B12: viral chemotherapy Flashcards
What are the types of vaccines used for smallpox, polio, measles, influenza, hepatitis B, and HPV?
Smallpox: Heterologous virus (vaccinia)
Polio: Killed virus (Salk - parenteral), Live attenuated (Sabin – oral)
Measles: Live attenuated (injected)
Influenza: Live attenuated (nasal), Killed virus (parenteral – tri-/tetravalent)
Hepatitis B: Recombinant subunit vaccine (parenteral)
HPV: Recombinant subunit vaccine (virus-like particles; parenteral)
What does ‘parenteral’ mean in the context of vaccines?
Parenteral means the vaccine is administered via injection (subcutaneous or intramuscular).
What type of vaccines are used for SARS-CoV-2?
Replication-deficient viral vector vaccines, mRNA vaccines, protein subunit vaccines.
Why is it hard to treat viral infections?
Viruses are intracellular parasites — drugs must target infected cells without harming healthy cells.
High mutation rates, especially in RNA viruses, lead to rapid development of resistance.
Viruses have diverse life cycles, making universal treatments difficult.
What is passive immunotherapy, and how is it used against viruses?
Passive immunotherapy uses externally sourced antibodies or immune molecules to fight infection, such as:
Post-exposure IgG
Monoclonal antibody therapy
Interferon therapy
What is Respiratory Syncytial Virus (RSV), and who is most at risk?
RSV infects the upper and lower respiratory tracts. Nearly all children are infected by age 2. High-risk groups include infants, the elderly, and those with conditions like cystic fibrosis.
What are RSV-Ig (RespiGam) and Palivizumab, and how do they work?
RSV-Ig: Intravenous IgG from pooled sera, providing passive immunity. Superseded due to risks (e.g., difficulty in sick infants, interference with other vaccines).
Palivizumab: Humanised monoclonal antibody targeting RSV’s F protein. Inhibits fusion with cells and promotes immune destruction of virus particles. FDA approved for at-risk infants in 1998.
What is ZMapp, and how is it developed?
ZMapp is a monoclonal antibody cocktail for Ebola Virus (EBOV), combining humanised, chimeric, and mouse antibodies (e.g., h13F6, c6D8, c13C6).
How do interferons fight viruses?
Create an antiviral state in neighbouring cells.
Upregulate MHC-I presentation, enhancing CD8 T-cell killing of infected cells.
Effective in Hepatitis B (~50%) and Hepatitis C (40-80% with ribavirin).
Side effects (flu-like symptoms) and high doses limit broader use.
What are the main strategies for antiviral drug action?
Block virus/receptor binding: e.g., Palivizumab for RSV.
Block uncoating: e.g., Amantidine (Influenza A M2 inhibitor).
Block nucleic acid synthesis: e.g., Aciclovir (herpes virus).
Block maturation/release: e.g., HIV protease inhibitors, Tamiflu (NA inhibitor for influenza).
How does Aciclovir work?
Aciclovir is a prodrug activated by a viral enzyme, converting to aciclovir triphosphate. It selectively inhibits viral DNA polymerase, acting as a chain terminator.
What are neuraminidase inhibitors, and how do they stop influenza?
Drugs like oseltamivir (Tamiflu) inhibit neuraminidase (NA), preventing the virus from being released from the cell surface, causing viruses to clump.
How do HIV protease inhibitors work?
HIV protease inhibitors (e.g., Saquinavir) block the viral protease needed for maturation, preventing the release of infectious virions.
What is combination therapy, and why is it effective?
Combination therapy (e.g., HAART for HIV) targets multiple stages of the virus life cycle. This reduces the chance of resistance developing. Example:
Nucleoside analogue (Zidovudine)
Non-nucleoside polymerase inhibitor (Nevirapine)
Protease inhibitor (Saquinavir)
What are key treatments for SARS-CoV-2?
Tocilizumab: Blocks IL-6 receptor (anti-inflammatory).
Baricitinib: JAK1/2 inhibitor (anti-inflammatory).
Casirivimab/Imdevimab: Monoclonal antibodies against the spike protein.
Remdesivir: Inhibits viral RNA polymerase.
Nirmatrelvir/Ritonavir: Protease inhibitors blocking viral replication.
What are the core principles of antiviral therapy?
Target virus-infected cells with minimal harm to healthy cells.
Exploit natural immune molecules (antibodies, interferons).
Block key life cycle steps: attachment, uncoating, nucleic acid synthesis, maturation.
Use combination therapies to reduce resistance.
