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

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
Example of nucleoside reverse transcriptase inhibitors NRTIs
Zidovudine
26
NRTI MOA
Inhibits viral reverse transcriptase Active when in triphosphate form Triphosphate competes for proviral synthesis Termination of viral DNA elongation
27
Indications of NRTIs
Advanced HIV infection
28
Adverse effects of NRTIs
Headaches Nausea Anaemia
29
What is zidovudine structurally similar to
Thymidine
30
Non nucleoside reverse transcriptase inhibitors NNRTIs MOA
Doesn’t look like nucleotide Denatures reverse transcriptase
31
NNRTI example
Nevirapine
32
Protease inhibitor example
Ritonovir
33
Protease inhibitor MOA
Inhibition of virus protease Protease essential for post-translational processing of gag and gag-pol poly proteins into functional proteins
34
Protease inhibitors clinical pharmacology
Highly effective in suppressing viral load CYP450 interactions Resistance issues
35
Highly active anti-retroviral therapy (HAART)
NRTI + NNRTI or PI
36
What is atripla
One combination pill per day
37
What is given to HIV patients with resistant strains of HIV
Integrase inhibitors (Raltegravir) Inhibits integration or transcribed viral DNA into host cell chromosomes