GMS6540: VIRAL PHARMACOLOGY EXAM QUESTIONS AND
ANSWERS WITH COMPLETE SOLUTIONS VERIFIED
viral chemotherapy
-viral pathogens use host and cell machinery to do the work
-bring in some viral specific proteins
1. virus binds to host cell = entry process occurs
2. once it penetrates it has to uncoat before early protein synthesis
3. after early protein synthesis it undergoes nucleic acid synthesis
4. after nucleic acid synthesis = late protein synthesis and processing occurs
5. package and assembly = released to affect more cells
Antiinfluenza drugs
-oseltamavir
process:
-binding to cell surface via hemagglutinin
-endocytosis = virus enters
-M2 protein (promotes influx of H+ protons) = leads to viral uncoating
-viral RNA released = can be replicated or transcribed
-viral proteins packaged --> gets released
oseltamavir
-Antiviral
-neuraminidase inhibitor = inhibits release of virus from infected cells and reduces viral
spread in respiratory tract
,-used in the treatment and prophylaxis of influenza A and B
-can reduce the duration of infection if administered within 48 hours following the onset
of clinical illness
herpes virus
-lifecycle:
-binds to receptors on cell surface + is taken up into the cell
-undergoes uncoating and releases double stranded viral DNA
-viral DNA is replicated and transcribed
-protein synthesis by host cell ribosome
-assembly of virion = release from cell
-primary target for treating herpes virus is inhibition of viral DNA polymerase
-virus can maintain a latent viral state in the nucleus of the cell
-only treating an actively replicating cells NOT latent stage
acyclovir
-herpes virus drug
-blocks viral DNA synthesis
-prodrug that is SELECTIVELY phosphorylated by viral thymidine kinase
-inhibits viral DNA polymerase
-causes DNA chain termination when it becomes incorporated into viral DNA
-used for herpes infections (herpes simplex, varicella zoster) but not very active against
cytomegalovirus (CMV)
-emergence of drug-resistant strains in immunosuppressed patients (loss of viral TK)
, -adverse effects = renal toxicity when solubility limits of drug are exceeded (drug
participates)
Ganciclovir
-similar to acyclovir
-nucleoside analogue that is more active against CMV
-can cause bone marrow suppression
Anti HIV drugs
-reverse transcriptase inhibitors = nucleoside reverse transcriptase inhibitors (NRTI) and
non-nucleoside reverse-transcriptase inhibitors (NNRTI)
-protease inhibitors
-entry inhibitors
-integrase inhibitors
HIV life cycle
-Binds to CD4 + fuses into cell
-reverse transcriptase copies viral RNA into dsDNA = provirus enters into host DNA
-transcription of HIV proteins = assembly and spread of new virus
-latent cells = virus persists in body
nucleoside reverse transcriptase inhibitors (NRTI)
-thymidine analogs
-cytidine analogs
-purine analogs
AZT/zidovudine
ANSWERS WITH COMPLETE SOLUTIONS VERIFIED
viral chemotherapy
-viral pathogens use host and cell machinery to do the work
-bring in some viral specific proteins
1. virus binds to host cell = entry process occurs
2. once it penetrates it has to uncoat before early protein synthesis
3. after early protein synthesis it undergoes nucleic acid synthesis
4. after nucleic acid synthesis = late protein synthesis and processing occurs
5. package and assembly = released to affect more cells
Antiinfluenza drugs
-oseltamavir
process:
-binding to cell surface via hemagglutinin
-endocytosis = virus enters
-M2 protein (promotes influx of H+ protons) = leads to viral uncoating
-viral RNA released = can be replicated or transcribed
-viral proteins packaged --> gets released
oseltamavir
-Antiviral
-neuraminidase inhibitor = inhibits release of virus from infected cells and reduces viral
spread in respiratory tract
,-used in the treatment and prophylaxis of influenza A and B
-can reduce the duration of infection if administered within 48 hours following the onset
of clinical illness
herpes virus
-lifecycle:
-binds to receptors on cell surface + is taken up into the cell
-undergoes uncoating and releases double stranded viral DNA
-viral DNA is replicated and transcribed
-protein synthesis by host cell ribosome
-assembly of virion = release from cell
-primary target for treating herpes virus is inhibition of viral DNA polymerase
-virus can maintain a latent viral state in the nucleus of the cell
-only treating an actively replicating cells NOT latent stage
acyclovir
-herpes virus drug
-blocks viral DNA synthesis
-prodrug that is SELECTIVELY phosphorylated by viral thymidine kinase
-inhibits viral DNA polymerase
-causes DNA chain termination when it becomes incorporated into viral DNA
-used for herpes infections (herpes simplex, varicella zoster) but not very active against
cytomegalovirus (CMV)
-emergence of drug-resistant strains in immunosuppressed patients (loss of viral TK)
, -adverse effects = renal toxicity when solubility limits of drug are exceeded (drug
participates)
Ganciclovir
-similar to acyclovir
-nucleoside analogue that is more active against CMV
-can cause bone marrow suppression
Anti HIV drugs
-reverse transcriptase inhibitors = nucleoside reverse transcriptase inhibitors (NRTI) and
non-nucleoside reverse-transcriptase inhibitors (NNRTI)
-protease inhibitors
-entry inhibitors
-integrase inhibitors
HIV life cycle
-Binds to CD4 + fuses into cell
-reverse transcriptase copies viral RNA into dsDNA = provirus enters into host DNA
-transcription of HIV proteins = assembly and spread of new virus
-latent cells = virus persists in body
nucleoside reverse transcriptase inhibitors (NRTI)
-thymidine analogs
-cytidine analogs
-purine analogs
AZT/zidovudine
