1. Viruses
    • Major cause of infectious disease
    • Cannot replicate on their own - non-living
    • No genus species classification
    • Can cause cancer
  2. Virus Characteristics
    • Small, aceullar
    • Obligate intracellular parasites
    • DNA or RNA genome
    • Limited host range/specificity
    • Hard to treat clinically
    • Depend on our organelles (ribosomes) to replicate- no metabolism
    • Infect all living organisms
  3. Ways to classify viruses
    • Type of nucleic acids (DNA or RNA)
    • Shape, host range, +/- envelope
    • Common English name
  4. Virus Structure
    • Nucleic Acid (DNA or RNA, double or single stranded)
    • Capsid: (Protein shell) determines shape, composed of capsomeres
    • Envelope - Some viruses possess phospholipid (derived from host cell)
    • Glycoprotein Spikes: Allow attachment and determine viral specificity
  5. Viron
    • A virus particle
    • Metabolically inert until entry into host cell, dependent on host resources
  6. Bacteriophage
    • Viruses that infect bacteria
    • Head: Contains genome
    • Collar, tail, sheath, plate, pin
  7. Bacteriophage
    • Lytic Cycle
    • Absorption: Phage is absorbed onto cell wall
    • Penetration: Phage DNA is injected -- bacterial DNA disrupted
    • Biosynthesis: Viral components produced from disrupted DNA
    • Maturation: Phage heads and pieces of viral DNA are synthesized -- parts assembled -- cell wall breaks open \
    • Release: Bacterial cell lyses -- virus released
  8. How are bacteriophage identified in lab?
    Phage plaques on 'lawns' of susceptible bacteria
  9. Types of human viruses
    • Lytic: Acute disease (ebola)
    • Latent: Usually cause chronic disease (Chicken pox, HIV, herpes)
  10. Lytic
    • Acute Disease - influenza
    • Virus invades host cell, produces new virus, and lyses so the new viruses can be relased
    • Virus then moves onto another cell
    • Replicate immediately
  11. Latent
    • Cause chronic disease
    • Virus intergrates host cell DNA
    • Replication is delayed
    • Lysis when the cell feels threatened
  12. Animal Virus Replication
    • 1.Attachment/Abs using viral spike binding to host cell receptor (membrane protein)
    • *Antibodies can neutralize (block attachment)
    • 2. Entry/penetration into host cell by membrane fusion (enveloped) or endocytosis (non-enveloped)
    • 3. Uncoating of nucleic acid via capsid digestion
    • *Latent: Integrate as dsDNA into host genome, delay replication/lysis, cause chronic disease
    • *Lysis: viruses replicate fast
    • 4.Biosythesis: Rapid for lytic and delayed for latent viruses until induction
    • 5. Virus assembly and maturation
    • 6. Release (virons exit host cell), lysis (may not be immediate some bud from host cell during shedding)
  13. Advantages/Disadvantages of Lytic
    • Advantages: Produce virons quickly
    • Disadvantages: Easily detected by immune system
  14. Advantage/disadvantages of Latent
    • Advantages:Not detected by immune system
    • Disadvantages: Will not replicate it host cell dies
  15. How does HIV attach to host cell?
    • Viral Glycoportein Spikes
    • Membrane protein reception - viral glycoprotein
  16. How do non-enveloped viruses enter the host cell?
  17. HIV transmission
    Blood semen, vaginal fluid, breast milk
  18. HIV origin
    From Chimps 1920-30s in Africa
  19. HIV Lifestyle
    • Retrovirus: RNA genome, only in humans
    • Attaches to CD4 receptor in T(helper) cells via gp120 viral spike, enter via membrane fusion, uncoating
    • Latent virus: RNA genome reverse transcribed to dsDNA, integrates into genome as provirus
    • Provirus transcribed into mRNAs and RNA viral genomes, mRNA translated into protein
    • Translated pre-protein cleaved into mature forms by viral protease, virus assembles, buds from cell, eventually lyses T(helper) host cell
  20. Seroconversion
    Appearance of anti-HIV antibodies (within 3 mos exposure)
  21. Clinical HIV Infection
    • Seroconversion
    • Strong initial immune response followed by long chronic phase (9-12 yrs)
    • Viral RNA load followed clinically, predicts course of infection
    • Low T(h) cell count leads to opportunistic infections, onset of full blown AIDS
    • Death from opportunistic ifections
  22. Opportunistic infections
    TB, pneumonia, cancer, neurodegeneration
  23. AIDS therapies
    • Antiretrovirals target viral enzymes RT, protease, and membrane fusion
    • 1. Reverse transcriptionase inhibitors
    • 2. Protease inhibitors inhibit viral protein maturation
    • 3. Fusase inhibits membrane fusion
  24. AZT
    • Nucleoside analog, terminates reverse transcription of viral RNA to DNA
    • Disadvantages: Anemia, virus resistance
  25. Protease inhibitors disadvantages
    large doses, side effects
  26. HAART
    Combination (cocktail) therapy effective
  27. Influenza Virus
    • Recurring epidemics, millions died in 1918-19
    • Spike proteins are hemagglutinin (H) and neuraminidase (N), main viral antigens
    • New strain each time
    • Strains identified by H and N combination
  28. Spike proteins change due to
    • Antigenic Drift
    • Antigenic Shift
  29. Antigenic drift
    Point mutations cause minor antigenic (H and N) changes over time
  30. Antigenic shift
    • Genetic reassortment between human virus and other animal virus
    • Causes sudden major shift in viral surface protein/antigen(s), produce virus no human has ever seen before
  31. Antigens
    viral proteins on surface
  32. Influenza virus structure
    • Enveloped
    • RNA genome
    • Lipid bilayer from host cell
    • N and H spikes
  33. Virus and Cancer
    • Associated with latent viruses such as HPV
    • Uncontrolled cell division
  34. Oncogene
    • Cancer causing gene
    • Growth out of control
    • genetic disruption
Card Set