treatment, prevention and control of viral diseases Flashcards

1
Q

antiviral drug

A

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

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2
Q

immune system stimulation

A

interferons, class of proteins that has antiviral effects and modulate functions of the immune system

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3
Q

last way to treat:

A

synthesize AB or admin of natural antiserum (AB)

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4
Q

class of med used for treating viral infection

A

antiviral drugs!

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5
Q

Acyclovir
-what does it treat? + 3 specific types
-how is it administered?
-how does it work?
-

A

-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

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6
Q

Acyclovir
-what is it an analog of?
-mechanism of effect

A

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

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7
Q

acyclovir
-effect to host ?

A

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

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8
Q

Amantadine
-inhibits what virus?
-how does it stop it?

A

inhibits replication of influenza A virus by blocking uncoating of the virus

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9
Q

Amantadine
-mechanism of action

A

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

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10
Q

Neuraminidase inhibitors
-inhibits what enzyme
-stops what virus

-what med?

-mechanism

A

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

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11
Q

nucleoside analog reverse transciptase inhibitors (NRTIs)
-2 examples

A

Zidovudine (ZDV) or azidothymidine (AZT)
and Didanosine - DDI

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12
Q

ZDV/AZT is an analog of what

mechanism of action

dosage in what species and against what

A

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

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13
Q

what are proteases required for?
what do they do?

A

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

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