treatment, prevention, control Flashcards
antiviral drugs
interfere with the ability of a virus to infiltrate a target cell or target different stages of replication/synthesis of components required for replication of the virus
why are antiviral drugs on effective sometimes?
most viruses that interfere with virus replication are toxic to the cell and not many drugs interfere with replication without harming the infected host cell
treatment for viruses
antiviral drugs
immune system stimulation (IFNs)
synthesize antibodies or administer natural serum
antiviral chemotherapeutic drugs are not commonly used in vet practice because
high cost, virus specific (narrow spectrum)
yet, things may change since antiviral chemotherapy has been more successful in humans
mechanism of an antiviral drugs
can target any portion of virus life cycle
- receptor binding
- cell entry
- uncoating
- nucleic acid and protein synthesis
- assembly
- release
Acyclovir
a prodrug for treating herpes (humans, feline HPV-1 for corneal ulcers, and equine HPV-1 for encephalomyelitis)
interferes with virus replication
mechanism of Acyclovir
its a synthetic nucleoside analog of deoxyguanosine
acyclovir has 3 phosphates added to it (by TK, GMPK, NDPK) then two phosphates are cleaved and acyclovir monophosphate is added to the growing DNA viral chain because it is similar to guanine, yet DNA elongation stops because acyclovir monophosphate lacks the attachment point to continue
also acyclovir triphosphates compete directly with viral DNA polymerase
acyclovir facts
- non toxic to uninfected cells
- resistance to the drug may occur because of mutations in kinases and in viral polymerase
amantadine
synthetic tricyclic amine
anti-viral and anti-parkinson drug
inhibits replication of influenza A by blocking uncoating of virus
amantadine mechanism of action
M2 channel protein that lets in the replicated virus is the target
the drug clogs the channel and prevent it from pumping protons into the virion-> virus replication is inhibited
-resistance may occur with change of amino acids of M2 protein
how amantadine blocks influenza A
pH change of endosomes resulting from M2 inhibition alter the conformation of hemmaglutinin, blocking viral assembly
neuraminidase inhibitors
treat influenza A and B viruses
- tamiflu
- Laninamivir
- Zanamivir
- Peramivir
neuraminidase
meant to cleave sialic acid receptors on cell, important for cell to cell spread of virus
-target for neuraminidase inhibitors, allowing the immune system to “catch up”
targets for anti-retroviral therapy
- inhibit reverse transcriptase
- inhibit protease
- inhibit integrase
- inhibit fusion
nucleoside analog reverse transcriptase inhibitors (NRTIs)
AZT/ Zidovudine
analog of thymine-> resembles deoxyribonucleotide containing the base thymine
mechanism of AZT/ Zidovudine
the host cell kinases add 2 phosphates, it incorporates into CDNA and Viral RNA to it-> no further elongation occurs
- AZT triphosphate competes with Reversre transcriptase
- Zidovudine has an Azide instead of OH-> cannot elongate cDNA