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Microbiology E-Books > Anti-Viral Drugs I > Flashcards

Anti-Viral Drugs I Flashcards

1
Q

The genomes of non-retroviruses are made of either

A

DNA or RNA

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2
Q

What are 3 examples of DNA viruses?

A

Herpes, Varicella, and Cytomegalovirus

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3
Q

Replicate inside host nuclei using virus-encoded machinery

A

DNA viruses

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4
Q

In DNA viruses, the viral genome is transcribed and translated by

A

Host proteins

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5
Q

A DNA virus that replicates through an RNA intermediate

A

HBV

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6
Q

What are two examples of RNA viruses?

A

Influena and Hepatitis A and C

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7
Q

(-)RNA genome serves as template for viral mRNA production

A

Influenza

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8
Q

In influenza, the genome is copied into a

A

(+) RNA intermediate

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9
Q

This (+) RNA intermediate is then used to produce more

A

(-) RNA genomes

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10
Q

(+) RNA genome is used directly as mRNA. The genome is copied to a (-) RNA intermediate, which is used to produce more (+) RNA genomes

A

Hepatitis

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11
Q

Analogs of naturally occurring nucleosides inhibit viral

A

DNA replication

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12
Q

All compete with natural nucleotides for binding viral DNA polymerase

A

Nucleoside analogs

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13
Q

Requires HSV thymidine kinase (TK) for first phosphaste

A

Acyclovir

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14
Q

Guanosine derivative that functions as a viral DNA replication inhibitor

A

Acyclovir

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15
Q

Acyclovir undergoes monophosphorylation by viral

A

Thymidine Kinase (HSV-TK)

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16
Q

Phosphorylation traps acyclovir within

A

Infected cells

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17
Q

The triphosphate form competes with dGTP to bind viral DNA polymerase

-Also acts as chain terminator

A

Acyclovir

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18
Q

Resistance to acyclovir is due largely to mutations in

A

HSV-TK and viral DNA polymerase

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19
Q

HSV-TK mutations cause cross-resistance to other drugs activated by

A

HSV-TK

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20
Q

A derivative of acyclovir that has increased bioavailability of the drug

A

Valacyclovir

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21
Q

Limited by renal insufficiency and CNS effects

-Use slow infusion rate

A

IV acyclovir

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22
Q

No evidence of teratogenic or carcinogenic effects despite nucleoside structure

A

Acyclovir

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23
Q

Drug Treatments for Herpes Simplex Virus (HSV) and Varicella Zoster Virus (VZV) are

A

Nucleoside analogs (acyclovir)

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24
Q

Which drugs do we use to treat Cytomegalovirus (CMV)?

A

Valganciclovir, ganciclovir, and letermovir

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25
Q

Valganciclovir and ganciclovir are both

A

Guanosine derivatives

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26
Q

The valyl protecting group in valganciclovir is removed at the

A

Intestinal wall

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27
Q

Taken orally

A

Valganciclovir

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28
Q

Given by IV

A

Ganciclovir

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29
Q

Ganciclovir is a prodrug that must be

A

Triphosphorylated

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30
Q

Adds the first phosphate to ganciclovir

A

Viral UL97 kinase

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31
Q

Binds viral polymerase competitively and causes chain termination

A

Ganciclovir

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32
Q

Ganciclovir resistance is caused by mutations in the viral

A

UL97

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33
Q

Approved in 2017 for CMV suppression during hematopoietic stem cell transplant (HSCT)

A

Letermovir

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34
Q

Inhibits the CMV DNA terminus complex required for viral packaging

A

Letermovir

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35
Q

Cleaves viral concatemers after DNA replication into monomers

A

Letermovir

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36
Q

Letermovir is an inhibitor and inducer of

A

CYP3A4 and other P450s

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37
Q

Contraindicated for use with pimozide, ergot alkaloids

A

Letermovir

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38
Q

Letermovir is also contraindicated for use with pitavastatin or simvastatin when co-administered with

A

Cyclosporine

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39
Q

Recommended treatments for first clinical episode for HSV and VZV

A

Acyclovir, valacyclovir, and famciclovir

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40
Q

Recommended first-line treatments for CMV in immunocompromised patients

A

Valganciclovir, ganciclovir, and letermovir

41
Q

For influenza, we want early treatment within

A

48 hours of illness onset

42
Q

This early treatment within 48 hours of illness onset shortens the duration of fever and illness symptoms by about a

A

Day

43
Q

Sialic residues on host receptors bind viral hemagglutinin causing viral particles to

A

Aggregate

44
Q

Cleaves these sialic residues, thereby permitting viral escape

A

Viral Neuramidase

45
Q

These drugs are sialic acid, transition-state analogs that inhibit viral neuraminidase activity

A

Neuramidase inhibitors

46
Q

Zanamivir, Oseltamivir (tamiflu), and Peramivir are the three

A

Neuramidase inhibitors

47
Q

Reduce viral escape from infected cells, preventing infection of others

A

Neuramidase inhibitors

48
Q

Neuramidase inhibitors work on the neuraminidase of both

A

Influenza A and B

49
Q

Resistance to neuramidase inhibitors appears with mutations in the

A

Neuraminidase gene or hemagglutinin

50
Q

A prodrugthat is taken orally. Activated by esterasesin GI or liver

A

Oseltamivir

51
Q

An inhaled drug to overcome low oral bioavailability

A

Zanamivir

52
Q

Administered as single IV dose (versus 5 days of Oseltamivir)

A

Peramivir

53
Q

Virus enters cell by endocytosis. Particles arrive in endosomes, which are

A

Acidic

54
Q

Low pH cleaves hemagglutinin on viral surface and activation of the viral

A

M2 ion channel

55
Q

Bind to the M2 protein and block viral acidification and unsheathing

A

Amantadine and Rimantidine

56
Q

Amantadine and rimantidine are not effective against

A

Influenza B

57
Q

Well absorbed by oral administration

-Very large Vd

A

Amantadine and Rimantadine

58
Q

Excreted unmetabolized in urine. Levels rise with renal insufficiency

A

Amantidine

59
Q

Metabolized by hydroxylation, conjugation and glucuronidation before excretion

A

Rimantidine

60
Q

There are reports of HBV reactivation during treatment of

A

HCV

61
Q

Chain terminator of HCV NS5B polymerase

-Part of first ALL oral treatment for HCV

A

Sofosbuvir

62
Q

Uridinechain terminator of the NS5B RNA-dependent RNA polymerase

A

Sofosbuvir

63
Q

Once daily pill. No induction of P450s

A

Sofosbuvir

64
Q

Sofosbuvir is a substrate for the p-glycoprotein drug

A

Efflux pump

65
Q

Abnormal slow heartbeat may occur in patients taking sofosbuvir-based drugs along with

A

Amiodarone

66
Q

Coformulated with pibrentasvir (NS5A drug) as fixed dose oral Mavyret

A

Glecaprevir

67
Q

A pan-genomic drug that is more than 92% effective and requires only 8 weeks of treatment

A

Glecaprevir

68
Q

Maintains activity against NS3/4A variants that are resistant to other drugs

A

Grazoprevir

69
Q

Coformulatedwith elbasvir (NS5A drug) as fixed dose oral Zepatier

A

Grazoprevir

70
Q

Coformulated with sofosbuvir (NS5B drug) and velpatasvir (NS5A drug) as fixed-dose oral Vosevi

A

Voxilaprevir

71
Q

Approved for use with patients who were treated previously with other HCV drugs that failed

A

Vosevi

72
Q

A structural protein of HCV with no enzymatic function

A

NS5A protein

73
Q

Binds NS5A tightly and blocks viral RNA replication and packaging

A

Ledipasvir

74
Q

A coformulationof ledipasvirand sofosbuvirwas approved in 2014 for

A

Genotype 1

75
Q

Principle drug interactions are associated with sofosbuvir component because it is a substrate for

A

P-glycoprotein

76
Q

Coformulated with grazoprevir (NS3/4A drug) as fixed dose oral Zepatier

-More than 94% Effective for genotypes 1 and 4.

A

Elbasvir

77
Q

Coformulated with sofosbuvir (NS5A drug) as fixed-dose oral Epclusa

A

Velpatasvir

78
Q

Over 90% effective for ALL genotypes

A

Velpatasvir

79
Q

More than 94% effective for genotypes 1 and 4

A

Elbasvir

80
Q

Coformulated with glecaprevir as fixed-dose oral Mavyret

A

Pibrentasvir

81
Q

Considered a first-line treatment for HBV

A

PEG-IFN

82
Q

Also first-line treatments, and have fewer associated side effects and restrictions

A

Nucleoside analogs

83
Q

Human proteins with antiviral, immunmodulating, and anti-proliferative actions

A

Interferon (IFN)

84
Q

Activate JAK-STAT signal transduction pathway, activating IFN responsive genes

A

Interferons

85
Q

IFN-induced major histocompatability antigens enhance the lytic effects of

A

Cytotoxic T-lymphocytes

86
Q

What are the 4 sites of interferon-mediated viral inhibition?

A
  1. ) Transcription inhibition
  2. ) Translation inhibition
  3. ) Protein processing inhibition
  4. ) Viral maturation
87
Q

Linked to polyethylene glycol (PEG), which increases its half-life from 2-3 to 54 hours. Allows less frequent injections

A

IFN

88
Q

Up to 1/3 of people taking IFNs must stop early due to

A

Side effects

89
Q

Dose-limiting toxicities are myelosuppression with granulocytopeniaand thrombocytopenia

A

IFN side effects

90
Q

Contraindicated for hepatic decompensation, autoimmune disease, severe heart disease, kidney disease, poorly controlled psychiatric conditions

A

IFN

91
Q

IFN reduces P450 metabolism of

A

Other drugs

92
Q

What are 2 drugs that target nucleic acid synthesis in HBV

A

Entecavir and Tenofovir

93
Q

Guanosine nucleoside analog recently approved by FDA for HBV.

-Prodrug that is tri-phosphorylated inside cells

A

Entecavir

94
Q

Drug is chain terminator for HBV RT

-Inhibits both first and second strand synthesis

A

Entecavir

95
Q

Entecavir’s distortion of DNA end blocks further

A

Synthesis

96
Q

With entecavir, with discontinuation of treatment, we have to watch for

A

Rebounding

97
Q

Resistance to entecavir requires

-Thus we have not seen much resistance yet

A

2 mutations

98
Q

Was first drug of this class for HBV and it is still in wide-spread use

A

Lamivudine

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