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Pharm Test 2 > Lecture 8 Antivirals > Flashcards

Lecture 8 Antivirals Flashcards

1
Q

What is the most severe constraint limiting the use of antivirals?

A

toxicity to the mammalian cell

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2
Q

Antivirals are said to have ____ ____ toxicity

A

poor selective

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3
Q

antivirals should interfere with a virus specific function that is either ____________ or _________

A

unique to the virus;

similar host function is much less susceptible to the drug

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4
Q

antivirals also can interfere with a _____ function necessary for viral _____

A

cellular; replication

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5
Q

Effective antiviral drugs have a therapeutic index of ___ to ___

A

100, 1000

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6
Q

All antivirals are viro___

A

static

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7
Q

2 examples of drugs that inhibit entry into host cells:

A

maraviroc; enfurvitide

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8
Q

____ is a CCR5 receptor antagonist

A

maraviroc

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9
Q

What is noncompetitive resistance and what drug is it especially associated with?

A

HIV uses drug bound form of CCR5 as the co-receptor; resistance in maraviroc

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10
Q

Maraviroc dosage should be modified when used with drugs that inhibit or stimulate

A

CYPA3

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11
Q

____ works by inhibiting the function of the gp41 transmembrane glyoprotein

A

enfuvirtide

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12
Q

Enfuvritide has low _____ _______, so it is mainly used for salvage therapy

A

oral availability

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13
Q

Viral uncounting is pH ____ in the endosomes/lysosomes but is pH _____ when fusing with the plasma membrane

A

dependent; independent

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14
Q

Example of drugs that inhibit viral uncoating:

A

amantidine and rimantidine

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15
Q

Raltegravir, dolutegravir, and elvitegravir work by inhibiting ______

A

integrase

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16
Q

Advantages of dolutegravir (2nd gen) or raltegravir):

  1. limited _______ profile
  2. prolonged serum ____
  3. minimal metabolization via ____, decreasing drug drug interactions
A

cross-resistance;
half-life;
CYP450

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17
Q

There is lesser risk of transmitting ____ ____ among individuals when using integrase inhibitors

A

drug resistance

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18
Q

Viral mutations leading to resistance against dolutegravir also diminish HIV ____ and ____ enzymatic activity

A

replication; integrase

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19
Q

Antivirals that inhibit polymerases are selective because:
1.
2.

A

virus uses its own enzyme to activate the drug;

viral polymerases are much more sensitive to drug than host

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20
Q

The fact that thydmidine kinase can phosphorylate the nucleoside analogs permits administration of the drug in a nonphosphorylated form that has what advantage over phosphorylated forms?

A

enters cell much more easily

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21
Q

2 examples of drugs that inhibit mRNA transcription and processing

A

ribavirin, interferon

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22
Q

____ nonspecifically inhibit protein translation

A

interferons

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23
Q

_____ helps the spread of influenza by removing scialic acid from the surface of infected cells so viruses can escape

A

neuraminidase (sialidase)

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24
Q

_____ is an inhibitor of viral neuraminidase

A

zanamivir

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25
Q

____ blocks gycosylation of viral hemagglutinin in the golgi apparatus, preventing viral maturation

A

nitazoxanideā€“used in influenza

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26
Q

Amantadine/rimantadine are _____ blockers that inhibit __

A

M2 channel, uncoating

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27
Q

Amantadine is thought to inhibit ____ in the _____

A

acidifcation, golgi

28
Q

Amantadine also acts on maturation of the influenza _____ glycoprotein, decreasing the ____ potential of virus progreny

A

HA; infective

29
Q

_____ was the first liscensed antiviral, but was too toxic for systemic use due to lack of ____

A

Idoxuridine; specificity

30
Q

Idoxuridine and trifluridine are used ____ to treat herpes ____ and primary _______

A

topically; keratitis; keratoconjunctivitis

31
Q

Ribavirin is a ____ nucleoside analog that inhibits ____ formation on mRNA

A

purine;

5ā€™ cap

32
Q

Ribavirin is used to treat _____ as an aerosol and hepatitis ____; limited use due to toxicity

A

RSV; C

33
Q

1st step of acyclovir activation:

A

phosphorylation by HSV thymidine kinase

34
Q

Acyclovir is a ___ analog that competes with _____

A

guanosine, dGTP

35
Q

Triphosphate acyclovir acts as a _____ because it does not have a ____ group

A

chain terminator;

3ā€™ OH

36
Q

____ toxicity may be seen with high doses of acyclovir

A

renal

37
Q

After receiving its 2nd and 3rd Pā€™s from ____ enzymes, acyclovir binds to _____ and inhibits it

A

cellular

DNA polymerase

38
Q

_____ has better _____ _____ than acyclovir because it is a prodrug

A

valacyclovir; oral bioavailability

39
Q

____ is a monophosphate nucleoTIDE analog that is used to treat acyclovir resistant HSV

A

cidofovir

40
Q

___ is a helicase primase inhibitor that is also used in treatment of HSV

A

pritelivir

41
Q

Azidothymidine/zidovudine (AZT) is a ______

A

nucleoside reverse transcriptase inhibitor

42
Q

AZT must be _____ to become active. It binds ______, aka reverse transcriptase

A

phosphoryalted; RNA dependent DNA polymerase

43
Q

Side effects of AZT: ______ surpression, _____ disturbances.

A

bone marrow; GI

44
Q

There is an increased risk of side effects with AZT if used with drugs that interact with the _______ pathway such as _____

A

glucuronyl transferase; aspirin/acetaminophen

45
Q

Lamivudine is a ___ analog and is a _____

A

cytosine; NRTI

46
Q

What else does lamivudine treat?

A

Hep B

47
Q

_____ is a nucleTide reverse transcripase inhibitor used to treat HIV

A

tenofovir

48
Q

sofosbuvir is used in ____ treatment by interfering with the _____ ____

A

Hep C; NS5B RNA polymerase

49
Q

NNRTIs such as efravirenz work by ______ inhibting RT. ___ develops rapidly

A

physically; resistance

50
Q

Dasabuvir (NNRTI) is used in treatment of _____ by acting as an analog of _______

A

Hep C; nonstructural NS5B

51
Q

Favipiravir is used in treatment of _____ and inhibits the viral ______

A

influenza A and B; polymerase heterotrimer

52
Q

Favipiravir is a ____ analogue that inhibits viral polymerase _____. It has a high barrier for _____

A

nucleobase; PB1; drug resistance

53
Q

Protease inhibitors end in _____

A

navir

54
Q

Protease inhibitors bind to the active site of _____ protease of HIV

A

aspartyl

55
Q

_____ is used to increase the efficiency of other protease inhibitors of HIV

A

ritonavir

56
Q

____ is given with ritonavir as a salvage option for patients with resistance to other protease inhibitors

A

tipranavir

57
Q

____ and ____ are examples of direct acting antivirals that treat HEP c

A

telaprevir, bocepravir

58
Q

Telaprevir and bocepravir target _____ in treatment of HCV

A

NS3/4A non structural protein

59
Q

HCV drugs are beginning to focus on Direct acting antivirals that permit increased sustained virologic ____, _____, and shortened ______ of treatment

A

response, tolerability, duration

60
Q

_____ is an example of an inhibitor of viral complexes

A

daclatasvir

61
Q

Daclatasvir treats ____ by inhibiting ______ protein

A

HCV, NS5A nonstructural

62
Q

inhibitors of ____ end in asvir

A

viral complexes

63
Q

New directions for antivirals include:

  1. targeting the viral _____ complex (ie CMV),
  2. targeting virus-host interaction,
  3. iSAVE-based gene therapeutics that use genetically modifed host ____
  4. baseline ____ testing
  5. taking into account _____ genotypes
A

terminase;
T-Cells;
resistance;
viral

64
Q

alpha and beta interferons prevent viral infection of noninfected cells by binding to _____ _____; also enhance expression of _____

A

surface receptors; MHC

65
Q

_____ interferon enhances the specific T cell mediated immune response

A

gamma

66
Q

Why were interferons hoped to be so effective?

A

act at several levels of the viral cycle

67
Q

What is an example of Pre-exposure prophylaxis for HIV?

A

Truvada (emtricitabine/tenofovir disoproxil fumarate)

Pharm Test 2 (10 decks)

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