Anti-virals Flashcards
Discuss viral replication
- Can not replicate on its own
- Attach and enter a host cell
- Uses the host cell to synthesize protein, DNA and RNA
Why are viruses difficult to kill?
Drugs that kill viruses also kill host cells (live inside host cells)
Discuss the characteristics of viruses
- Can not replicate on their own, no metabolic machinery
- No cell wall, made up of nucleic acid components
- Some can contain an envelope
- Certain viruses multiply in the cytoplasm but others do in the nucleus
- Most multiplication take place before diagnosis is made
Discuss the characteristics of anti-viral drugs
- Purine or pyramidine analogs
- Many are prodrugs–> phosphorylated by virus or cellular enzymes
- Inhibit active replication, growth resumes after drug removal
Explain some of the actions of antiviral drugs
- Enter cell infected with virus
- Interfere with viral nucleic acid synthesis
- Interfere with the ability of viruses to bind to cells
- Stimulate the body’s immune system (immunotherapy) Competent immune system works synergistically with anti-viral drugs
Classify the anti-viral medications
Antiviral (infections other than HIV)
Anti-retroviral
Herpes simplex virus
Varicella Zoster Virus
Explain the MOA, examples and adverse effects of nonretroviral anti-viral drugs
- Inhibits viral replication
Used to treat:
Influenza viruses
HSV (herpes simplex virus), VZV (vericella zoster virus)
CMV (cytomegalovirus)
Hepatitis A, B, C (HAV, HBV, NCV
Healthy cells often killed
What is the limitations of anti-viral drugs
- Only inhibit actively replicating virus, viral growth returns once drug is stopped
- Does not eliminate latent viruses
- Immune response is important for the elimination of the viral infection
Explain the stages of viral replication
- Attach/bind to cell and entry
- Uncoating
- Transcription of viral genome
- Translation
- Assembly of viral components
- release
What are some anti-viral mechanisms
- Fusion inhibitors
- Cytokine receptor antagonists
- Reverse Transcriptase inhibitors
- Integrase inhibitors
- Viral protease inhibitors
Explain the MOA of attachment fusion inhibitors and give examples
- Enfuvirtide (HIV)
- Ribavirin (Hep C)
- Oseltamivir (influenza)
- Inhibit attachment and fusion to host cells preventing the virus from entering the host cell
Explain the MOA and examples of chemokine receptor antagonisits
Acyclovir (herpes)
Zanamivir (influenza
Interfere with the binding receptor, blocking the interaction, fusion and entry
Differentiate between NRTis and NNRTIs
nucleotide reverse transcription inhibitors (NRTIs): amalogues of the nucelotides gaunine, cytosine, thymidine and adenine. When incorporated into the DNA strand during reverse transcription, it terminates the chain.
Non- nucleotide reverse transcription inhibitors directs inhibit the reverse transcriptase enzyme
Explain the viral protease inhibitors and examples
Doultegravir
Inhibitors of the proteases which is responsible for the cleavage of the viral polyprotein
Prevents the maturation of viral particles
Disuss integrase inhibitors in terms of examples and MOA
- Raltegravir, Bictegravir, doultegravir
Prevent the integration of viral DNA into host DNA
They work by blocking the activity of the enzyme integrase, which is essential for the replication of the virus. The mechanism of action of integrase inhibitors involves three main steps:
Binding: Integrase inhibitors bind to the integrase enzyme, preventing it from interacting with viral DNA.
Strand transfer inhibition: Integrase inhibitors block the strand transfer step of the integration process, which is necessary for the viral DNA to be inserted into the host cell’s DNA.
Viral integration: By blocking the integration step, integrase inhibitors prevent the virus from replicating and spreading throughout the body.
