immune cells, the cells
use them to make the protein piece. After the protein piece is made,
the cell breaks down the instructions and gets rid of them.

Next, the cell displays the protein piece on its surface. Our immune
systems recognize that the protein doesn’t belong there and begin
building an immune response and making antibodies, like what
happens in natural infection against COVID-19.

At the end of the process, our bodies have learned how to protect
against future infection. The benefit of mRNA vaccines, like all
vaccines, is those vaccinated gain this protection without ever having
to risk the serious consequences of getting sick with COVID-19.

6. How to work(Oxford-AstraZeneca)

The researchers added the gene for the coronavirus spike protein to another
virus called an adenovirus. Adenoviruses are common viruses that typically
cause colds or flu-like symptoms. The Oxford-AstraZeneca team used a
modified version of a chimpanzee adenovirus, known as ChAdOx1. It can
enter cells, but it can’t replicate inside them.

the Oxford vaccine doesn’t have to stay frozen. The vaccine is expected to last
for at least six months when refrigerated at 38–46°F (2–8°C).

The cell engulfs the virus in a bubble and pulls it inside. Once inside, the
adenovirus escapes from the bubble and travels to the nucleus, the chamber
where the cell’s DNA is stored.

the gene for the coronavirus spike protein can be read by the cell and copied
into a molecule called messenger RNA, or mRNA.

The mRNA leaves the nucleus, and the cell’s molecules read its sequence and
begin assembling spike proteins.

These protruding spikes and spike protein fragments can then be recognized
by the immune system.

7. In early 2020, the Beijing Institute of Biological Products created an inactivated coronavirus vaccine
called BBIBP-CorV. Clinical trials run by the state-owned company Sinopharm showed that it had an
efficacy rate of 79 percent. China approved the vaccine
A Vaccine Made From Coronaviruses
The antibodies attach to viral proteins, such as the so-called spike proteins that stud its surface.
To create BBIBP-CorV, the Beijing Institute researchers obtained three variants of the coronavirus from
patients in Chinese hospitals.
They picked one of the variants because it was able to multiply quickly in monkey kidney cells grown in
bioreactor tanks.
Killing the Virus
Once the researchers produced large stocks of the coronaviruses, they doused them with a chemical called
beta-propiolactone.
The compound disabled the coronaviruses by bonding to their genes.
The inactivated coronaviruses could no longer replicate. But their proteins, including spike, remained intact.
The researchers then drew off the inactivated viruses and mixed them with a tiny amount of an aluminum-
based compound called an adjuvant Adjuvants stimulate the immune system to boost its response to a
vaccine.
How to work(Sinopharm)

8. Prompting an Immune Response

Because the coronaviruses in BBIBP-CorV are dead, they can be injected into the arm without
causing Covid-19. Once inside the body, some of the inactivated viruses are swallowed up by
a type of immune cell called an antigen-presenting cell.
The antigen-presenting cell tears the coronavirus apart and displays some of its fragments on
its surface.

A so-called helper T cell may detect the fragment.

If the fragment fits into one of its surface proteins, the T cell becomes activated and can help
recruit other immune cells to respond to the vaccine.

Making Antibodies

Another type of immune cell, called a B cell, may also encounter the inactivated coronavirus.

B cells have surface proteins in a huge variety of shapes, and a few might have the right
shape to latch onto the coronavirus. .

9. Coronavirus disease (COVID) has caused a great global
threat to public health. The World Health Organization
(WHO) has declared COVID-19 disease as a pandemic,
affecting the human respiratory and other body systems,
which urgently demands for better understanding of
COVID-19 histopathogenesis. The lungs are affected the
most, with patients presenting symptoms related to the
respiratory system such as sore throat, fever, malaise,
and respiratory distress, and in worst cases may The
entry of virus in the host cells induces immune response
with wide secretion of inflammatory cytokines and
chemokines. Because SARS-CoV-1 and SARS-CoV-2
have the same mechanism of action, both can cause
rapid production of multiple cytokines in body fluids
following infection, leading to acute respiratory distress
and multiple organ failure.

10. This also explains why most patients with COVID-
19 have mild symptoms at the onset of the
disease, while conditions of a few affected
patients are suddenly worsened after being
diagnosed in hospital, which may be related to
the body producing excessive cytokines after the
disease, leading to ‘cytokine storm’ in the body.
The association of viral infection with any
comorbid conditions such as hypertension,
diabetes and renal failure has shown more
severe form of clinical presentations such as
respiratory failure to multiple organ failure.

11. Patients with affected upper respiratory tract
usually present with mild to moderate symptoms
but patients with lower respiratory tract infection
show features of pneumonia and land up with
organ failure. The severity increases with presence
of comorbidities like hypertension, chronic
kidney disease, obstructive sleep apnoea and
metabolic diseases like diabetes and obesity, and
the pathological changes may even vary between
right and left lung. Macroscopically, lungs appear
congestive, with patches of haemorrhagic
necrosis.

16. Alveolitis with atrophy, vacuolar degeneration,
proliferation, desquamation and squamous metaplasia
of alveolar epithelial cells ,with presence of exudative
monocytes and macrophages are prominent features
microscopically. There may be presence of massive
fibrinous exudate, multinucleate giant cells and
intracytoplasmic viral inclusion bodies and presence of
epithelial cells in the lumen suggesting necrotic
changes (necrotising bronchiolitis). There may be
presence of diffuse alveolar damage (DAD), hyaline
membrane formation and vascular congestion with
occasional inflammatory cells, damaged pneumocytes
with focal sloughing and formation of syncytial giant
cells, along with focal infiltration of immune cells in the
form of lymphocytes, monocytes and increased stromal
cells .

19. Additional findings included intra-alveolar
haemorrhages, cluster or plug formation due to
the accumulated fibrin and degraded hyaline
membrane remnants in some of the alveoli .There
may be presence of patchy and sparse chronic
inflammation, composed mainly of lymphocytes,
along with thrombi in branches of pulmonary
artery and focal areas of congestion in alveolar
septal capillaries along with septal capillary injury
with mural and luminal fibrin deposition.

22. Renal histopathology
Kidney changes were observed with interstitial
infiltration by lymphocytes, tubular epithelial cell
necrosis, fibrinoid necrosis of blood vessels, and
microthrombi in small vessels . All findings present in
acute kidney injury. There were also erythrocyte casts in
some of the tubules - erythrocyturia, as well as
ballooned glomeruli .