Antivirals

• Why don’t antibiotics work on viruses?

  Viruses don’t grow or metabolize like cells. (Don’t have membranes or cell walls)
• Most antiviral drugs are _.

  Synthetic
• Antibiotics kill _.

  Normal flora, which then helps viruses to grow
• What are the 4 antiviral modes of action?

  1. Inhibit attachment
  2. disrupt genomic replication (through nukes)
  3. Inhibit viral enzymes (through non-nukes)
  4. Interferons (generate antiviral proteins)
• What are drugs that block viral attachment?

  Amantadine

  • For influenza

  Vidarabine

  • For herpes zoster and simplex

  Enfuvirtide

  • For HIV (2003)
• What are base analogues (substitutes for nucleic acids)?

  AZT

  • Nuke
  • Used for retrovirus

  Zovirax

  • Neither nuke or non-nuke
  • used for genital herpes and chicken pox

  PrPE

  • daily med for people at risk of contracting HIV
  • combination of 2 nukes

  Truvada (Tenofovir + emtricitibine)

  • Acts like AZT
  • 90% reduction in sex disease —> HIV
• What are drugs that inhibit viral enzymes?

  Invirase (Protease Inhibitor)

  • Inhibits enzyme that processes HIV proteins

  Viramune (non-nuke)

  • inhibits enzyme that turns RNA to DNA

  Tamiflu(Neuraminidase inhibitor)

  • inhibits spike enzyme
• What are some monoclonal antibody treatments?


  All end in “vimab”
• Monoclonal antibody treatments are sp_.

  Sporadic
• Monoclonal antibody treatments are used in…

  • high risk groups
  • given early (within 10 days of infection)
• Monoclonal antibody treatments are not a replacement for 


  Vaccines.
• What is the treatment for SARS-CoV-2?

  1. Remdesivir
  2. Paxlovid
  3. Molnupiravir
• Remdesivir

  • Stops reproduction of RNA
  • Originally effective against Ebola and HepC, now used in Canada for severe SARS-CoV 2
• Paxlovid? (Nirmatrelvir, ritonavir)

  • combination drug
  • Nirmatrelvir inhibits CoV protease, while ritonavir slows down metabolism of protease inhibitors.
  • Oral and at-home prescription treatment
  • Treats mild cases in high risk groups
• Molnupiravir?

  • Shifts configuration of RNA strands
  • Being investigated by health cananda (birth defects)
• What are the 3 categories of interferons


  A, b, g
• What does group A and B do?

  • come from virally infected cells
  • AVP production
• What does group G do?

  • comes from tumor cells
  • natural killer cells
• AVPs stop viral protein synthesis by

  Binding viral mRNA
• INF-a is approved for use in hep…

  B, C, genital warts, HIV, CoV2
• What is required to develop a drug?

  1. Lab testing
  2. Animal Testing
  3. Clinical Trials (3 phases)
• Describe phase 1

  • 20 - 100 healthy subjects
  • Test different doses
  • judge side effects and bioavailability
• DEscribe Phase 2

  • 100 sick
  • monitor side effects
  • compare new drug to control
• describe phase 3

  • Thousands sick
  • test drug tints established method
  • triple blinded
  • sets stats on efficacy and safety
• Trials take..

  7-15 years
• What are the odds of drugs

  1/1000 make it to humans

  1/5000 make it through trials
• What are superbugs?

  bacteria that is resistant to most antibiotics.
• How do superbugs resist antibiotics?

  1. destroy the drug
  2. prevent drug penetration
  3. alter the target site
  4. rapid reflux of drug before it can act
• What contributes to resistance?

  • Abusing antibiotics!
• How do we abuse antibiotics?

  • overprescribe - 150 million prescriptions per year, 1/2 are for common cold)
  • self medication
  • Incomplete antibiotic regimens
• What are 3 major superbugs?

  1. MRSA
  2. C. Diff
  3. VRE
• What is an emerging superbug?

  KPC
• MRSA is derived from

  penicillin
• How many people carry staphylococcus aureus?

  1 in 3, 2% carry MRSA in nostrils
• What is the carrier rate of MRSA in nurses?

  5%
• MRSA is spread by

  direct contact
• MRSA infection is sporadic or..

  epidemic
• What is effective against MRSA

  Vancomycin
• MRSA is gram

  +
• C. difficile is gram

  +