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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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