Mechanisms of Antivirals Flashcards

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1
Q

Why do we need anti-virals ?

A

because viruses are quick killers

slow progressing viruses cause chronic disease that leads to cancer

to treat inflammatory acute infections like herpes and shingles

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2
Q

Use of anti-virals

A

Treatment of acute infection
Influenza ; Chickenpox; herpes infections -(aciclovir)

Treatment of chronic infection:
HCV, HBV, HIV (numerous different agents)

Post-exposure prophylaxis and preventing infection:
HIV (PEP)

Pre-exposure prophylaxis: HIV (PrEP)

Prophylaxis for reactivated infection: e.g. in transplantation
CMV (ganciclovir, foscarnet)

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3
Q

Selective Toxicity - what is this?

A

when an anti-viral drug has a selective action against the pathogen and not the host
-due to the differences in structure and metabolic pathways between host and pathogen

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4
Q

Why is it hard to make anti-virals?

A

they are intracellular organisms and they use cellular processes in order to replicate themselves

so, if you inhibit the replicative processes inside the cell, it stops the virus from replicating but it also damages the cell

some viruses are able to remain in a latent state e.g. herpes, HPV - hide from the antiviral

viruses enter cells using cellular receptors which may have other functions - blocking the receptors could be detrimental

high mutation rate - quasispecies (viruses can escape the effects of anti-viral drugs because the target mutates very rapidly)

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5
Q

Modes of action of selected

anti-virals

A
  • Preventing virus adsorption onto host cell
  • Preventing penetration
  • Preventing viral nucleic acid replication (nucleoside analogues)
  • Preventing maturation of virus
  • Preventing virus release
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6
Q

Herpes virus treatment

A

Acyclovir

  • low toxicity
  • HSV and VZV

Ganciclovir
-CMV

both given IV/oral
both inhibit nucleic acid polymerization by targeting RT’s/DNA polymerases

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7
Q

Ribavarin

A

compromises DNA replication

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8
Q

give an example of a target for selective toxicity

A

viral enzymes that are sufficiently different from human counterparts

for example
-RT and protease (HIV), thymidine kinase (HSV)

act as selective targets with minimal effect on host enzymes or processes

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