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STEP1 > Antivirals > Flashcards

Antivirals Flashcards

1
Q

HIV entry inhibitors: example and mechanism

A

Maraviroc

Binds CCR5 on cell, so HIV virus cannot enter cell

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2
Q

HIV fusion inhibitor: example and mechanism

A

Efuviritide binds viral gp41 (viral surface protein that normally facilitates viral fusion to host cell)

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3
Q

HIV Fusion inhibitor mechanism of resistance

A

Env encodes structural genes; mutations in env –> resistance

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4
Q

HIV integrase inhibitors: example and mechanism

A

“-tegravir” (raltegravir, dolutegravir, elvitegravir)

Blocks viral integrase, which normally allows viral DNA (post reverse transcription) to integrate with host DNA

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5
Q

HIV Integrase inhibitors mechanism of resistance

A

Integrase encoded by pol; mutation here–>resistance

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6
Q

Mechanism of HIV infection–>release

A
  1. Attachment (viral gp120 to cell CXCR4 or CCR5)
  2. Fusion (via viral gp41)
  3. Uncoating
  4. Reverse transcription
  5. Integration into host DNA via integrase
  6. Transcription, translation
  7. Protease (bc HIV proteins translated as long polyproteins that need to be cleaved by proteases from immature precursors–>mature virion
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7
Q

NRTIs: what are they?

A

Nucleoside reverse transcription inhibitors
Indirectly inhibit reverse transcription
Nucleotides or nucleosides with absent hydroxyl @ 3’ end–>DNA elongation terminated because can’t make 3’-5’ phosphodiester bond

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8
Q

NRTIs: how do they get activated in cells?

A

Nucleosides need to be phosphorylated by cell enzymes to be activated
Nucleotides (ie tenofovir) do not (“naht for tenofovir”)

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9
Q

NRTIs: important SEs overall

A

Mitochondrial toxicity, lactic acidosis

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10
Q

Lamivudine, stavudine, didanosine SE

A

peripheral neuropathy

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11
Q

NNRTIs: what are they and how do they work?

A

Non-nucleoside reverse transcriptase inhibitors
Directly inhibit reverse transcriptase by direct binding–>allosteric inhibition
Doesn’t need intracell phosphor

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12
Q

NNRTIs mechanism of resistance

A

Mutation in viral pol gene

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13
Q

NNRTIs important side effects

A

Liver failure
Stevens Johnson Syndrome
Teratogenic (elfavirenz and dilavirdine)

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14
Q

Protease inhibitors: suffix and mechanism

A

“-navir”
HIV needs proteases bc gene translated as long polyprotein that must be cleaved
Protease encoded by pol gene

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15
Q

Protease resistance?

A

Mutations of pol gene; never use as monotherapy bc of this

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16
Q

Protease SEs

A

Hyperglycemia due to insulin resistance, dyslipidemia, lipodystrophy
Ritonovir inhibits CYP450 strongly

17
Q

Interferons: what are they

A

Immunomodulatory cytokines released from virus infected cells; upregulated by interleukins

18
Q

Interferon alpha treats

A

Hep B and C, hairy cell leukemia, malignant melanoma, kaposi sarcoma, HPV condyloma accuminata, renal cell carcinoma

19
Q

Interferon alpha SEs

A

Flu like syndrome (can be very severe), retinopathy, confusion, myelosuppression, drug-induced lupus

20
Q

Interferon beta tx

A

multiple sclerosis

21
Q

Interferon gamma tx

A

Chronic granulomatous disease

Via activating macrophages

22
Q

Ribavarin mechanism

A

Guanosine nucleoside analogue; must be phosphorylated 3x into its active nucleotide form

23
Q

Ribavirin use

A

Hep C (not anymore)

24
Q

Sofosbuvir mechanism

A

Nucleoside analog, direct polymerase inhibitor

25
Q

Simeprevir mechanism

A

Protease inhibitor

26
Q

HSV, VZV drugs

A

Acyclovir, valacyclovir, famcyclovir

27
Q

Acyclovir mechanism

A

Guanosine nucleoside analog; must be activated by viral thymidine kinase (HSV virus specific)
Absence of viral thymidine kinase confers resistance
Acyclovir gets incorporated into replicating viral DNA, halting synthesis

28
Q

HSV antivirals that do not need to be activated by virus

A

Foscarnet and cidofovir

Directly inhibit viral DNA polymerase

29
Q

Acyclovir SE

A 
CNS (delirium, confusion, hallucinations)
Interstitial nephritis (prevent with hydration)
30
Q

CMV antivirals

A

gancyclovir, valgancyclovir, foscarnet, cidofovir

31
Q

Ganciclovir main toxicity

A

Myelosuppression

32
Q

When do people get CMV infections?

A

CD4<50

33
Q

Ganciclovir mechanism

A

Like acyclovir (guanosine analog, must be phosphor by viral kinase)

34
Q

Oseltamivir, zanamivir mechanism and tx for

A

inhibit influenza NA–>decrease release of progeny virus
Tx and prevent influenza A and B (doesn’t work if already widely replicated virus though, since only inhibits release of more progeny)

35
Q

Ganciclovir mech of resistance

A

Mutated viral kinase

36
Q

Foscarnet mechanism of resistance

A

Mutated DNA polymerase

STEP1 (11 decks)

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