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PED2006 - Systems Pharmacology > Antiviral [20] > Flashcards

Antiviral [20] Flashcards

1
Q

3 DNA viruses

A

Adenovirus
Herpesvirus
Papilomavirus

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2
Q

2 RNA viruses

A

Influenza virus
Retrovirus (AIDS)

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3
Q

Explain virus replication cycles

A
  1. Attachment to host cell
  2. Un-coating of virus
  3. Control of DNA/RNA/protein production
  4. Production of viral subunits
  5. Assembly of virions
  6. Release of virions (cell lysis)
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4
Q

Describe specificity of antiviral drugs

A

Hard to achieve distributional selectivity
Target enzymes, metabolic pathways, viral Nucleic acid synthesis

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5
Q

3 viral specific targets of antivirals

A

Viral cell binding
Interrupting uncoating
Stimulating host immune system

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6
Q

What is viral latency

A

Recurrence of infection
(Acute, persistent, reactivating, slow)

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7
Q

Are most AV drugs virustatic or viruscidal

A

Virustatic
No AV drugs can eliminate latency

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8
Q

Acute virus infection example

A

Influenza

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9
Q

Persistent virus infection example

A

Meningitis

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10
Q

Reactivating virus infection example

A

Herpes

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11
Q

Slow virus infection example

A

HIV

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12
Q

What increases AV resistance

A

Rapid replication rates
Spontaneous mutation
Mutations prevent protease and reverse transcriptase binding

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13
Q

Traits of herpes virus

A

Cold sores, varicella zoster (chicken pox), Epstein Barr (glandular fever)

Blisters

Infects sensory ganglia where becomes latent

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14
Q

Herpes treatment

A

Aciclovir
Synthetic guanosine analogue
High specificity to simplex
Require intracellular phosphorylation to become active

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15
Q

Aciclovir activation

A

Uses simplex’s thymidine kinase to monophosphorylate Aciclovir

Host cell kinases di and tri phosphorylate

Triphosphate form is active

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16
Q

Aciclovir MOA

A

G analogue so binds DNA
Makes a kink
DNA polymerase can’t cause elongation

17
Q

HIV and AIDS general information

A

1981 discovery
Sexually transmitted
Destruction of host immune system
HIV1 - AIDS
HIV2 - less virulent

18
Q

HIV MOA

A

Viral DNA -(RNA polymerase)-> viral RNA —> translation to viral components —> viral assembly —> host cell death

19
Q

What does HIV target

A

CD4 and CD8 cells

20
Q

HIV treatments

A

Fusion inhibitors
CCR5 inhibitors
NRTIs and NNRTIs
Protease inhibitors

21
Q

Example of fusion inhibitors

A

Enfurvitide

22
Q

Fusion inhibitor MOA

A

Identical to HIV gp41
Stops gp41 changing shape to allow HIV to enter host cell
Inhibits fusion of cellular and viral membranes

23
Q

CCR5 inhibitor example

A

Maraviroc

24
Q

CCR5 inhibitor MOA

A

Binds CCR5 receptor on CD4
Prevents interaction of gp120 and CCR5
Needed for entry to cell
Not a first line therapy

25
Q

Example of nucleoside reverse transcriptase inhibitors NRTIs

A

Zidovudine

26
Q

NRTI MOA

A

Inhibits viral reverse transcriptase
Active when in triphosphate form
Triphosphate competes for proviral synthesis
Termination of viral DNA elongation

27
Q

Indications of NRTIs

A

Advanced HIV infection

28
Q

Adverse effects of NRTIs

A

Headaches
Nausea
Anaemia

29
Q

What is zidovudine structurally similar to

A

Thymidine

30
Q

Non nucleoside reverse transcriptase inhibitors NNRTIs MOA

A

Doesn’t look like nucleotide
Denatures reverse transcriptase

31
Q

NNRTI example

A

Nevirapine

32
Q

Protease inhibitor example

A

Ritonovir

33
Q

Protease inhibitor MOA

A

Inhibition of virus protease
Protease essential for post-translational processing of gag and gag-pol poly proteins into functional proteins

34
Q

Protease inhibitors clinical pharmacology

A

Highly effective in suppressing viral load
CYP450 interactions
Resistance issues

35
Q

Highly active anti-retroviral therapy (HAART)

A

NRTI + NNRTI or PI

36
Q

What is atripla

A

One combination pill per day

37
Q

What is given to HIV patients with resistant strains of HIV

A

Integrase inhibitors (Raltegravir)
Inhibits integration or transcribed viral DNA into host cell chromosomes

PED2006 - Systems Pharmacology (19 decks)

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