CORONA VIRUS DISEASE 2019

Corona virus – found in animals & humans

7 Types
4 – low pathogenic
2 – highly pathogenic

Middle East Respiratory Syndrome (MERs) – 2012

-camels

Severe-Acute Respiratory Syndrome (SARs) – 2002

-found in palm civets & raccoon dogs

o COVID-19
-bats & pangolins
 STRUCTURE:
Protein Spikes - crown-like under electron microscope
- gives rise to corona virus
4 Structural Proteins
S – spike
E – envelope
M – membrane
N – nucleocapsid
SPIKE
 A crown-like structure
 Responsible for allowing
the virus to attach to the
membrane of the host cell.
 Contains a receptor binding
domain which recognizes a
specific receptor.
Functional Subunits:
S1- binds to the host cell
S2- mediates the fusion of the viral &
cellular membranes.
(Focus in the design of vaccines &
medical treatment)
MEMBRANE
 The most abundant on the
viral surface
 Defines the shape of the viral
envelope
 Central organizer of
assembly & interacts with the
other structural protein.
ENVELOPE
 Smallest of the major
structural protein on the viral
membrane
 Integral on the assembly &
release of virus from host
cells & during viral replication
 Largely localized at the site of
intracellular trafficking
specifically in the
endoplasmic reticulum &
Golgi apparatus
Viral envelope – viruses’ outer &
fatty layer (contact w/ soap will
breakdown)
NUCLEOCAPSID
 Bound to the viruses’ single
strand RNA
 All genetic information is held
to allow itself to replicate.
Capsid – protein shell that encloses
the genetic material of the virus
Function:
-Inhibits the host cells defense
mechanism
-Assist the viral RNA replication
 PATHOGENESIS

Exposure to respiratory droplets

cough & sneeze direct contact surface

Aerosolized allowing it to travel Inoculation to mucous membrane

into:

Nasal cavity
&
Oral cavity

 Average of 5-6 days to develop symptoms

 14 days for a person to contaminate
others
 Upper Airway
Angiotensin Converting Enzymes-2 (ACE-2)
(Nasal or throat area)
Was identified as the receptor that the virus
utilizes to infect the host cell.
Symptoms:
Mainly present in:  Common cold
 Stuffy nose
 Headaches
 Sore throat
 Fever

Lower Respiratory Tract

Trachea (Windpipe)
|
Bronchi (Left-2 & Right-3) Alveoli are tiny air-filled
Lung epithelial cells namely type 2 pneumocytes in Bronchioles pockets responsible for gas
the alveoli | exchange. (02 &CO2)
Alveoli (600 millions)

Binds in ACE-2

Mechanism of Entry
Direct cell entry Endocytosis

1. SARS COV-2 binds spike or S- 1. Material enters a cell after being surrounded by an area of the cell
protein to ACE-2 receptor. membrane which then buds off inside the cell to form a vesicle.
2. The host cell has proteases which 2. Once inside the cell, viruses’ specific RNA and proteins are
are enzymes that breakdown synthesized within the cytoplasm.
proteins & cleaves the spike 3. Further, viral proteins are then assembled with the blueprint
protein. contained within the viral RNA using the host cellular machinery.
3. This process activates the protein (endoplasmic reticulum & Golgi apparatus)
in order to trigger the process of 4. With specific processes to form the envelope glycoproteins, new
membrane fusion before injection variants are then assembled by fusing to the plasma membranes &
of the viral genome into the host released as vesicles via cellular exocitic secretion processes.
cell. (like influenza)
The virus uses the cell’s organelles to
replicate & release more viruses to infect VIRAL REPLICATION
the surrounding cells.
Injured alveolar cells

Cell death (Apoptosis)

1. Cellular stressors
2. Immune antigen inflammation

Can lead to exaggerated immune

response with the huge release
of pro-inflammatory mediators
causing cytokine storm
(Cytokine Release Syndrome)
Cytokines are small
proteins involved in cell
signaling and are crucial in
mediation and immune
response.

Activation of innate immune system:

 IL-2
 TNF-Alpha
 IL-6
(pyrogens)
 Multiple inflammatory mediators are
released which creates an
Alveolar cell damage inflammatory response leading to:
& inflammatory = Pneumonia

1. Build up of mucus & thickening &

hyperplasia of cells within the airways.
2. Inflammation causes irritation of the cell
lining which leads to cough.
Triggers nerve endings in the
lungs to initiate cough reflex.

Impaired ability to exchange gases

Symptom: Shortness of breath

 Systemic inflammatory state causes increased
Damage to type-2 pneumocyte will Collection of fluid in the alveoli:
capillary permeability pulmonary
Non-cardiogenic & results inedema
even more
stop the production of surfactant.
fluid entering the alveoli. 1. Alveolar cell damage
Surfactant: reduce surface tension 2. Alveolar inflammation
(Noncardiogenic pulmonary edema)
& prevent lung collapse. 3. Alveolar collapse

= Acute Respiratory Distress Syndrome

(ARDS)
Noncardiogenic Pulmonary Edema Impairs the ability of the lungs to
is caused by changes in permeability of the exchange oxygen & carbon dioxide
pulmonary capillary membrane. (Decrease gas exchange)

Acute Respiratory Distress Syndrome

(ARDS)

DEATH