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CMOD > Sweatman Antiviral Drugs > Flashcards

Sweatman Antiviral Drugs Flashcards

1
Q

NRTI’s

A

ABACAVIR
LAMIVUDINE (3-TC)
TENOFOVIR
ZIDOVUDINE (AZT)

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2
Q

HIV-1 PROTEASE INHIBITORS

A

ATAZANAVIR

RITONAVIR

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3
Q

DNA STRAND TRANSFER INHIBITORS

A

RALTEGRAVIR

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4
Q

NNRTI’S

A

EFAVIRENZ

NEVIRAPINE

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5
Q

FUSION INHIBITORS

A

ENFUVIRTIDE

MARAVIROC

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6
Q

CLASSES OF ANTI-RETROVIRAL DRUGS

A 
NRTI's
NNRTI's
HIV-1 PROTEASE INHIBITORS
DNA STRAND TRANSFER INHIBITORS
FUSION INHIBITORS
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7
Q

ANTIVIRAL DRUGS

A 
ACYCLOVIR- (ZOVIRAX)
VALCYLOVIR- (VALTREX)
RIMANTIDINE
PEGINTERFERON ALFA
VALGANCICLOVIR
BECEPREVIR
FOSCARNET
GANCICLOVIR
OSELTAMVIR (TAMI-FLU)
RIBAVARIN
TELAPREVIR
TRIFLURIDINE
ZANAMIVIR
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8
Q

REASONS WHY VIRUSES ARE HARD TO TREAT

A
  1. fewer targets sufficiently different than host cells to exploit
  2. heterogeneous group of infectious agents (harder to make a broad spectrum drug)
  3. replicate by co-opting host cell machinery
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9
Q

general steps involved in a DNA virus replication

A
  1. attachment and entry
  2. uncoating
  3. genome replication
  4. RNA synthesis
  5. protein synthesis
  6. assembly and maturation
  7. Eggress and release
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10
Q

MOA for most antiviral agents that are currently approved

A

neucleoside analogues that target genome replication (DNA polymerase or reverse transcriptase)

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11
Q

Attachment and entry inhibitors and their target

A

Maraviroc
Enfuviritide (t-20)
*attachment and entry

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12
Q

Ion channel blockers and their target

A

amantidine
rimantadine
*M2 ion channel–> prevents uncoating

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13
Q

polymerase inhibitors and their target

A

acyclovir
zidovudine
efavirenz
*reverse transcriptase or DNA polymerase

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14
Q

integrase inhibitor and their target

A

raltegravir

*prevents viral dna from being inserted into the host DNA

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15
Q

protease inhibitors and their target

A

saquinavir
ritonavir
*prevents assembly an maturation

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16
Q

Neuroaminidase inhibitors and their target

A

zanamavir
oseltamvir
*prevents mature virions from exiting host cell

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17
Q

Steps in HIV-1 retrovirus replication

A
  1. virus attachment
  2. Fusion
  3. uncoating
  4. integration
  5. transcription and post-transcriptional processing
  6. translation
  7. assembly
  8. proteolytic cleavage—> fully infective virions
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18
Q

Virus attachment for HIV depends on

A

gp41-gp120 complex binding to host cell CD4+ T cell receptors and certain chemokine receptors

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19
Q

Fusion of HIV virus relies on–>

A

HR1 and HR2 complex forming a fusion pore

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20
Q

type of genetic material in HIV virus

A

ssRNA

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21
Q

what does uncoating stage of HIV replication accomplish

A

permits ssRNA HIV genome to be copied by RT in to dsDNA

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22
Q

integration step relies on

A

HIV encoded protein “integrase”

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23
Q

Stages of Influenza A replication

A
  1. Hemagglutinin bind sialylated glycoprotein receptors on host-cell
  2. virus enter cell via receptor-mediated endocytosis
  3. ATP dependent proton pump acidifies cell
  4. hemagglutinin reminds to endosome, virus-host membranes fuse
  5. RNP’s now released into cytoplasm
  6. RNP’s taken to nucleus for replication
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24
Q

M2 ion channels are located where?

A

viral membrane

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25
Q

M2 channel blockers

A

amantadine

rimantadine

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26
Q

Neuaraminidase inhibitors

A

oseltamvir

zanamivir

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27
Q

know why antiviral drugs are limited based on time course of infection–>symptom presentation

A

by the time someone feels like shit…virus has already proliferated and the virus has spread all over
*this s why tami-flu must be taken in the first 2-3 days of contracting influenza A

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28
Q

know the steps involved in HIV infection

A

too many to type justt know them in your soul

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29
Q

Enfuvirtide (t-20) MOA

A

mimics HR2, binds HRI–> prevents HR1 and Hr2 interaction

*traps the process at the atachment stage–>no membrane fusion

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30
Q

Maraviroc MOA

A

blocks “other chemokine receptors”

–>therefore cells that rely on CCR5 for attachment and entry are inhibited

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31
Q

M2 ion channel MOA

A

pH gated ion channel that opens up in response to acidification of endosome–> necessary step for uncoating of Influenza A RNP’s and viral genetic material into cytosol

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32
Q

Which are HIV-1 specific NRTI’s or NNRTI’s

A

NNRTI’s

33
Q

Require metabolic activation usually to a triphosphate form

A

NRTI’s

34
Q

Indirectly inhibits polymerization

A

NRTI’s

35
Q

prevents elongation of newly formed nucleic acid by polymerase

A

NRTI’s

36
Q

most common uses of NRTI’s

A

herpes

HIV

37
Q

MOA of nucleoside analogues

A

competitive inhibition with endogenous nucleosides for DNA polymerase/reverse transcriptase–>ultimately leading to termination of elongation

38
Q

toxicity associated with NRTI’s

A

*they also inhibit mitochondrial DNA synthesis–>leading to depletion of mitochodnrial DNA

39
Q

MOA for NNRTI’s

A

Direct-Specific inhibition of HIV-1 RT:

bind to hydrophobic pocket on HIV-1 reverse transcriptase changing its form and function

40
Q

Does NNRTI’s require metaoblic activation (ie intracellular phosphorylation)

A

HELL NAW

41
Q

NNRTI’s are innefective against HIV-2, or other retroviruses

A

binding site is virus strain specific

42
Q

Raltegravir MOA

A

blocks activity of HIV 1 and 2 integrase

*cannot insert cDNA into host chromosome

43
Q

HIV-1 protease inhibitors MOA

A

“inhibit precursors of polypeptide cleavage”
-inhibit ASPARTYL PROTEASE (responsible for HIV gag and pol precursors that go on to make many CRUCIAL prot components required for replication–> enzymes and strcutral
(reverse trasncriptase, proteases, integrases, many structural prots)

44
Q

Some Protease inhibitors used in HIV treatment—WHY?

A

Some of them inhibit CYP3A4 activity–>(RITONAVIR) in low doses will prolong plasma persistence of drugs broken down by CYP3A4

45
Q

What limits Protein INhibitors presence in Blood Brain Barrer

A
  1. P-gp pump (ABC transporter—> MDresistance)

2. strong plasma-protein biding

46
Q

What is unique about peginterferon

A

log-lasting formulation of interferon that is conjugated to ethylene glycol to increase durability in the circulation of active drug

47
Q

Interferons affect what types of viruses

A

DNA and RNA

48
Q

Interferon MOA

A

BInding if an IFN causes cell to produce a series of antiviral proteins MOST OF WHICH ACT TO INHIBIT THE TRANSLATION OF VIRAL PROTEINS

49
Q

Drugs which inhibit release of influenza virus form infected cell

A

Zanamivir, Oseltamvir

*selective sialic acid analogue inhibitors

50
Q

MOA for drugs that inhibit Influenza A release

A

produce conformational changes in active site of influenza A and B NEURAMINIDASES

51
Q

What do neuraminidases do?

A

destroy terminal sialic acid residues–>which destroys the receptors recorgnized by viral hemagglutinin that are present on the cell surface in progeny virions and respiratory secretions

52
Q

Use of these drugs leads to local aggregation of progeny virions on infected cell surface and results in decreased viral spread within the respiratory tract

A

neuroaminindase inhibitors

53
Q

Principle of chemo:

ALL ASPECTS OF THE DISEASE ARE DERIVED FROM VIRAL EFFECTS UPON ______

A

CD4+ Helper T Cells

54
Q

Principle of HIV chemo:

Current drugs require ______

A

actively replicating virus

55
Q

Principle of HIV chemo:

If the viral genetic material is hiding in quiescent T cells____

A

it is unlikey that drug treatment will eradicate ALL infected T cells

56
Q

Principle of HIV chemo:

It is likely that some infected T cells_____

A

will survive decades if not throughout the life of the patient

57
Q

Principle of HIV chemo:

Drug therapy does NOT cause mutations

A

rather it provides selective presure to promote growth of the naturally ocuring mutant viruses
(i’m not following this?)

58
Q

Principle of HIV chemo:

Clinically beneficial of HIV chemo?

A
  1. long-term suppression (decrease in plasma RNA levels

2. replenishment of CD4+ T cells

59
Q

Result of using 3 HIV drugs simultaneously

A

initial treatment will reduce plasma RNA copies <50copies/mL by 24 weeks

60
Q

Limiting factor in using 4+ drugs?

A
  1. toxicity

2. inconveneince (pt’s ability to tolerate)

61
Q

If viral resistance is observed?

*implying RNA levels increase despite continued adherence to the regimen

A

regimen must be changed

62
Q

Principle of HIV chemo:

resistant strains remain in?

A

T lymphocytes forever

63
Q

Principle of HIV chemo:

the relative “forgiving nature” of a given regimen towards missed doases is based on?

A

duration of of drug persistence in pt’s blood

longer half lives are better

64
Q

Principle of HIV chemo:

failed treatment usually resultant of

A

non-adherence

65
Q

preferred agents used against HBV polymerase

A

tenofovir disproxil fumarate, and entacavir

66
Q

tx for HCV is defined by?

A

genotype of the infected virus

67
Q

Genotype 1 HCV is treated with?

A

peginteferon-alfa + ribavarin + telaprevir + boceprevir HCV NS3/4A

68
Q

Major factor in recent H1N1 resistant to neuraminidase inhibitors?

A

overuse of drugs and veterinary usage

69
Q

DOC for early events (viral entry of uncoating)

A

enfurvitide, maraviroc, amantadine, rimantadine

70
Q

DOC for nucleic acid synthesis by herpes viruses

A

Acyclovir, Ganciclovir, Valcyclovir, Valganciclovir

71
Q

DOC for Nucleic acid synthesis by HIV

*NRTI’s

A

abacavir, lamivudine (3-tc), tenofivir, disproxil, zidovudine (AZT), emtricitabine, didanosine (ddl), stavudine

72
Q

DOC for Nucleis acid synthesis in HIV

**NNRTI’s

A

efevirenze, nevirapine

73
Q

DOC for Nuecleic acid synthesis by HBV

A

adefovir

74
Q

DOC for nucleic acid synthesis for other viruses

A

ribavarin, trifluridine

75
Q

DOC for HIV integrase inhibition

A

raltegravir

76
Q

DOC for cleavage (protease) of precursor polypeptides

A

atazanavir, ritonavir

77
Q

DOC Cleavage of precursor polypeptides of HCV

A

boceprevir, telaprevir

78
Q

DOC for synthesis directed by viral mRNA

A

Peginterferon-alfa

79
Q

DOC for release of influenza from infected cell

A

Oseltamvir, Zanamivir

CMOD (19 decks)

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