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Medical Microbiology > 8 Antivirals > Flashcards

8 Antivirals Flashcards

1
Q

why are the less antiviral drugs

A

Not as many antiviral drugs as there are antibacterials - as viruses can only replicate in living cells

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2
Q

what do viruses use to replicate

A

Use cellular machinery to do all the processes that are necessary to replicate the virus

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3
Q

what do viruses effect

A

Interfere with the host cell – kill host cell = kill virus (isn’t useful clinically)

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4
Q

Schematic virus replication cycle

A
  1. Attachment
  2. Entry
  3. Uncoating
  4. Macromolecular synthesis
  5. Assembly
  6. Release
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5
Q

Acyclovir drug

A

first proof that drug can interfere with virus and not harm host

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6
Q

what does ACV interfere with

A

DNA synthesis

cause termination of DNA synthesis as nothing for next base to come into – when part of the chain

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7
Q

what is ACV

A

analogue of guanosine

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8
Q

what is the ACV active form

A

Adding 3 phosphate to ACV – eukaryotes cannot do this but if infected with virus that has particular enzyme then these virally encoded enzymes can phosphorylate ACV

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9
Q

what does ACV compete with

A

guanosine triphosphate to get into growing DNA chain (to terminate) this molecule is recognized much better by viral DNA enzymes compared to host cell DNA enzymes – selectively antiviral

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10
Q

ACV: selectivity of action

A
  • Only activated in infected cells
  • Becomes concentrated in infected cells
  • Higher affinity for viral DNA polymerase than cellular enzymes
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11
Q

what activates ACV

A

viral enzyme – thymidine kinase

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12
Q

ACV spectrum of activity

A

NARROW only works against – but they’re pretty common (HSV herpes virus, VZV) Will only work against a virus with both thymidine kinase to phosphorylate it and a DNA polymerase

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13
Q

ACV: resistance

A

thymidine kinase absence
- exist pretreatment and are selected for
- but are non-pathogenic
Alteration of thymidine kinase – TK mutants
- Do appear during therapy
- but are also of attenuated virulence
Altered DNA polymerase
- Fully virulent, and a real clinical problem

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14
Q

what drug is dervived from ACV

A

Valine ester of ACV

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15
Q

how is valine ester ACV administered

A

orally

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16
Q

what happens when valine ester ACV is taken

A

breaks into ACV and valine

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17
Q

which drug is better ACV or valine ester ACV

A

Valine ester is much better - most 3x a day or 1x a day (better blood levels)

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18
Q

Anti-cytomegalovirus drugs

A

Ganciclovir
Cidofovir
Foscarnet

19
Q

what is Ganciclovir

A

Acyclic guanosine analogue

20
Q

what does ganciclovir require

A

phosphorylation – by the gene UL97

21
Q

what does ganciclovir inhibit

A

acts as DNA polymerase inhibitor

22
Q

what is ganciclovir active against

A

all herpesviruses

23
Q

why was valganciclovir made

A

ganciclovir poorly absorbed orally

24
Q

con of ganciclovir

A

Toxic e.g. bone marrow suppression– easier to phosphorylate so host start to

25
Q

what is cidofovir

A

Acyclic phosphonate nucleotide analogue

has a phosphate group on it already

26
Q

what does cidofovir require

A

Non-viral dependent phosphorylation

27
Q

what does cidofovir inhibit

A

viral DNA polymerase

28
Q

what is the benefit of cidofovir

A

Broader spectrum – potentially all DNA viruses

29
Q

how is cidofovir administered

A

Given by intravenous infusion (not given orally) given by inject once a week

30
Q

con of cidofovir

A

Toxicity VERY as host can easily phosphorylate (phosphate already there) – nephrotoxic – secreted into renal tubules and damages them = kidney damage

31
Q

what is foscarnet require

A

doesn’t need to be phosphorylated by anything

32
Q

what is CMV

A

mostly harmless virus

33
Q

when is CMV harmful

A

crosses the placenta in pregnant women will damage the foetus or if immunosuppressed CMV is a multisystem pathogen

34
Q

CMV and HIV

A

HIV immunosuppressed CMV common - better HIV treatment now that they will unlikely reach the immunosuppressed stage to get CMV and then latent reinfection

35
Q

Ribavirin effect

A

Don’t know for sure how this drug works

? Interferes with 5’ capping of mRNA processing (recognised by the ribosome)

36
Q

ribavirin benefit

A

If effects mRNA processing – all viruses have to make mRNA and get onto ribosome to make viral protein = broad spectrum of activity in vitro, incl both DNA and RNA viruses

37
Q

what are the uncoating inhibitors

A
  • Amantadine

- rimantadine

38
Q

what does amantadine inhibit

A

uncoating of influenza A virus

39
Q

what is the problem with amantadine

A
  • Poorly tolerated because of CNS stimulation
  • Resistance rapidly emerges
  • No longer recommended
40
Q

how does amantadine work

A

hydrogen ions enter through ion channel

blocks the ion channel – blocks the acidification of the viral capsid = prevents uncoating

41
Q

how do neuraminidase inhibitors work

A

Virus has hemagglutnin on its surface and cell trying to leave has sialic acid – virus would get stuck when trying to bud out
Neuraminidase cleaves sialic acid, allow virus get away, can infect more respiratory epithelial cells
Block neuraminidase then can stop the virus going to infect another cell can’t carry on replicating

42
Q

what are the neuraminidase inhibitors

A

Zanamavir

43
Q

what do neuraminidase inhibitors work against

A

against all known influenza NA (all viruses have a hemagglutnin and neuramnidase –inhibit all the NA)

Medical Microbiology (13 decks)

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