2 Student Learning Outcomes Differentiate 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.
3 The ability of a virus to infect an organism is regulated by the host species.the type of cells.the availability of an attachment site.cell factors necessary for viral replication.all of the above
4 Foundations of Virology Non-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
6 General Characteristics of Viruses Obligatory intracellular parasitesFilterableVirus = Latin for poisonContain DNA or RNAContain a protein coat = capsid made up of capsomeres. Various shapesSome are enclosed by an envelope (naked vs. enveloped)Some viruses have spikes (COH/protein)Most viruses are tissue specificHost range is determined by specific host attachment sites and cellular factors
7 Host Range and Specificity Usually narrow host range – due to?Tissue tropismPhage TherapyOncolytic viruses
9 Which of the following statements about viruses is FALSE? Viruses use their own catabolic enzymesViruses contain a protein coatViruses contain DNA or RNA but never bothViruses use the anabolic machinery of the cell
10 Virion Structure Nucleic acid Capsid Envelope Spikes DNA or RNA CapsomeresEnvelopeSpikesFig 13.2
11 Morphology of an enveloped helical virus Example of a enveloped polyhedral virus: Hepes simplex
12 PolyhedralSmallpox virusComplex symmetryCompare to Figs
13 Electron micrograph of Aeromonas virus 31, an unassigned virus in the family Myoviridae photograph by Dr Hans Ackermann.
14 Taxonomy of Viruses No evidence for common viral ancestor. Classification based on genomics and structure.Family names end in –viridaeGenus and species 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.
15 Examples of Naming Viruses Family: HerpesviridaeGenus: VaricellovirusSpecies and subspecies: Human herpes virus 3 (HHV-3Briefly review Table 13.2Family: RetroviridaeGenus: LentivirusSpecies and subspecies: Human immunodeficiency virus 1 and 2 (HIV-1, HIV-2)Family: PicornaviridaeGenus: HepatovirusSpecies and subspecies: Hepatitis A virus
18 The viral envelope closely resembles the CapsomereCytoplasmProkaryotic cell wallEukaryotic cell membraneNone of the above
19 Isolation, Cultivation, and Identification of Viruses Fig 13.6Viruses must be grown in living cellsBacteriophages form plaques on a lawn of bacteriaAnimal viruses may be grown in cell culture, embryonated eggs (Fig 13.7), or living animalsFig 13.8
20 Virus Identification Serological tests Nucleic acids methods Detect antibodies against viruses in a patientUse antibodies to identify viruses (more after Immunology chapter discussion)Nucleic acids methodsRFLPsPCR
21 Viral MultiplicationObligate intracellular parasites using host cell machineryVery limited number of genes encode proteins forCapsid formationViral nucleic acid replicationMovement of virus into and out of cellKill or live in harmony within the host cell – Outside the cell, viruses are inert
22 2 Mechanisms of Bacteriophage Multiplication Lytic cycle (by lytic or virulent phage)Phage multiplies, eventually causing lysis and death of host cellLysogenic cycle (by lysogenic or temperate phage)Phage DNA incorporated in host DNA Prophage. No host cell lysis, cell lives. 3 results of lysogeny:Lysogenic cell immune to reinfection by same phagePhage conversionPossibility for specialized transductionMastering: Viral Multiplication
23 T-Even Bacteriophage: The Lytic Cycle Attachment to cell surface receptors (chance encounter – no active movement)Penetration – only genome entersBiosynthesis – Production of phage DNA and proteinsMaturation – assembly to form intact phageRelease due to phage induced lysozyme productionSee Fig 13.11
24 Lytic Cycle of a T-Even Bacteriophage 123Fig 13.11
25 Some animal viruses exit the host cells via budding HSV envelopment and releaseFig
30 Cancer - Oncology Cancer uncontrolled mitotic divisions Benign vs. malignant tumorsCarcinoma vs. SarcomaAdenocarcinoma3 important characteristics of cancer cells:Rapid cell divisionLoss of anchoring junctions and contact inhibition ______________Dedifferentiation of cells
31 Viruses and Cancer Root of all cancers: Chemicals and ___________ directly damage the genes through mutation rateViruses damage/alter genes by bringing new genes into the cell. what kinds of genes?Normal cell cycle ends in cell division. Necessary for normal growth & development and wound healing….
32 Viruses and Cancer Normal cell cycle regulator genes Proto-oncogenes Tumor suppressor genesGenetic material of oncogenic viruses becomes integrated into the host cell’s DNA _____ virus.
33 Provirus leads to….……conversion of proto-oncogenes to oncogenes or suppression of Tumor suppressor genesFoot on accelerator model:Proto-oncogenes turned ______Foot off brake model:Inhibitors of tumor suppressor proteins
34 Oncogenic Viruses are responsible for 10 % of human cancers DNA Viruses RNA VirusesHepatitis C virus (HCV) liver cancerhuman T-cell leukemia virus (HTLV-1)HPV _________cancerEpstein-Barr virus (EBV) Burkitt’s lymphomaHHV8 Kaposi’s sarcomaHBV _________cancer
35 carcinogens in cigarette smoke. Proto-oncogenes can be activated to become oncogenes and cause cancer bycarcinogens in cigarette smoke.overexposure to UV radiation in sunlightspontaneous mutations.virus infection.all of the above.
36 Latent and Persistent Viral Infections Latent: Virus remains in asymptomatic host cell for long periodsPersistent: Disease processes occurs over a long period; generally is fatalFig 13.21
37 Prions =Inherited and transmissible by ingestion, transplant, and surgical instrumentsCause spongiform encephalopathies Human and 9 animal diseases, such as:Scrapie,Mad cow diseaseCJD,KuruPrPC: Normal cellular prion protein, on cell surface. Involved in cell death regulation.PrPSc: Scrapie protein; accumulates in brain cells, forming plaques.Review Fig 13.22
38 Spongiform Encephalopaties Caused by altered protein:Mutation in normal PrPc gene (sporadic CJD), orcontact with the abnormal PrPSc protein (Kuru)Mastering: Prions
39 Fig 13.22 PrPc produced by cells is secreted to the cell surface. PrPSc1PrPc produced by cells is secreted to the cell surface.2PrPSc may be acquired or produced by analtered PrPc gene.3PrPSc reacts with PrPcon the cell surface.4PrPSc converts the PrPc to PrPSc.5The new PrPSc converts more PrPc.6The new PrPSc is taken in, possibly by receptor-mediated endocytosis.Lysosome78PrPSc continues to accumulate as the endosome contents are transferred to lysosomes. The result is cell death.PrPSc accumulates inendosomes.EndosomeFig 13.22