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Pharmacology > Antiviral Drugs > Flashcards

Antiviral Drugs Flashcards

1
Q

What are come of the biological characteristics of viruses?

A
  • obligate intracellular parasites
  • no cell wall or plasma membrane
  • no metabolism- so tough to target
  • few drugs block reproduction selectivity
  • pharmacology focused on late symptoms
  • few virus groups can be effectively treated with drugs
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2
Q

What are the cytopathic effects of viruses?

A
  • host cell metabolism is hijacked
  • there is a viral induced suppression of host homeostasis
  • viral proteins induce lysis or apoptosis
  • viral proteins trigger hose IS
  • inflammatory reaction kills host
  • ** all involve the lytic cycle- generation of new virus
    • virus can become latent- the host cell survives
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3
Q

Describe the characteristics of Herpes simplex virus

A
  • neurotrophic
  • complex dsDNA viruses- at least 8 members
  • HSV-1 is cold sores, and HSV-2 is genital herpes
  • chicken pox (varicella zoster) is an example of this, shingles and cyclomegalovirus as well
  • transmitted by close contacts
  • latent infection
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4
Q

What is the life cycle of the HSV?

A
  • lytic cycle in epithelial cells - 80 genes in a cascade
  • viral progeny spread to sensory neurons
  • retrogradely transported to the cell body
  • latent- circular episomal DNA (nucleosome)
  • no immune signature
  • no cytotoxic effect
  • stress related reactivation
  • anterograde transport
  • shingles - varicella zoster, rash and pain ( neuralgia)
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5
Q

What is the replication process of herpes simplex virus?

A
  • viral DNA enters the nucleus and circularizes
  • immediate early genes- use host RNA polymerase (2-4 hr post infection)
  • host transcription factors
  • VP16 viral activator
  • binds host cell factor that activates OCT1 (host)
  • IEG trigger early genes
  • E proteins control viral DNA replication
  • DNA replication initiates late genes- viral structure and assembly
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6
Q

What is the main antiviral drug that is used to treat HSV? How does it work?

A
  • main antiviral is acyclovir
  • synthetic nucleoside analog
  • viral thymidine kinase converts to acyclo-GMP
  • Acyclo-GTP inhibitor of viral DNA polymerase
  • viral DNA chain termination
  • treatment of genital herpes, shingles, cold sores and chicken pox
  • oral or intravenous
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7
Q

What is famciclovir used to treat?

A

HSV-1, HSV-2, and VSC - prodrug of 6-deoxypenciclovir. 1st pass metabolism converts to penciclovir

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8
Q

What is penciclovir and what is it used to treat?

A

guanosine analog, used to tx HSV. Topical formulation

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9
Q

What is docosanol and what is it used to treat?

A

inhibitor of fusion of HSV-1 virus with host cell- topical formulation

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10
Q

Cyclomegalovirus is a major problem in _______ patients

A

immunocompromised

organ transplantation

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11
Q

CMV can lead to what?

A

liver failure, colitis and retinitis (inflammation of the retina)

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12
Q

What is ganciclovir and how does it work?

A
  • used to treat CMV
  • analog of acyclovir: x 20-100 more effective against CMV
  • targets specific protein kinase phosphotransferase UL97
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13
Q

What is valganciclovir and how does it work?

A
  • used to treat CMV
  • prodrug of ganciclovir
  • oral admin
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14
Q

What is foscarnet and how does it work?

A
  • used to treat CMV
  • reversible inhibitor of viral DNA/RNA polymerases
  • CMV infection and resistant HSV, range of SE
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15
Q

What family of virus family does HIV fall under?

A

retrovirus family - (+) sRNA virus

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16
Q

What makes HIV so infective?

A
  • has a fast replication and can infect multiple times (there can be multiple viruses going into one cell)
  • reverse transcriptase - error prone- can lead to drug resistance
  • latent infection- via viral integrase enzyme
  • can lead to AIDS
  • spreads via blood/fluid transfer (HIV viruses completely integrate into the DNA cells- can be used to transfer DNA from one cell to another one)
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17
Q

What kind of cells does HIV invade?

A

helper T cells, as well as macrophages and dendritic cells

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18
Q

What are the targets of HIV once they get into the helper cells and macrophages?

A
  • targets are CD4 receptors and chemokine co-receptors (CCR5 and CCR4)
  • loss of CD4+ cells
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19
Q

What is lost when HIV invades helper T cells and macrophages ?

A

cell mediated immunity is lost

-90% of patients progress to AIDS within 10-15 years

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20
Q

What is the origin of HIV in NA?

A
  • started by eating monkey meat- this is the way that HIV first spread to humans , as it originated from monkeys
  • a single individual from haiti visited africa and transferred the virus back to haiti
  • haiti has dirty blood donating programs- transferred the blood amongst the haitian people
  • american visitors came to haiti, got infected, and transferred it back to the US
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21
Q

Nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs) are analogs of what part of the cell?

A

native ribosides- they lack the 3’ hydroxyl

- gets incorporated into viral DNA once phosphorylated to triphosphate by hose enzymes

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22
Q

The lack of the 3’ hydroxyl leads to what?

A

DNA chain termination

- the drug affinity is more than the HIV reverse transcriptase

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23
Q

Why is there toxicity associated with NRTIs?

A

due to inhibition of mitochondrial DNA polymerase

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24
Q

What does HAART stand for?

A

highly active anti-retroviral therapy

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25
Q

Zidovudine treats what and is an analog of what nucleotide?

A
  • tx HIV
  • pyrimidine analog, converted to triphosphate by cellular enzymes
  • good penetration across BBB
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26
Q

How is zidovudine toxic to bone marrow?

A
  • inhibits DNA polymerase- gamma in mitochondria
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27
Q

What is abacavir? (NRTIs)

A
  • guanosine analog- t1/2 1.5 hr
  • resistance develops slowly
  • hypersensitivity reactions can be severe. Higher risk of MI
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28
Q

What is lamivudine? (NRTIs)

A
  • cytosine analogue
  • good bioavailability and unaffected by food
  • t1/2 is 2.5 hr
  • recommended in pregnant women
  • inhibits RT in HIV and HBV
  • does not inhibit tDNA or bone marrow
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29
Q

What is emtricitabine? (NRTIs)

A

fluor-derivative of lamivudine- inhibits RT in HIV and HBV - long intracellular half life of 39 hr makes OD tx feasible. Good bioavailability and unaffected by food

30
Q

What is tenofovir? (NRTIs)

A

acyclic analogue of adenosine. Long half life allows OD dosing. GI complaints and renal dysfunction contraindicated

31
Q

What is the action of non nucleoside/nucleotide reverse transcriptase inhibitors (NNRTIs)

A
  • non competitive inhibitors if HIV-1 reverse transcriptase
  • no activation required
  • no effect on bone marrow or mitochondrial DNA polymerase
32
Q

What is efavirenz (NNRTIs)

A
  • once daily tx w/o food

- metabolized by CYP3A4 and CYP2B6. CNS SE. Some severe, such as psychosis. Skin rash. Avoid in pregnancy. Indued CYP3A4

33
Q

What is nevirapine (NNRTIs)

A
  • good oral bioavailablilty and not food dependent
  • metabolized by CYP3A isoforms. Recommended in pregnancy. Severe rash can occur. Liver toxicity. Can induce CYP 3A4 system
34
Q

HIV protease inhibitors reversibly inhibit what?

A

HIV aspartyl protease

  • also prevents proteolysis of viral polyprotein
  • prevents maturation of viral particles
  • non-infectious virus produced
35
Q

What are the pharmacokinetics of HIV protease inhibitors?

A
  • poor oral bioavailability
  • substrates for CYP 3A4 isozyme of cut p450
  • substrates for P-glycoprotein multidrug efflux pump in endothelial cells of the brain - restricts access to CNS
  • binds to plasma PRO - alpha1 acid glycoprotein
36
Q

What are the adverse effects of HIV protease inhibitors?

A
  • parasthesia, nausea, vomiting and diarrhea
  • diabetes phenotype
  • fat redistribution
37
Q

What are the most common adverse effects associated with lopinavir?

A

GI adverse effects are the most common

38
Q

What are the most common adverse effects of ritonavir?

A
  • diarrhea, nausea, taste perversion, vomiting, anemia, increased hepatic enzymes, increased triglycerides
  • required refrigeration, takes with meals
39
Q

What are the drug interactions of HIV proteases inhibitors associated with?

A
  • associated with the inhibition of CYP isozymes
40
Q

What is the mechanism of action of HIV integrate inhibitors?

A

the inhibitors block the ability of the integrates to integrate into the host DNA

41
Q

What is dolutegravir? (HIV integrate strand transfer inhibitors)

A

metabolized by UGT1A1 and CYP3A. Inhibits renal transported OCT2 and so contraindicated with dofetilide and metformin. Rash and hypersensitivity can form

42
Q

What is raltegravir (HIV integrase strand transfer inhibitors)

A

metabolized by UGT1A1. Does not interact with the Cytp450 system. Antacids should be used with caution. Severe hypersensitivity and rash can occur
- this is the most common one

43
Q

What is the viral fusion inhibitor class of HIV drugs?

A
  • enfuvirtide is an example
  • HIV protein gp41 mediates cell fusion
  • 36 amino acid peptide binds to p41
  • given subcutaneously
  • used typically as salvage therapy - for multi drug resistant HIV
44
Q

How does maraviroc work?

A
  • specifically binds to host CCR5 (V3 loop)- this it is only effective against HIV-1 tropic for CCR5.
  • contraindicated in renal impairment. Caution required with hepatic problems- substrate for CYP3A4. Resistance linked to mutations in gp120 protein
45
Q

What is flu A carried in?

A

aquatic birds and domestic birds

46
Q

What is more severe - flu A or B?

A

Flu B

47
Q

Why is influenza resistant to drugs?

A

there is no RNS proof reading

48
Q

Influenza is a ____ virus

A

(-) ssRNA

49
Q

Influenza virus attacks ____

A

epithelial cells

50
Q

Hemagglutinin (Hag) binds to _____ sugars on cells

A

sailic acid

51
Q

Neuramidase cleaves ____ residues to release the virus

A

sailic

52
Q

What does the protein channel M2 modulate?

A

pH

53
Q

Describe the influenza virus life cycle?

A
  • Hag binds to cell surface
  • Mediates endocytosis of the particle
  • M2 regulates uncoating
  • M2 also controls Hag processing
  • Release of particles from buds requires neuraminidase
54
Q

What enzyme is viral neuraminidase?

A

glycoside hydrolase enzyme

55
Q

Zanamivir (inhale), oseltamivir (oral) - works effectively as a ____ treatment against the spread of infection in flu A and B. What is the main problem with this however?

A

prophylaxis

- main problem is that it needs to be taken within 6-12 hours after contact with the virus

56
Q

What are the 2 drugs that act as inhibitors of viral uncoating?

A

amantadine and rimantadine

57
Q

What is the action of inhibitors of viral uncoating?

A
  • block the M2 channel
  • precent acidification of viral particle
  • stop release of viral genome and uncoating
  • early therapy is effective against influenza A
58
Q

What are the potential complications of the hepatitis B virus?

A
  • hepatitis, cirrhosis, and carcinoma
59
Q

Hepatitis B is a dsDNA virus, but still used ______

A

reverse transcriptase

60
Q

How is hepatitis B transferred?

A

blood-blood transfer

61
Q

What happens to the DNA of the hepatitis B virus if the infection becomes persistent ?

A

get a covalently closed circular DNA

62
Q

Hepatitis C is a _____ virus

A

(-) ssRNA

63
Q

What is the transmission of hepatitis C?

A

blood-blood transmission

treats only those with a chronic infection

64
Q

What is interferon treatment used for? How does it work?

A
  • used for a chronic hepatitis infection only
  • interferon alpha 2a/2b
  • raises cell resistance - antiviral state
  • innate induction of interferon by high levels of dsRNA or foreign RNA
  • elevates MHC1- presentation of cytotoxic CD8 T cells
  • increases p53- leading to apoptosis
65
Q

What drug class is typically used as an anti-HBV drug?

A

nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs)

66
Q

What does NRTIs do to the the HBV virus?

A

causes DNA chain termination

67
Q

What are the 2 NRTIs that are used to treat HBV? What is it usually combined with?

A
  • lamivudine, tenofovir

- typically combined with interferons

68
Q

What is the standard therapy as an anti-HCV drug? How does it work?

A
  • ribavirin is the standard therapy in combination with peg interferon alpha
  • inhibits capping of viral mRNA and viral RNA dependent RNA polymerase - also inhibits HIV and influenza
69
Q

How do protease inhibitors act against HCV? What are the two drugs that fall into this class?

A
  • inhibits NS3/4A protease that cleaves HCV- encoded poly-proteins
  • there are numerous SE and interactions with other drugs that are metabolized by CYP 3A
  • examples are boceprevir and telaprevir
70
Q

What is the main polymerase inhibitor that is used to treat HCV? How does it work?

A
  • sofosbuvir

- inhibits HCV NS5B RNA-dependent RNA polymerase, Combined with ribavirin and peg interferon alfa. Very expensive

Pharmacology (23 decks)

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