Download Viral Structure and Life Cycles

Ch 5
Viral
Structure and
Life Cycles
SLOs
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Explain what it means when viruses are described as filterable.
Identify better terms for viruses than alive or dead.
Discuss the size of viruses relative to other microorganisms.
Describe the function and structure(s) of viral capsids.
Distinguish between enveloped and naked viruses.
Explain the importance of viral surface proteins, or spikes.
Diagram the possible configurations that nucleic acid viruses may
possess.
Diagram the different steps in the cycle of animal viruses.
Discuss both persistent and transforming infections.
Provide thorough descriptions of both lysogenic and lytic
bacteriophage infections.
List three principal purposes of cultivating viruses.
Describe three ways in which viruses are cultivated.
Name and summarize two noncellular infectious agents besides
viruses.
Viruses as part of the Biological Spectrum
• Infect every cell type (phages vs. animal viruses)
• Pasteur: “living things” smaller than bacteria are
causing diseases  “Filterable units”
• Virus = Latin for poison
• Obligatory intracellular parasites using
host cell machinery
• Dead or alive?
• Better terms:___________________
• Kill or live in harmony within the host cell.
Outside of cell: Viruses are inert.
General Properties of Viruses
• Nucleic acid core: DNA or RNA
• Protein coat = capsid made up of capsomeres.
• Some are enclosed by an envelope (naked vs.
enveloped)
• Viruses have spikes (COH/protein)
• Lack enzymes for metabolism, incl. protein
synthesis and energy production.
• Host range is determined by specific host
attachment sites and cellular factors
• Most viruses are also tissue specific
Virus Shapes and Sizes
Advent of EM
allowed for
visualization of
viruses
Compare to Fig 5.1
Naming of Viruses
Often based on hosts
and diseases they
cause.
Clinicians usually use
common vernacular
names (e.g.: polio
virus, chickenpox
virus, measles virus,
etc.)
Most recent
considerations:
Structure and
genomics
Examples of Naming Viruses
• Family: Herpesviridae
• Genus: Varicellovirus
• Species and subspecies:
Human herpes virus 3
(HHV-3
 Family: Picornaviridae
 Genus: Hepatovirus
 Species and subspecies:
Hepatitis A virus
Family Names end in –viridae
Genera and species names end
in -virus.
Subspecies are designated by a
number.
• Family: Retroviridae
• Genus: Lentivirus
• Species and
subspecies: Human
immunodeficiency
virus 1 and 2 (HIV-1,
HIV-2)
Virion Structure
• Capsid
– Capsomeres
– Helical, icosahedral,
or complex
• Nucleic acid
– DNA or RNA
• Envelope
• Spikes (on envolpes)
Fig 5.3
Table 5.2
Variety in Viral Nucleic Acid
• DNA viruses: ds, ss, linear, circular
• RNA viruses
- Ds, but more often Ss
- Positive-sense RNA: ready for immediate translation
- Negative-sense RNA: must be converted before
translation can occur
- Segmented
Some carry their own enzymes, e.g.: Reverse transcriptase
(Retroviruses)
Multiplication in
Animal Viruses
General phases of animal
viral replication cycle:
-
Adsorption
Penetration
Uncoating
Synthesis
Assembly
Release
Length of replication cycle
varies: 8 h in polioviruses;
36 h in herpesviruses
Kill or live in harmony within
host cell (carrier relationship)
Table 5.4
2 types of penetration modes
Fig 5.5
Multiplication of Animal DNA Viruses
Naked animal viruses are predominantly released
by host cell lysis!
Multiplication of
a Retrovirus
Enveloped animal viruses may exit the
host cells via budding
HSV envelopment and release
https://www.youtube.com/watch?v=bgj
1YpevA6A
Damage to Host Cell
Cytopathic Effects (CPEs): virus-induced cell
damage visible microscopically
Examples of CPEs:
- Inclusion bodies: compacted
masses of viruses or damaged
cell organelles in the nucleus and cytoplasm
- Syncytia
Accumulated damage kills most cells.
Viruses and Cancer - Oncology
Cancer  def.?
Expanded
from book.
Discard Fig 5.8
Benign vs. malignant tumors
Carcinoma vs. Sarcoma vs. Adenocarcinoma
3 important characteristics of cancer cells:
1. Rapid cell division
2. Loss of anchoring junctions  ______________
3. Dedifferentiation of cells and changes in cell’s
surface molecules (“cancer markers”)
Oncoviruses can transform cells  Tumors
Viruses and Cancer cont.
• Root of all cancers:
• Chemicals and ___________ directly damage
the genes through mutation rate
• Normal cell cycle ends in cell
division. Necessary for normal
growth & development and
wound healing….
Viruses and Cancer cont.
Normal cell cycle regulator genes:
1. Proto-oncogenes
2. Tumor suppressor genes
Genetic material of oncogenic viruses
becomes integrated into the host cell’s DNA
 _____ virus.
Oncogenic Viruses are responsible for 20%
of human cancers
Oncoviruses lead to….
• addition of oncogene or conversion of protooncogenes to oncogenes, or
• suppression of Tumor suppressor genes
1. Foot on accelerator model:
Proto-oncogenes turned ______
2. Foot off brake model:
Inhibitors of tumor suppressor proteins
Oncogenic Viruses
DNA Viruses
HPV 
_________cancer
Epstein-Barr virus (EBV)
 Burkitt’s lymphoma
HHV8  _________
sarcoma
HBV  ______cancer
RNA Viruses
Hepatitis C virus
(HCV)  liver cancer
human T-cell
leukemia virus
(HTLV-1)
Bacteriophages Infect Bacteria
• Mostly ds DNA viruses
• Lytic or lysogenic cycles
• 2008: Discovery of virophages
• Relevant for medical microbiology because
– easy to study, and
– can make bacteria more pathogenic through
lysogenic conversion. (See below) E.g: C. diphtheria,
V. cholerae, C. botulinum)
– Phage therapy!
T-Even Bacteriophage:
The Lytic Cycle
1. Adsorption to cell surface receptors (chance
encounter – no active movement)
2. Penetration – only genome enters
3. Biosynthesis and Assembly – Production and
assembly of phage DNA and proteins
4. Maturation –
assembly to form
intact phage
5. Release due to
lysis of host cell
Fig 5.9
2 Mechanisms of Bacteriophage Multiplication
• Lytic cycle (by lytic or virulent phages)
Phage multiplies, eventually causing lysis and
death of host cell
• Lysogenic cycle or Lysogeny (by lysogenic
or temperate phages)
Phage DNA incorporated in host DNA 
Prophage. No host cell lysis, cell lives. Allows
virus to spread without killing host.
Induction: Activation of lysogenic prophage to
go into lytic cycle
Lytic and Lysogenic Cycles ( Phage)
Compare to Fig 5.9
Cultivation and Identification of
Animal Viruses
• Viruses are obligate ……………………….
• Culture methods:
- In vivo: lab animals and embryonic bird tissues
- In vitro: cell or tissue culture methods
• Primary purposes of viral cultivation:
- Isolate and identify viruses in clinical specimens.
- Prepare viruses for vaccines.
- Research
Other Noncellular Infectious Agents
• Prions: Infectious Proteins
• Cause chronic persistent spongiform encephalopathies
• Long latency, progressive and universally fatal
• Human and 9 animal diseases, such as:
–
–
–
–
CJD
Kuru
Scrapie
Mad cow disease = _________________
• PrPC: Normal cellular prion protein, on cell surface.
Involved in cell death regulation.
• PrPSc: Scrapie protein; accumulates in brain cells,
forming plaques.
Spongiform Encephalopathies
Caused by altered prion protein:
– Mutation in normal PrPc gene (sporadic CJD), or
– contact with the abnormal PrPSc protein (Kuru)
Spontaneous or
transmissible by
ingestion, transplant,
and surgical
instruments
Satellite Viruses
• Dependent on other viruses for replication
• Adeno-associated virus (AAV):
- Originally thought to only replicate in cells infected
with adenovirus
• Delta agent:
- Naked circle of RNA
- Expressed only in presence HBV
- Worsens severity of liver damage
Case File: The Domino Effect
Inside the Clinic: Shingles
Who will present?