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Ch 13
Viruses and
Prions
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Student Learning OutcomesDifferentiate a virus from a bacterium.Explain the difference between enveloped and
nonenveloped viruses.Define viral species.Describe how bacteriophages and animal viruses are
cultured.Compare and contrast the lytic and lysogenic cycles of
bacteriophages.Define oncogene and transformed cell.Discuss the relationship between viruses and cancer.Explain latent viral infections and give an example.Discuss how a proteins can be infectious.
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Foundations of VirologyNon-living agents that infect all life forms
(phages vs. animal viruses)
Viral cultivation differs from bacterial cultivation
∼ 1,500 known viruses (estimates: ∼ 400,000 exist)
Advent of EM allowed for visualization of viruses
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General Characteristics of Viruses Obligatory intracellular parasites Filterable Virus = Latin for poison Contain DNA or RNA Contain a protein coat = capsid made up of
capsomeres. Various shapes Some are enclosed by an envelope (naked vs. enveloped)
Some viruses have spikes (COH/protein) Most viruses are tissue specific Host range is determined by specific host attachment
sites and cellular factors
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Host Range and Specificity
Virus / host cell interaction usually very specific (narrow host range) – due to?
Tissue tropism
Fig 13.1
Virus Shapes and Sizes
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Virion Structure
Figure 13.2a
Nucleic acid DNA or RNA
Capsid Capsomeres
Envelope Spikes
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Morphology of an enveloped helical
Helical viruses:• rabies• ebola
Polyhedral virus
and
Polyhedral
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Taxonomy of Viruses No evidence for common viral ancestor. Classification based on type of NA, strategy for
replication, and morphology. Family names end in -viridae. Genus names end in -virus. Viral species: A group of viruses sharing the same
genetic information and ecological niche (host). Common names are used for species.
Subspecies are designated by a number.
Nucleic Acid Diversity of
Virus Families
Also compare to Table 13.2
, Orthomyxoviridae
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Isolation, Cultivation, and Identification of Viruses Viruses must be grown in
living cellsBacteriophages form plaques
on a lawn of bacteria
Animal viruses may be grown in cell culture, embryonatedeggs (Fig 13.7), or living animals
Fig 13.6
Fig 13.8
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Virus Identification Cytopathic effects Serological tests Detect antibodies against viruses in a patient Use antibodies to identify viruses in neutralization tests,
viral hemagglutination, and Western blot Nucleic acids RFLPs PCR
Novel methods such as Biophotonics
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Viral Multiplication Obligate intracellular parasites using
host cell machinery
Very limited number of genes encode proteins for Capsid formation Viral nucleic acid replication Movement of virus into and out of cell
Kill or live in harmony within the host cell – Outside the cell, viruses are inert
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2 Mechanisms of Bacteriophage Multiplication Lytic cycle (by lytic or virulent phage)
Phage multiplies, eventually causing lysis and death of host cell
Lysogenic cycle (by lysogenic or temperate phage)Phage DNA incorporated in host DNA ⇒ Prophage. No
host cell lysis, cell lives. 3 results of lysogeny:1. Lysogenic cell immune to reinfection by same phage2. Phage conversion3. Possibility for specialized transduction
ANIMATION Viral Replication: Temperate Bacteriophages
ANIMATION Viral Replication: Virulent Bacteriophages
Bacteriophage:The Lytic Cycle
1. Attachment to cell surface receptors (chance encounter – no active movement)
2. Penetration – only genome enters
3. Biosynthesis – Production of phage DNA and proteins
4. Maturation – assembly to form intact phage
5. Release due to phage induced lysozyme production
See Fig 13.11
1
2
3
Lytic Cycle of a T-even Bacteriophage
Fig 13.11
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Some animal viruses exit the host cells via budding.
HSV envelopment and release
Compare to Fig. 13.20
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Lytic and Lysogenic Cycles
Multiplication of DNA VirusesFoundation Fig 13.15
ANIMATION Viral Replication: Animal Viruses
Fig 13.17
Multiplication of RNA Viruses
Fig 13.19
Multiplication of a Retrovirus
CancerCancer → uncontrolled mitotic divisions
Benign vs. malignant tumors
Oncology3 important characteristics of cancer
cells:1. Rapid cell division2. Loss of anchoring junctions and contact
inhibition → metastasis3. Dedifferentiation of cells
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Viruses and Cancer The genetic material of oncogenic viruses
becomes integrated into the host cell’s DNA (→provirus).
Conversion of proto-oncogenes to oncogenes Activated oncogenes transform normal cells into
cancerous cells Transformed cells have increased growth, loss
of contact inhibition, tumor-specific transplantantigens, and T antigens
Oncogenic Viruses are responsible for ∼10 % of human cancers
OncogenicDNA Viruses and RNA Viruses
Papilloma virus (HPV) → cervical cancer
Epstein-Barr virus(EBV) → Burkitt’slymphoma
HV8 → Kaposi’s sarcoma
Hepatitis B virus (HBV) → liver cancer
Hepatitis C virus (HCV) → liver cancerhuman T-cell
leukemia virus (HTLV-1)
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Fig 13.21
Latent and Persistent Viral InfectionsLatent:Virus remains in asymptomatic host cell for long periods
Persistent:Disease processes occurs over a long period; generally is fatal
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Prions Small proteinaceous infectious particles (very
resistant to inactivation) Inherited and transmissible by ingestion, transplant,
and surgical instruments Causes spongiform encephalopathies: Sheep scrapie, Creutzfeldt-Jakob disease, Gerstmann-Sträussler-Scheinker syndrome, fatal familial insomnia, mad cow disease
PrPC: Normal cellular prion protein, on cell surface. Involved in cell death.
PrPSc: Scrapie protein; accumulates in brain cells, forming plaques.
Spongiform EncephalopatiesCaused by altered protein: Mutation in normal PrPc gene (sporadic CJD), or contact with the abnormal PrPSc protein
ANIMATION Prion: Diseases
ANIMATION Prion: Characteristics
ANIMATION Prion: Overview
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