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Chapter 17-Virus • What do you know about virus? Virus characteristics • Small • Only view with an electron microscope LE 18-2 Virus Bacterium Animal cell Animal cell nucleus 0.25 µm Virus characteristics • Not alive • Obligate intracellular parasites. Infect cells-turn into a virus factory. • Computer virus analogy Virus Characteristics • Contain only protein and nucleic acid (either DNA or RNA) • Nucleic acid can be SS or DS-makes up virus core • Core surrounded by a protein capsid. Shape of capsid gives the virus its characteristic shape. Some virus have envelope (animal virus onlyproduced by budding) • Some virus have enzymes. LE 18-4a Capsomere of capsid RNA 18 250 mm 20 nm Tobacco mosaic virus LE 18-4b Capsomere DNA Glycoprotein 70–90 nm (diameter) 50 nm Adenoviruses LE 18-4d Head Tail sheath Tail fiber DNA 80 225 nm 50 nm Bacteriophage T4 Figure 18.02x2 Phages LE 18-4c Membranous envelope Capsid RNA Glycoprotein 80–200 nm (diameter) 50 nm Influenza viruses LE 18-9 Glycoprotein Viral envelope Capsid Reverse transcriptase RNA (two identical strands) Table 18.1 Classes of Animal Viruses, Grouped by Type of Nucleic Acid Virus characteristics • • • • • Virus are host specific A. animal virus B. plant virus C. bacterial virus (phage) Sometimes a virus can mutate so it can infect a new host (avian flu) Figure 18-01 Virus characteristics • • • • • Virus cause diseases Rabies Influenza Colds Etc. Figure 18-03 LE 18-11 Young ballet students in Hong Kong wear face masks to protect themselves from the virus causing SARS. The SARS-causing agent is a coronarvirus like this one (colorized TEM), so named for the “corona” of glyco-protein spikes protruding form the envelope. Figure 17.8 1 m (a) 2009 pandemic H1N1 influenza A virus (b) 2009 pandemic screening Virus Life cycle Simplified virus life cycle (lytic). Virulent virus. What kind of cell can be infected by a virus (any-plant, animal, bacteria) Typical cycle-20-30 minutes. • A. Attachment (specific-received e-mail) • B. Entry (don’t open that e-mail) • C. Synthesis • D. Assembly (spontaneous) • E. Release LE 18-5 Entry into cell and uncoating of DNA VIRUS DNA Capsid Transcription Replication HOST CELL Viral DNA mRNA Viral DNA Capsid proteins Self-assembly of new virus particles and their exit from cell Enveloped Virus life cycle LE 18-8 Capsid Capsid and viral genome enter cell RNA HOST CELL Envelope (with glycoproteins) Viral genome (RNA) Template mRNA ER Glycoproteins Capsid proteins Copy of genome (RNA) New virus LE 18-10 HIV Membrane of white blood cell HOST CELL Reverse transcription Viral RNA 0.25 µm HIV entering a cell RNA-DNA hybrid DNA NUCLEUS Provirus Chromosomal DNA RNA genome for the next viral generation New HIV leaving a cell mRNA Treatment of viral diseases Infectious cycle becomes an uncontrolled chain reaction. How can you deal with it? A. Antibiotics? No B. Immune system. Can’t respond quick enough first time you see virus (immunization). Colds, flu. C. Antiviral drugs-AIDS (AZT, protease inhibitors); Tamiflu (neuramindase inhibitor) D. Restriction enzymes-if you’re a bacteria. Why do virus infections cause disease symptoms? • Damage to tissue-cell destruction (some cells regenerate (epithelium of upper respiratory tract), some can’t (nerves-polio) • Cause infected cells to produce toxins (infected cell becomes transformed) • Viral cancer-oncogenes. Hep B-liver cancer; Herpes-Burkitt’s lymphoma; papovaviruscervical cancer • Immune system-inflammation, lymphokines Emerging virus • Typically not new virus-Existing virus that: a. Evolve and infect individuals who are only resistant to ancestral virus (influenza B and C) b.Spread from small populations to larger. AIDS c.Environmental disturbances can increase emergence. Roads into tropical rainforest, global warming, airplanes. d.Spread from species to species. Hanta virusdeer mice to humans. Influenza A- Avian virus. Porcine virus. Triple Re-assorted H1N1Influenza virus • Three processes contribute to the emergence of viral diseases – The mutation of existing viruses, which is especially high in RNA viruses – Dissemination of a viral disease from a small, isolated human population, allowing the disease to go unnoticed before it begins to spread – Spread of existing viruses from animal populations; about three-quarters of new human diseases originate this way Lysogenic life cycle (temperate virus) Characteristics of the Lysogenic life cycle • Steps Provirus inserts into infected cell’s genome. Repressor gene usually represses viral gene expression. Induction. • Differences in lytic and lysogenic life cycle LE 18-7 Phage DNA The phage attaches to a host cell and injects its DNA. Daughter cell with prophage Many cell divisions produce a large population of bacteria infected with the prophage. Phage DNA circularizes Phage Bacterial chromosome Lytic cycle The cell lyses, releasing phages. Occasionally, a prophage exits the bacterial chromosome, initiating a lytic cycle. Lysogenic cycle Certain factors determine whether Lytic cycle or Lysogenic cycle is induced is entered New phage DNA and proteins are synthesized and assembled into phages. The bacterium reproduces normally, copying the prophage and transmitting it to daughter cells. Prophage Phage DNA integrates into the bacterial chromosomes, becoming a prophage. Consequences of Lysogeny • none-(viral genetic info lies dormant) • Transformation-makes cell cancerous (viral gene is an oncogene) • Induction-Herpes- Prions • Infectious proteins • Proteins are misfolded-cause other proteins to be misfolded • Misfolded proteins impair cellular function • “Mad cow” disease LE 18-13 Prion Original prion Many prions Normal protein New prion Origin of Virus? There are three main hypotheses regarding the origins of virus: a. The progressive, or escape, hypothesis states that viruses arose from genetic elements that gained the ability to move between cells; b.The regressive, or reduction, hypothesis asserts that viruses are remnants of cellular organisms; c. The virus-first hypothesis states that viruses coevolved with their current cellular hosts. Progressive hypothesis Genetic material moved from cell to cell via injured cell surfaces? Evolution of capsid proteins may have facilitated infection of undamaged cells. Candidates for sources of viral genomes? a. plasmids? b. Transposons? (Mobile genetic elements) Mirror image rna sequences Often associated with rna virus AAAAAAUUUUUXXXXXAAAAAAUUUUUU RNA folds back on itself DS RNA recognized by a system of enzymes and proteins (the COP) The COP then destroys an DS m-rna with these mirror image sequences RNai Fig. 18-13 Hairpin miRNA Hydrogen bond Dicer miRNA 5 3 (a) Primary miRNA transcript mRNA degraded miRNAprotein complex Translation blocked (b) Generation and function of miRNAs RNAi Video • http://www.nature.com/nrg/multimedia/rnai /animation/index.html