treatment, prevention, control Flashcards
(41 cards)
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
AZT/ZDV facts
-selective activity on Reverse transcriptase and low mammalian toxicity occurs
-signs of toxicity include anemia and granulocytopenia
-considered a maintenance drug
does not eliminate the virus
-can reduce clinical signs in FIV positive cats
gag polyprotein
polyprotein associated with HIV
HIV must have own proteases to cleave into functional protein units
will cleave by proteases binding to active site
HIV protease inhibitors
Saquinavir Ritonavir Indinavir Nelfinavir these will bind to the active site, preventing the proteases from binding here to cleave the gag polyprotein
breaking the chain of infection at any point leads to
control of the disease! for new susceptible host->immunization treatment for host reservoir-> neutralization for ode of transmission-> interruption for route/portal entry->protection
Immunization-> vaccinations
where-endemic/enzootic areas
when-disease is in season or outbreak of non-endemic disease occurs
who-people at risk
why-because loss caused by disease is greater than cost of immunization
good vaccine features
safe to use effective against diverse strains of same pathogen few side effects give long lasting protection stable/long shelf life easy to administer inexpensive benefit outweighs the risk
live-attenuated vaccine
from naturally occurring viruses
originally introduced by Jenner (cowpox/smallpox)
sometimes when vaccinated for one disease, can protect for a genetically similar disease
live-attenuated by serial passage
in cultured cells
most vaccines used today
repeated passage allows for –substitutions in genome which lead to attenuation
