treatment, prevention and control of viral diseases Flashcards
antiviral drug
interfere with ability of a virus to infiltrate a target cell or target different stages of replication/synthesis of components required for replication of the virus
immune system stimulation
interferons, class of proteins that has antiviral effects and modulate functions of the immune system
last way to treat:
synthesize AB or admin of natural antiserum (AB)
class of med used for treating viral infection
antiviral drugs!
Acyclovir
-what does it treat? + 3 specific types
-how is it administered?
-how does it work?
-
-treats herpes virus (specifically herpes in humans, feline herpesvirus 1 induced corneal ulcers and equine herpesvirus 1 induced encephalomyelitis)
-admin as a prodrug, an inactive form
-requires virus enzymes in infected host cell to convert itself into an active form, which then interferes with virus replication
Acyclovir
-what is it an analog of?
-mechanism of effect
GUANOSINE - deoxyguanosine
-herpes simplex’s DNA polymerase enzyme incorporates the acyclovir monophosphate into the growing DNA strand as if it were 2-deoxyguanosine monophosphate (a G base) –> further elongation of the chain is now impossible because acyclovir monophosphate lacks the attachment points for adding new nucleotides = viral DNA synthesis stops
-also, competitive inhibition of viral DNA polymerase, as acyclovir - triphosphate competes with dGTP for viral DNA polymerase
acyclovir
-effect to host ?
non toxic to uninfected host cell
-since the enzymes thymidine kinase and herpes virus DNA polymerases are viral enzymes and not found in uninfected host cells, acyclovir cannot be phosphorylated and incorporated into the host DNA = nontoxic to uninfected host cells = safe drug
Amantadine
-inhibits what virus?
-how does it stop it?
inhibits replication of influenza A virus by blocking uncoating of the virus
Amantadine
-mechanism of action
M2 ion channel is the target, these compounds clog the channel and prevent it from pumping protons into the virion
-with drug: viral RNAs remain bound to M1 and cannot enter the nucleus = virus rep is inhibited
Neuraminidase inhibitors
-inhibits what enzyme
-stops what virus
-what med?
-mechanism
inhibits neuraminidase enzyme
made by INFLUENZA A and B
EX: oseltamivir (tamiflu)
mechanism: blocks function of neuraminidase with NA inhibitors, prevents release of virus and spread of infection, as the HA of virus is still bound/attached to sialic acid containing receptors on surface of already infected host cell, inhibition of neuraminidase slows virus spread = gives immune system time to catch up and mediate virus clearance
nucleoside analog reverse transciptase inhibitors (NRTIs)
-2 examples
Zidovudine (ZDV) or azidothymidine (AZT)
and Didanosine - DDI
ZDV/AZT is an analog of what
mechanism of action
dosage in what species and against what
thymine !! -resembles deoxyribonucleotide containing thymine
mechanism: competitive inhibition of reverse transcriptase activity: AZT triphosphate competes with thymine deoxyribonucleotide trisphosphate for reverse transcriptase, inserting AZT- monophosphate into cDNA blocks the growth of cDNA being transcribed from the viral RNA by reverse transcriptase
reduces clinical signs in FIV positive cats when administered at dose of 10mg/kg twice a day, subQ for 3 weeks
what are proteases required for?
what do they do?
cleaving the HIV polyproteins into functional proteins
-protease inhibitors inhibit proteases, HIV polyproteins cannot be cleaved into functional proteins; they bind to the active site of the HIV protease and prevent the enzyme from cleaving HIV polyproteins into functional proteins, as a result, HIV can not mature and noninfectious viruses are produced