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Antivirals Flashcards

1
Q

Classes of Antivirals

A

– Hepatitis inhibitors
– Non‐nucleoside reverse transcriptase inhibitors
– HIV protease inhibitors
– Fusion/Entry
– Integration inhibitors.

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2
Q

Antiherpes/CMV Drug list

A
  • Acyclovir
  • Ganciclovir
  • Foscarnet
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3
Q

Antihepatitis Drug List

A
  • Interferons
  • Ribavirin
  • Simepravir
  • Sofosbuvir
  • Ledipasvir/Sofosbuvir
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4
Q

Anti-influenza

A

• Amantidine, Oseltamivir, Zanamivir

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5
Q

Inhibition of Viral DNA polymerase

A
  1. acyclovir
  2. vidarabine
  3. foscarent
  4. ganciclovir
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6
Q

DNA structure

A

base + sugar = nucleoside
base + sugar + phosphate = nucleotide

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7
Q

Herpes simplex virus agens

A

Acyclovir
*guanosine look alike

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8
Q

Antiherpes MOA

A

Hase to undergo 3 phosphorylations . . .
inhibits polymerization and causes chain termination.

Competes with deoxyGTP and competitively inhibits viral DNA polymerase, therefore no DNA synthesis.

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9
Q

What is the first step for the MOA of Acyclovir?

A

Metabolically activated via 3 phosphorylations. Initial
phosphorylation occurs by viral thymidine kinase

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10
Q

Acyclovir ADME

A

– May be administered topically and via i.v.
(unique to acyclovir)
– Diffuses into most tissues/body fluids including CSF

The earlier in the infection that you take it, the better.

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11
Q

Acyclovir is a first-line agent against:

A

Herpes simplex encephalitis

neonatal HSV

severe HSV or

VZV infections

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12
Q

Main acyclovir TOXICITIES

A

neuro and renal toxicity

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13
Q

Acyclovir mechanism of resistance

A

Alteration (mutation) in viral thymidine kinase or viral _DNA
polymerase_ (Primary mechanism)
– Cross resistant to valacyclovir, famciclovir, ganciclovir

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14
Q

Acyclovir resistance can be treated with:

A

Foscarnet (doesn’t require viral phosphorylation)

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15
Q

Anti CMV agents

A
  • Ganciclovir
  • Foscarnet
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16
Q

Ganciclovir MOA

A

Acyclic guanosine analog (requires tri‐phosphorylation similar to acyclovir), first phosphorylation cataylzed by CMV kinase

Active against: CMV (100x > acyclovir)

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17
Q

What is the main toxicity of Ganciclovir?

A

Myelosuppression

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18
Q

When is the treatment of CMV related to transplant?

A

Used as treatment/prophylaxis for CMV post‐transplantation

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19
Q

Foscarnet MOA

A

Inhibits Viral DNA polymerase, RNA polymerase, HIV RT. No activation required!!!!

Looks like phosphate

Useful in strains resistant to acyclovir

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20
Q

Foscarnet Administration

A

IV only!!!!

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21
Q

Foscarnet TOXICITIES

A
  • Renal toxicity
  • Hyperphosphatemia, hypokalemia/calcemia/magnesemia
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22
Q

AntiHepatitis Agents

A
  • *Ribavarin**
  • *Pegylated (Peg) Interferon**

HCV Protease Inhibitors **not HIV*

Simeprevir (Olysio)

HCV Polymerase Inhibitors
Sofosbuvir (Solvadi)
Sofosbuvir/Ledipasvir (Harvoni)

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23
Q

How do the interferons work?

A

Pegylated forms = LONG half lives! (once per week injection)
antiviral

immunomodulatory (boosts immunity)

antiproliferative actions

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24
Q

How does INterferon work?

A

Interferon alpha

_ Induces_ intracellular signals leading to _inhibition of viral
penetration/translation/transcription/protein
processing/maturation_, and release
↑ major histocompatibility complex antigens

↑ phagocytic activity of macrophages
↑ the proliferation and survival of cytotoxic T cells.
Has direct effect on virus as well

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25
Q

What are the toxicities of alpha interferon?

A

“flu-like symptoms”
= biggest downfall

abortifacent

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26
Q

Ribavirin (HCV)

A

Guanosine analog that is phosphorylated intracellularly . Blocks capping of viral mRNA _inhibits viral RNA‐dependent
polymerase_
*Can be used in combination with interferon

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27
Q

Ribavarin (HCV) Toxicities

A

Hemolytic anemia

teratogenic

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28
Q

How is Simeprevir used?

A 
Oral use in **_combination w/peginterferon alfa and ribavirin to treat HCV_**
genotype 1  (Standard of care, 24‐48 weeks)
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29
Q

Simeprevir MOA

A

Protease inhibitor: Targets NS3/4A protease

30
Q

Simeprevir toxicities

A

P‐glycoprotein transporter/CYP3A4 inhibitors/substrates =

Rx‐Rx interactions (rosuvastatin/atorvastatin)

31
Q

What is the most effective drug for HCV?

A

Sofosbuvir

32
Q

Sofosbuvir MOA

A

RNA‐dependent NS5B RNA Polymerase inhibitor.

33
Q

What’s special about Sofosbuvir?

A

Activity against all HCV genotypes (1‐6) AND those resistant to PIs. Use in combo with w/peginterferon alfa and ribavirin

34
Q

What are Sofosbuvir Toxicities?

A

P‐glycoprotein transporter substrate, contraindicated with P‐gp inducers (rifampin). $1,000 per pill!!!!!!

35
Q

Ledipsavir/Sofosbuvir

A

Inhibits NS5A protein which impacts replication (interacts with NS5B), assembly, release and host cell function

36
Q

Ledipsavir/Sofosbuvir Effectiveness

A

Activity against all HCV genotypes (1‐6) AND those resistant to PIs. 99% SVR!! FDA approved combo without peg or ribavarin.

37
Q

When do you give anti-influenza agents?

A

Quicly, withing 48 hrs of onset of symptoms

38
Q

How do Tamiflu and Relenza work?

A

Oseltamivir (Tamiflu,oral) and zanamivir (Relenza, inhalation)
– Neuraminidase inhibitors: Analogs of sialic acid = inhibit release

39
Q

Tamiflu and Relenza Targets

A

Activity against influenza A and B. Zanamivir is useful against oseltamivir‐resistant strains

40
Q

Anti-retroviral

Non-Nucleoside/Nucleotide RTI

A
  1. Abacavir
  2. Tenofovir
  3. Lamivudine/Emtricitibine
  4. Efavirenz

Don’t wanna b LATE!!

41
Q

Antiretroviral
HIV protease inhibitors

A
  1. Ritonavir
  2. Darunavir
  3. Atazanavir
42
Q

Antiretroviral

Fusion, entry, and integration inhibitors

A
  1. Enfuvirtide
  2. Maraviroc
  3. Dolutegravir
43
Q

How do proviruses enter a cell?

A
  1. Bind to **CD4/Chemokine **receptors
  2. Fuse with cell, uncoating
  3. Synthesize dsDNA copy of
    ssRNA genome by RT
  4. Translocate to nucleus
  5. Integrate into DNA
  6. Transcribe/Translate viral
    proteins (by cell)
  7. Assemble new virions
    = Proteolytically “mature” virus
44
Q

Why are retroviruses prone to resistance?

A

Retroviral replication ERROR PRONE = Increased mutation frequency

45
Q

What is Cobicistat used for?

A

CYP3A4 inhibitor therefore increases bioavailability of other drugs

46
Q

Combo THERAPY

A

Standard of care. Drugs are selected based on patient’s strain resistance: Genotype strain for mutations in RT and protease genes.

47
Q

Nucleoside reverse transcriptase inhibitors

(NRTIs)

A

Competitive inhibition of RT
– Incorporation into viral DNA. Activated by cellular phosphorylation to triphosphate

48
Q

Why is there usually resistance to NRTIS?

A

Mutations in viral RT

49
Q

What is an example of NRTIs?

A

Zidovudine/AZT

50
Q

NRTI Toxicity

A

_ Lactic acidosis w/hepatic steatosis_ – life‐
threatening
– Due to NRTI‐mediated inhibition of mitochondrial function **Build‐up of triglycerides = hepatic steatosis

51
Q

Abacavir Toxicities

A

Myocardial infarction

_Hypersensitivity reactions _

52
Q

Who should not receive Abacavir?

A

_Individuals with HLA‐B*5701_ or a reaction should NEVER receive abacavir!!!!

53
Q

Lamivudine & Emtricitabine

A

Used in HBV treatment (inhibits HBV RT)
Emtricitabine = fluorinated analog of lamivudine = long t½
= once‐daily dosing

54
Q

Tenofovir

A

nucleotide analog of adenosine. Competitively inhibits HIV RT = chain termination after incorporation into DNA

55
Q

How is Tenofivir Administered?

A

Tenofovir is co‐administered with emtricitabine as a first‐line
RTI backbone therapy

56
Q

Tenofivir Toxicity

A

Renal Accumulation: Tubular necrosis, Renal failure, Fanconi’s
Syndrome

57
Q

Non‐nucleoside Reverse Transcriptase Inhibitors

(NNRTIs)

A

Efavirenz

Bind directly to HIV‐1 reverse transcriptase and inhibit RNA‐ and DNA‐dependent DNA polymerase activity
• Binding site of NNRTIs is distinct from that of NRTIs (allosteric)

58
Q

DDIs with NNRTs!

A

Extensive metabolism/induction via P450 (CYP3A4) pathway = drug‐drug interactions (limits use in HAART)

59
Q

Efavirenz

A

Half life is DAYS!!!

Toxicity: Nightmares/Psychiatric disturbances (at start
of therapy, then resolve)

60
Q

HIV protease inhibitors

A

Pepitdomimetics. Metabolized by, inhibitors of CYP3A4 (drug interactions)

61
Q

HIV protease inhibitors TOXICITIES

A

– Lipodystrophy
– ↑ triglycerides/LDL

62
Q

PI: Ritonavir

A

Inhibitor of CYP3A4 =
used with other PIs to ↑
their serum levels= less
frequent dosing, more
tolerability (“BOOSTING”)

↑ triglycerides/LDL, elevated serum
aminotransferase
levels

63
Q

Atazanavir

A

Concurrent use with antacids block absorption

64
Q

Darunavir

A

Don’t give with sulfa allergy!!!

65
Q

Lopinavir

A

Only available as a fixed dose combo w/ritonavir

ritonavir Inhibits CYP3A4 = ↑ lopinavir blood levels

66
Q

Entry Inhibitors

A

Maraviroc: Binds selectively to CCR5

67
Q

When is Maraviroc used?

A

Used in HIV‐1 strains resistant to other drugs

68
Q

Enfuvirtide

A

Binds to gp41 s

– Sub‐cutaneous injection (peptide)

Only for treatment experienced HIV patients
w/ongoing HIV replication

69
Q

Integrase Strand TransferInhibitors (INSTIs)

“gravir”

A

Dolutegravir: Inhibits viral DNA strand integration in host genome

*effective in INSTI resistance

70
Q

Treatment Targets

Pharmacology (9 decks)

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