Antiviral Agent Flashcards

1
Q

How do viruses work

A
  1. Binding and fusion of virus w/ host cell
  2. Penetration-uncoating and release of genetic material
  3. Insertion into host genome via integrase
  4. Genome replication
  5. Expression of viral proteins and protein processing
  6. Assembly of virus in host cell
  7. Release of virus from host

Viruses are obligate intracellular pathogens

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2
Q

Types of viral genome replication

Examples of each

A

DNA→DNA→mRNA

DNA pol

Herpes, CMV, varicella

DNA→RNA→DRNA

DNA pol, RNA dep DNA pol

HBV

+RNA→mRNA

HCV, HAV

-RNA→mRNA, +RNA template

RNA dep RNA pol

RSV, ebola

+RNA→DNA→+RNA

Reverse transcriptase

HIV

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3
Q

Viral infections

A

Many not life threatening

Some only show up when damage has been done-untreatable until damage is done (polio, resp. viruses)

Best tx for preventing/limiting viral inf is immunization (polio, MMR, smallpox, HPV)

Chronic viral inf. that can be treated:

  • Herpes
  • Varicella zoster
  • CMV
  • RSV
  • Influenza
  • HIV
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4
Q

What drugs are used to treat herpes infections?

A

Ciclovirs

Cyclovirs

Cidofovir

Foscarnet

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5
Q

Acyclovir

A

Antiviral drug

Tx: Herpes simplex and zoster

Mech: Incorporated into DNA and inh. viral DNA pol

Prodrug-must be phosphorylated by viral kinase

Only occurs in active cells

Much higher affinity for viral DNA pol

Route: IV and oral (not well absorbed though)

SE:

  • GI upset
  • Renal damage
  • CNS problems
    • Delerium when given IV
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6
Q

Valacyclovir

A

Antiviral drug

Tx: Herpes simplex and zoster

Mech: Prodrug converted to acyclovir

Must be given orally-prodrug metab. by 1st pass metab.

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7
Q

Famciclovir

A

Antiviral agent

Tx: herpes simplex and zoster

Mech: prodrug converted to acyclovir analog

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8
Q

Ganciclovir

A

Antiviral agent

Tx: CMV (herpes virus)

CMV→retinitis+ blindness

Mech: Inhibits viral DNA pol

Prodrug-activated by viral kinase

SE:

  • Neutropenia
  • Thrombocytopenia
  • Teratogen
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9
Q

Valganciclovir

A

Antiviral agent

Tx: CMV (herpes virus)

CMV→retinitis+ blindness

Mech: Inhibits viral DNA pol

Prodrug-converted to ganciclovir by viral kinase

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10
Q

Cidofovir

A

Antiviral agent

Tx: CMV (herpes virus)

CMV→retinitis+ blindness

Mech: Inhibits viral DNA pol

Prodrug-converted by host kinase

Used if resistance has occured so that host cells convert prodrug

SE: Renal damage

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11
Q

Foscarnet

A

Antiviral agent

Tx: CMV (herpes virus)

CMV→retinitis+ blindness

Mech: Inhibits viral DNA pol

Not a prodrug–directly inh. DNA pol

Route: IV 3x/day

SE: Renal damage

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12
Q

Agents used to treat Hep B

Names and mech

A

LATTE:

Lamivudine

Adefovir

Telbivudine

Tenofovir

Entecavir

Mech: Inh. Hep B reverse transcriptase

  • I HRT LATTE*
  • Inh. hep B rev. trans.–LATTE*
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13
Q

Lamivudine

A

Antiviral agent

Tx: Hep B

Mech: Inh. Hep B reverse transcriptase

Discontinuation→Increase hepatitis symptoms

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14
Q

Adefovir

A

Antiviral agent

Tx: Hep B

Mech: Inh. Hep B reverse transcriptase

SE: Liver and renal damage

Discontinuation→Increase hepatitis symptoms

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15
Q

Telbivudine

A

Antiviral agent

Tx: Hep B

Mech: Inh. Hep B reverse transcriptase

SE:

  • Lactic acidosis
  • Hepatomegaly

Discontinuation→Increase hepatitis symptoms

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16
Q

Tenofovir

A

Antiviral agent

Tx: Hep B

Mech: Inh. Hep B reverse transcriptase

SE:

  • Lactic acidosis
  • Hepatomegaly

Discontinuation→Increase hepatitis symptoms

17
Q

Entecavir

A

Antiviral agent

Tx: Hep B

Mech: Inh. Hep B reverse transcriptase

SE:

  • Lactic acidosis
  • Hepatomegaly

Discontinuation→Increase hepatitis symptoms

18
Q

Ribavirin

A

Antiviral agent

Tx: RNA virus (RSV)

Only for severe lower resp inf.

Mech: Inh RNA dep DNA pol

Phosphorylated in cell.

SE:

  • Preg cat X
  • Hemolytic anemia
  • Decrease pulmonary fxn in infants
  • Cardiac arrest

Not used much anymore. Very expensive

19
Q

Palivizumab

A

Antiviral agent

Tx: RNA virus (RSV)

Mech: vs antigenic site of RSV–blocks fusion of virus w/ target

Only used prophylactically

20
Q

Amantadine

A

Antiviral agent

Tx: RNA virus (Influenza A virus)

Virus taken up by cell endosome→opens channel in endosome→H enters→virus can release genes

Mech: Blocks process by which H channel forms in endosome

Blocks transporter or ion channel

Used proph. or very early

SE:

  • Renal failure
  • Teratogen
  • CNS fx
    • Dizziness
    • Slurred speech
    • Confusion
    • Seizures
    • Nausea
21
Q

Rimantadine

A

Antiviral agent

Tx: RNA virus (Influenza A virus)

Virus taken up by cell endosome→opens channel in endosome→H enters→virus can release genes

Mech: Blocks process by which H channel forms in endosome

Blocks transporter or ion channel

Used proph. or very early

Widespread resistance

SE: Fewer than amantidine but similar SE

  • Renal failure
  • Teratogen
  • CNS fx
    • Dizziness
    • Slurred speech
    • Confusion
    • Seizures
    • Nausea
22
Q

-amivir

A

Zanamivir

Oseltamivir

Antiviral agent

Tx: Influenza A+B virus (RNA virus)

Virus leaves cell and is attached by tether of neuraminic acid

Release of virus requires neuraminidase

Mech: Neuraminidase inh.

So virus cannot be released from cell and spread

SE:

  • Nausea
  • Diarrhea
  • Psychosis
  • Hallucinations
  • Zanamivir is a powder that must be inhaled so asthma issues

Only shorten influenza by about a day

23
Q

Recombinant interferon alpha

A

Antiviral agent

Tx: Hepatitis virus (esp Hep C)

Cytokine w/ multiple mech

Mech:

  • Immunostimulant
  • Inh. mRNA processing
  • Decrese viral synth

SE:

  • Fatigue
  • Flu-like symptoms
  • Depression
  • Hypertensino
  • Retinopathy
  • Myelosuppression→fewer platelets, granulocytes, etc.
24
Q

-previr

A

Boceprevir

Telaprevir

Simeprevir

Antiviral agent

Tx: Hepatitis virus (esp Hep C)

Mech: HCV protease inh.

Virus makes proteins but cannot be processed to final stage

Used in comb. w/ interferon

25
Q

Sofosbuvir

A

Antiviral agent

Tx: Hepatitis virus (esp Hep C)

Mech: Inh HCV RNA dep RNA pol

Ledipasvir+Sofosbuvir=harvoni

26
Q

Ledipasvir

A

Antiviral agent

Tx: Hepatitis virus (esp Hep C)

Mech: Binds to and inh. protein thats necessary for HCV replication

Ledipasvir+Sofosbuvir=harvoni

27
Q

Harvoni

A

DOC for HCV

Ledipasvir+sofosbuvir

28
Q

Nucleoside analog reverse transcriptase inh (NRTIs)

A

DAZLES T

Didanosine

Abacavir

Zidovudine

Lamivudine

Emtricitabine

Stavudine

Telbivudine

(Tenefovir=nucleoTide analog of RT inh)

**Nucleotides do not have to be processed like nucleosides* *

Tx: HIV

Mech: Inh reverse transcriptase

Nucleoside analog–competetive inh.

Phosphorylated in cell

SE:

  • Life threatening hepatomegaly
  • Systemic lactic acidosis
  • Anemia
  • Myopathy
  • Pancreatitis
  • Some neuropathy
  • Daves got flow*
  • DAVE PHLOA*

Didanosine

Abacavir

Vudine

Emtricitabine

Pancreatitis

Hepatomegaly

Lactic acidosis

-Opathy (retin- +my-)

Anemia

29
Q

Non nucleoside analog reverse transcriptase inh (NNRTIs)

1st gen

A

Nevirapine

Delavirdine

Efavirenz

Tx: HIV

Mech: Bind to non-active sites on reverse trans.

Non competetive inh.

30
Q

Non nucleoside analog reverse transcriptase inh (NNRTIs)

2nd gen

A

Etravirine

Rilpivirine

Tx: HIV

Mech: Bind to non-active sites on reverse trans.

Non competetive inh.

Differ from 1st gen:

  • Higher potency
  • Longer T1/2
  • Fewer SE
31
Q

Nevirapine

A

Antiviral agent

Tx: HIV

Mech: bind to non active sites and Inh reverse trans

Not competetive inh.

1st gen NNRTI

SE

  • Hepatotoxicity
  • Stevens Johnson syndrome
32
Q

Delavirdine

A

Antiviral agent

Tx: HIV

Mech: bind to non active sites and Inh reverse trans

Not competetive inh.

Not as effective

1st gen NNRTI

SE

  • Hepatotoxicity
  • Stevens Johnson syndrome
  • P450 inh.
33
Q

Efavirenz

A

Antiviral agent

Tx: HIV

Mech: bind to non active sites and Inh reverse trans

Not competetive inh.

1st gen NNRTI

SE

  • CNS- so some people crush it up and smoke it
    • hallucinations
    • memory loss
  • Rash
  • Smoke EFavirenz to get EFfed up*
  • hallucinations and mem loss*
34
Q

-virine

A

Etravirine

Rilpivirine

Antiviral agent

Tx: HIV

Mech: bind to non active sites and Inh reverse trans

Not competetive inh.

2nd gen NNRTI

Differ from first gen:

  • Higher potency
  • Longer T1/2
  • Fewer SE
35
Q

-navir

A

Antiviral agent

Tx: HIV

Mech: Protease inh.

Prevent formation of active viral proteins from their peptide precursor

Most inh. P450

Some are absorbed poorly via oral route and 18 capsules must be taken/day

Ritonavir is most potent known P450 inh so it is given w/ the poorly absorbed protease inh to avoid taking so many

Ritonavir given w/: SALTD

  • Saquinavir
  • Atazanavir
  • Lopinavir
  • Tipranavir
  • Darunavir

SE:

  • Alter fat distribution
    • Loss of fat in face and limbs
    • Gain fait in gut, chest, and back
  • Increase diabetes
  • Some have sulfur groups→allergies
    • Tipranavir
    • Fosamprenavir
36
Q

Enfuvirtide

A

Tx: HIV

Mech: binds to specific site on virus that binds to target

Fusion inhibitor

SE: Insomnia

37
Q

Maraviroc

A

Tx: HIV

Mech: Blocks binding site on macrophage preventing entry of virus

Fusion inhibitor

SE:

  • Hepatotoxicity
  • Allergies
  • Increase MI
38
Q

-gravir

A

Tx: HIV

Mech: Inh. HIV-1 integrase

Inh. insertion of viral genome into human

Prevents propagation

39
Q

HAART

A

Highly Active Anti Retroviral Therapy

Protease inh

NRTI

NNRTI