Download Viruses

Medical
Microbiology
Li Mei
Department of Microbiology
November, 2006
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
parvoviruses
nm
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: rodshaped
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
– Human Hepatitis D
a single circular RNA molecule
without a protein coat which
mainly cause plant diseases.
• Prion
– Proteinaceous infectious particle infectious agents composed of a
single glycoprotein with MW 27– Human diseases:
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
progeny viral DNA
late mRNA
(nonstructural proteins)
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
RNA Polymerase
Structural protein
Translation
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
A
B
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:
Phenol and its derivatives;
Formaldehyde/formalin;
70% ethanol;
Oxidizing agents;
Lipid solvents;
Biological agents
Antibiotic, interferon, etc.
-196℃
Differentiation of viruses from bacteria
Virus
Bacterium
Size
0.02～0.3um
0.5～3.0um
Structure
Non-cellular
microorganism
DNA or RNA
Prokaryotic
microorganism
DNA and RNA
Growth on cell free
medium
Mode of multiplication
Cannot grow
Can grow
Replication
Binary fission
Ribosome
None
Has ribosome
Antibiotic
Resistant
Sensitive
Interferon
Sensitive
Resistant
Nucleic acid