Microbiology Module 11.2

  1. Viruses, Viroids, and Prions overview
    • All infective non-cellular agents
    • Viruses abundant (over 1 million/milliter)
    • -Contain Nucleic Acid and capsid (protective cover)
    • -Some viruses have enveloppes derived from CM of -host cell
    • -Classified into groups into groups and families based on component differences
    • Viroids only infect RNA and infect plant cells
    • Virusoids contain RNA and infect animal cells (require helper virus)
    • Prions only contain AA and infect animals (infective proteins)
  2. Viral Varieties
    • All require Electron microscope to be seen
    • Bacteriophage are viruses that infect prokaryotic cells
    • Many phage are larger and more complex than viruses
    • Capsids enclose genome and made up of protomers (self assembling subunits)
    • Nucleocapsid: Capsid plus genomic material
  3. Baltimore System
    • Classifies viruses based on type of NA used for genome
    • (+)RNA viruses: Have ssRNA that serves as an mRNA
    • (-)RNA viruses: Have ssRNA that is compliment of mRNA. Must be replicated before it can be translated
    • Retroviruses: ssRNA converted to dsDNA that is inserted into host chromosome
  4. Types of Capsids: Helical
    • Are as large as the NA
    • NA made and then protomers bind to NA
    • Examples: TMV, Influenza
  5. Types of Capsids: Polyhedral/icosahedral
    • Contain self assembling capsids. (60-1500 capsomers)
    • Protomer: Basic building block
    • Capsomer: Made up of 3-5 capsomers
    • **Dont worry about numbers
  6. General Features of Viral Life Cycle
    • 1. Attachment (adsorption) to host cell
    • 2. Entry into cell
    • 3. Viral-directed synthesis of viral components
    • 4. Viral assembly (or insertion into host genome)
    • 5. Release of fully assembled virions (viral particles)
  7. Attachment to Host Cells
    Attachment events determine host specificitiesMany genes/proteins involved in production of tails
  8. Entry of Virus into cytoplasm
    • 1.Tail fibers attach to the OM protein
    • 2.Tail structure contracts
    • 3.Base plate (lysozyme coated) pushes thru cell wall
    • 4.DNA injected into cell
  9. 3 Main ways for entry into cell
    • 1. Fusion: virus bind to particular receptors, triggering a fusion of envelope w/cytoplasm of cell
    • 2. Endocytosis: Receptor bound virus w/envelope results in nucleocapsid surrounded by 2 lipid layers
    • 3. Endocytosis: Virus w/no envelopes. Same as above
    • All require uncoating of virus (can be therapeutic)
    • Amantadine prevents uncoating of Influenza A
  10. Viral Replication Strategies
    • DNA Viruses: Make way to nucleus and replicated by host cell DNA polymerases
    • RNA Viruses: Translated and must carry gene to make +RNA NAs from either -RNA or DS-DA template
    • -RNA viruses must bring replicase enzymes to create +mRNA
    • Retroviruses: +RNA viruses. Make & package reverse transcriptase to convert RNA genome into DS-DNA prior to integration into host chromosome
  11. Release Mechanisms
    • Lysing: non-enveloped viruses. Lead to short and acute infection
    • Budding: Enveloped viruses. Short and chronic infections
    • Some dont replicate and leave cell at all, they cause cancer. Cause host cell to de-differentiate causing host cell to replicate uncontrollably
  12. Influenza Viruses
    • Flu Caused by 2 species of orthomxoviruses (Type A&B). Type A responsible for most pandemics
    • Genome: 8 (-)ssRNAS (11packaged)
    • Hosts: Chickens, humans, pigs, horses, birds, sea mammals
    • Virions contain hemagglutinin which allows it to attach to respiratory cells
    • Neuraminadase break down mucus
    • Type B only infect humans and does not have antigenic shifts
  13. Influenza Life Cycle
    • PB1 enzyme is error-prone RNA dependent RNA transcriptase (1 mistake/genome). Responsible for antigenic drift (over flu season, influenza virus mutates w/in a single patient)
    • Therapeutic agents: Target neuraminadase, uncoating process.
    • Symptoms: Fever, cough, body aches
  14. Antigenic Shifts
    • Major change in antigenic character of influenza when common host is co-infected w/different new strains
    • Shifts are responsible for pandemics such as H1N1
  15. Useful Viruses
    • Used to treat viral infections in Russia. Issue is specificity (only specific to small group of bacteria)
    • Used to inhibit bacterial growth in foods. Inhibit lysteria (Deli Meat)
    • Used as vectors in biotechnology. AAvs used as vectors in gene therapy
    • Lysogenic pathogens harbor prophage that express virulence factors (useful to a bacteria)
  16. Lysogenic Pathogens
    • Corynebacterium diphtheriae: Harbors B phage
    • Vibrio Cholera: Harbors CTX phage.
    • E.Coli: Harbors phage encoding shiga-like toxins
    • S. Pyogenes:Causes scarlet fever and necrotizing fascitis
    • --All pathogens above only cause disease when harboring the prophage
  17. Viroid and Virusoids
    • Viroid infections caused by small naked RNAs that forms double stranded regions
    • Plant pathogens include: Coconut cadang cadand and Chrysanthemum stunt viroid
    • Get into cell by wounding. RNA copied by plant RNAp and transcribe viroid RNA
    • Virusoids: Only infect animal cells and contain no capsids and encode some proteins. Require helper virus. Example: Hepatitis D
  18. PRIONS
    • Infectious Prion: Enriched in Beta-Pleated sheet (43%)
    • Noninfectious Prion: 43% Alpha Helix
    • Prion proteins go into spinal cord and brain and convert normal prions to infectious forms
    • Prion proteins resistant to proteases and disinfectants
    • Cause holes in brains and severe immune response
    • Scrapie in sheep, CJD in humans, BSE in cows.
Card Set
Microbiology Module 11.2
Module 11.2