Something evil • They are not alive…yet

they are not dead

are on the • They prey on living
loose… things, especially
HUMANS
• We cannot see them,
but they are
everywhere
• They have already
killed millions
• You or your loved ones
could be their next
victim
I’m not talking about him…
Viruses!!
Things you need to know about viruses
• Viruses are everywhere
Over 5,000 have been described in detail
Millions and Millions Exist
• When they’re in the air, or on a doorknob
They’re inert = about as living as a rock.
• When they come into contact with host cells
They trigger the cell to engulf them
Or fuse with the cell
• Then use the cell’s machinery to reproduce
HIV virus; the mass killer
• Yearly Mortality: 3.1 million
Total Mortality: 25 million+
since 1981

• How it works:
Invades important immune
system cells and kills them.
Leaves patient open to
death by other illnesses
with lowered immune
function.
Ebola virus: the rapid killer with no cure

• Yearly mortality:
Mortality rate: 90%
within days[3]
• How it works:
[3]Disables tetherin, a
protein that disables
the spread of the virus
from cell to cell.
Spreads rapidly to cause
hemorrhaging, extreme
fever, and death.
Rotavirus: the child-killer
• Yearly Mortality:>500,000
children
• How it works:
Spread through fecal-oral
exposure, often through
play surfaces
or contaminated water.
Diarrhea, vomiting, and
abdominal pain can be
deadly, particularly in
the developing world
Smallpox: the monarch killer
• Mortality rate: Eradicated
20th century mortality rate:
300-500 million
• 80% of infected children died
20-60% of infected adults.
• How it works:
Localizes in the blood vessels of
the skin and in the mouth and
throat. One of two infectious
diseases to be eradicated by
humans. Ravaged populations
from 10,000 b.c.- 1979. Killing 5
reigning monarchs in the
1700′s.
Hepatitis B: killing your liver
• How it works:
The virus enters
the bloodstream
and heads for the
liver. Once in the
liver many other
viruses activate
and spread.[6]
Influenza: the pandemic that’s still around
• Yearly Mortality: 500,000
deaths
Pandemics occur around 3
times a century.
• How it works:
Attaches itself to receptors on
cells in the lungs and air
passages. As it takes over their
machinery, the cells die. Dead
cells cause runny nose, sore
throat, and other symptoms.
Measles (tigdas)
• Yearly Mortality:
197,000 deaths
• Over last 150 years:
200 million deaths
• How it works:
One of the most
contagious viruses.
Causes rash, high
fever, and for
weakened immune
systems can be
deadly
Hantavirus: Because rats are dirty
• yearly mortality:
70,0000 deaths
• How it works:
Spread through
rodent bites,
droppings, or
aerosolized
rodent fecal
matter.
• Can cause
hemorrhaging and
death.
Dengue Fever: the break-bone fever
• yearly mortality:
25,000 deaths
• How it works:
Spread by
mosquitoes. Leads
to severe pain in
muscles, joints, and
behind eyes.
• Occurs primarily in
urban tropical
areas.
 • yearly mortality: 55,000 deaths
Rabies: • How it works:
Enters the body and proceeds
to the brain, replacing nerve
cells in the process. By
proceeding through the
salivary glands it increases
salivation, causing foaming at
the mouth. This helps the virus
spread through saliva.
• The most common form is the
encephalitic or “furious” form
of rabies in which agitation and
aggression is heightened.
AVIAN FLU VIRUS
ZOMBIE VIRUS?
Virology
 Chapter 19

General Properties of Viruses

Structure
Replication
 What is virus?

Viruses
the smallest infectious and acellular microbe
consisting only one kind of nucleic acid (DNA or
RNA), and which obligately replicate inside host
cells.

 Virions
The complete mature viral particles.
(The intact infectious virus particles.)
 Distinctive features

• Acellular microbes
• Pass through 0.2μm filters
• Obligatory intracellular
parasites.
• Contain either DNA or RNA
• Self-replication
 I. Size, shape and structure

A. Size:
The unit of measurement nm

parvoviruses poxviruses
 Comparative sizes of virions and bacteria

• 1. Staphylococcus aureus
• 2. Rickettsia
• 3. Chlamydia
• 4. Poxviruses
• 5. Bacteriophage of E. coli
• 6. Influenza virus
• 7. Adenovirus
• 8. Encephalitis B virus
• 9. Poliovirus
 I. Size, shape and structure

B. Shape:
Tobacco mosaic virus: rod-shaped
Poxvirus: brick-shaped
 HIV

Spherical
VSV (Vesicular stomatitis virus):
bullet-shaped
Bacteriophage T4: tadpole-shaped
Ebola Virus: filamentous shape
 I. Size, shape and structure
C.Structure:
Basic structure:
Core: Viral nucleic acid
(DNA or RNA)

Capsid: Protein shell

capsomers (morphological subunit)
 polypeptide molecules (chemical subunit)

Core + Capsid → nucleocapsid

 I. Size, shape and structure

Naked virus:
Virion: nucleocapsid.
Enveloped virus:
Virion: nucleocapsid+Envelope
spikes (peplomers);

Others: enzymes, etc.

e.g. Retrovirus has reverse transcriptase
Influenza virus
HA - hemagglutinin

NA - neuraminidase

nucleocapsid

lipid bilayer envelope

 I. Size, shape and structure

2. Symmetry of viral nucleocapsids

-- is decided by arrangement of capsomers

• Helical symmetry
(e.g., tobacco mosaic virus)
• Icosahedral symmetry
(e.g., adenovirus)

 Complex symmetry
(e.g., poxviruses )
Influenza virus
 Unconventional viruses
• Viroid
– plant disease a single circular RNA molecule
– Human Hepatitis D without a protein coat which
mainly cause plant diseases.

• Prion
– Proteinaceous infectious particle infectious agents composed of a
– Human diseases: single glycoprotein with MW 27-
e.g., Kuru 30 kDa.
Creutzfeldt-Jakob disease (CJD)
Gerstmann-Straussler-Scheinker Syndrome (GSS)
Fatal Familial Insomnia (FFI)
– Animal diseases:
e.g., Scrapie
Bovine spongiform encephalopathy (BSE)
II. Replication

In host cell, virus replicates its nucleic acid and synthesizes

its proteins, then assembles them to form progeny viral
particles that are released by budding or cell lysis.
 II. Replication
A. Normal Replication
– Adsorption /Attachment
– Penetration
– Uncoating
– Biosynthesis
– Assembly

– Release
 II. Replication
 Attachment / Adsorption
Attachment / Adsorption
 II. Replication
 Penetration
Mechanisms:
A. Endocytosis
 II. Replication
B. Fusion between cell membrane and viral envelope
The enveloped viruses
 II. Replication
C. Nucleic acid translocation:
Some bacteriophages and naked viruses
• penetration
 outside

inner

A B C D
 II. Replication
 Uncoating:
The process that capsid is removed and viral nucleic acid is released in
the host cell.

 Biosynthesis:
Eclipse phase
Biosynthesis includes:
Viral genome replication
Viral protein synthesis

Types: dsDNA, ssDNA, dsRNA, +ssRNA, -ssRNA, Retrovirus

 Biosynthesis

dsDNA viruses: e.g., Herpes simplex virus

Cell’s DDRP
dsDNA (template) early mRNA

DDDP
early proteins
semi-conservative replication (nonstructural proteins)

progeny viral DNA late mRNA late proteins

(structural proteins)

assembly
progeny viral nucleocapsid
+ssRNA virus Examples: Poliovirus, HAV

(+) ssRNA

Translation

(-) ssRNA Replication

Release

Cleavage
RNA polymerase
Structural protein Viral
proteins
-ssRNA virus e.g., influenza virus

RNA Polymerase
Transcription Translation

RNA Polymerase

Structural protein
 II. Replication
 Assembly
Naked virus: capsid + viral genome → nucleocapsid (virion)

Enveloped virus: nucleocapsid + envelope → virion

Site: a. DNA viruses (except poxvirus): cell nucleus;

b. RNA viruses and poxvirus: cell cytoplasm;
Manner: a. assemble as empty shell (procapsids), then viral genome fill in.
b. Viral capsomers array around the viral genome to form helical
symmetry.
 II. Replication
 Release
The process of progeny viruses getting out of host cell.
– Naked viruses: released by cell lysis.
– Enveloped viruses: usually released by budding.
During budding enveloped viruses acquire
their envelope.
– Defective measles virus: release from cell to cell via cell bridges.

SSPE (Subacute sclerosing panencephalitis)
Host cell lysis Budding
• release
 II. Replication
B. Abnormal replication:
– Defective viruses
– Abortive infection
II. Replication
Defective viruses:
are genetically deficient and incapable of producing
infectious progeny virions.
Helper virus:
can supplement the genetic deficiency and make
defective viruses replicate progeny virions when they
simultaneously infect host cell with defective viruses.
e.g., AAV & adenovirus
 Defective Viruses

• Defective Viruses lack gene(s) necessary for a complete

infectious cycle

• helper viruses provide missing functions

A B

A B
 Defective interfering particles (DIP)

DIP:
• Defective viruses which can occupy the cell machinery
necessary for normal virus replication to prevent virus
production, are called "defective interfering particles"
(DIP).
 II. Replication
2. Abortive infection:
Virus infection which does not produce infectious progeny because the
host cell cannot provide the enzyme, energy or materials required for
the viral replication.

non-permissive cells
The host cells that cannot provide the conditions for viral replication.
permissive cells
The host cells that can provide the conditions for viral replication.
III. Viral interference:
Viral interference
When two viruses infect simultaneously one host cell, the virus A may
inhibit replication of virus B.

Range of interference occurrence

between the different species of viruses;
between the same species of viruses;
between the inactivated viruses and live viruses.
 III. Viral interference

Mechanisms of viral interference:

a.Virus A may inhibit virus B adsorption by blocking or destroying
receptors on host cell.
b.Virus A may compete with virus B for replication materials like
polymerase, translation initiation factors, etc.
c.Virus A may induce the infected cell to produce interferon that can
prevent viral replication.
 III. Viral interference:
Significance of interference:
Advantage
a. Stop viral replication and lead to patient recovery.
b. Inactivated virus or live attenuated virus can be used as vaccine to
interfere with the infection of the virulent virus.
Disadvantage
May decrease the function of vaccine when bivalent/trivalent vaccine is
used.
IV. Reaction to physical & chemical agents
Physical agents:
Temperature, pH, Irradiation

Chemicals: -196℃
Phenol and its derivatives;
Formaldehyde/formalin;
70% ethanol;
Oxidizing agents;
Lipid solvents;
Biological agents
Antibiotic, interferon, etc.
 Differentiation of viruses from bacteria
Virus Bacterium
Size 0.02～0.3um 0.5～3.0um
Structure Non-cellular Prokaryotic
microorganism microorganism
Nucleic acid DNA or RNA DNA and RNA
Growth on cell free Cannot grow Can grow
medium
Mode of multiplication Replication Binary fission
Ribosome None Has ribosome
Antibiotic Resistant Sensitive
Interferon Sensitive Resistant