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Year 3 - Clinical Science and Professionalism > Antiviral agents > Flashcards

Antiviral agents Flashcards

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1
Q

What is the difference between antiviral agents and antibacterial agents

A

Antiviral agents are more specific to one virus or one specific group of viruses whereas antibacterial are usually wide acting

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2
Q

list ways of how antiviral therapies work

A
  • Most of them block the enzyme
  • Some work by blocking the receptor to the ligand
  • block membrane fusion
  • uncoating blocked
  • replication of DNA/RNA
  • escape from the vacuole blocked
  • integration of DNA into the genome blocked
  • assembly and maturation of visions
  • escape from the host cell blocked
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3
Q

What is the most effective anti viral or anti disease treatment

A

Immunisation

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4
Q

name ways to enhance the immune response

A
  • Immunisation

- Interferon

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5
Q

describe how to enhance the immune response

A
  • Immunisation enhances antibody interaction with viruses extracellularly and CD8 T lymphocyte killing of infected cells
  • Interferon (human cytokine) upregulates the immune responses and upregulates intracellular suspicion of viral DNA/RNA
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6
Q

List the drugs that are effective against herpes virus

A
  • Aciclovir
  • Valaciclovir
  • Ganciclovir
  • Valganciclvoir
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7
Q

what is one of the most effective drugs in terms of the therapeutic ratio for herpes virus

A
  • Aciclovir

- Valaciclovir

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8
Q

What is aciclovir effective against

A

herpes simplex virus 1

herpes simplex virus 2,

herpes zoster

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9
Q

describe the structure of aciclovir

A
  • Guanosine analogue (acyclo-gaunosine, a partial nucleoside analogue)
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10
Q

describe how aciclovir works

A
  • It is converted by the viral enzyme, thymidine kinase to the monophosphate acylco-GMP and then by a human cellular enzyme to the triphosphate
  • the triphosphate then inhibits the action of the viral DNA polymerase by causing chain termination when incorporated into the growing chain
  • the triphosphate is attracted to the viral DNA polymerase more than the human one therefore it attacks the virus and not the human cells
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11
Q

Why does the aciclovir have a high therapeutic ratio

A
  • As the viral thymidine kinase is 3000x more effective at converting acyclo-guanosine to the monophosphate than the cellular thymidine kinase, & the viral DNA polymerase is much more effective in incorporating the triphosphate into the growing DNA chain than the cellular DNA polymerase, it has a very high therapeutic ratio
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12
Q

how can aciclovir be administered

A

admistered topically, orally, IV

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13
Q

out of aciclovir and valaciclovir which one is best to give orally

A

valaciclovir

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14
Q

describe the structure of valaciclovir

A
  • Valaciclovir is ester linked to valine
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15
Q

how does resistance occur to aciclovir and valaciclovir

A
  • Resistance occurs to these drugs via mutation of the viral thymidine kinase or DNA polymerase
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16
Q

what are the side effects fo aciclovir and valaciclovir

A
  • Psychiatric adverse effects are reported such as cotards syndrome where person thinks there dead,
  • toxicity due to overdose manifests such as lethargy, confusion and myoclonus
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17
Q

what are Ganciclovir and Valganciclvoir active against

A
  • These are active against cytomegalovirus.
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18
Q

describe the structure of ganciclovir

A
  • Ganciclovir is a synthetic analogue of deoxyguanosine
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19
Q

describe how ganciclovir and valganciclovir works

A
  • Ganciclovir is a synthetic analogue of deoxyguanosine, which is phosphorylated to the monophosphate by a CMV thymidine kinase, & then to the triphosphate by cellular kinases.
  • This inhibits the viral DNA polymerase more than the cellular DNA polymerase, by being incorporated & therefore acts as a chain terminator
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20
Q

describe the structure of valganciclovir

A
  • Valganciclovir is a valine ester of ganciclovir

- has greater oral bioavailability

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21
Q

what are the side effects of ganciclovir and valganciclovir

A

Both have adverse effects including bone marrow suppression

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22
Q

Name drugs that are effective against retroviruses

A
  • Nucleoside analogues (Lamivudine)
  • Nucleotide analogues (Tenofovir)
  • Non nucleoside/nucelotide reverse transcriptase inhibitors (Efavirenz)
  • Protease inhibitors (Darunavir, ritonavir)
  • Integrase inhibitors
  • fusion inhibitors
  • Entry inhibitors
  • Drug combinations
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23
Q

How do nucleoside and nucleotide analogues work

A

inhibit reverse transcriptase by being

incorporated into growing DNA chain & then being unable to link to the subsequent base.

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24
Q

name an example for a nucleoside analogues

A
  • Lamivudine
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25
Q

what are the adverse effects of nucleoside analogues

A 
Nausea
fatigue
headaches
diarrhoea
cough
pro-inflammatory response,
gives rise to autoimmunity. – of lamivudine
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26
Q

how many phosphorylations do nucleoside analogues need

A

require three phosphorylations for incorporation.

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27
Q

How many phosphorylations do nucleotide analogues need

A

only need two phosphorylation’s to be incorporated.

28
Q

Give an example of nucleotide analogue

A
  • Tenofovir - analogue of adenosine monophosphate
29
Q

What are adverse effects of nucleotide analogue

A

These are rare:

  • Renal insufficiency,
  • Fanconi syndrome
30
Q

How do non nucleoside/nucleotide reverse transcriptase inhibitors work

A
  • These bind to Reverse transcriptase enzyme not at the active site, hamper its activity by distortion but not my mimicking a nucleoside or a nucleotide
31
Q

Give an example of a nucleoside/nucelotide reverse transcriptase inhibitor

A
  • Efavirenz
32
Q

How do protease inhibitors work

A
  • Act by binding to viral protease that cuts viral precursor proteins into the components of virion structure.
  • Without this taking place it cannot mature to a virion therefore if this is inhibited the virus cannot mature
33
Q

Name examples of protease inhibitors

A
  • Darunavir

- Ritonavir

34
Q

different protease inhibitors are used in …

A
  • Note that different protease inhibitors are used in treatment of hepatitis C, though ritonavir inhibits their metabolism also (preserves them)
35
Q

How do integrase inhibitors work

A
  • Inhibit integrase, a viral enzyme that mediates integration of the HIV DNA (produced by reverse transcription) into the host genome
36
Q

What does integrase usually do

A

a viral enzyme that mediates integration of the HIV DNA (produced by reverse transcription) into the host genome

37
Q

How do fusion inhibitors work

A
  • Block gp41 on the surface of the HIV virion.
  • Gp 41 mediates fusion between the HIV envelope & the cell membrane. So by blocking this you block entry into the cell
38
Q

How do entry inhibitors work

A
  • Block CCR5 (a chemokine) receptor on the surface of the cell, which, together with CD4, enables gp 120 on the surface of the HIV virion to bind to the cell & gain entry.
  • GP120 binds to CD4 and CCR5 to gain entry to the cell
39
Q

what drug combinations do you usually use for anti retroviral therapy

A
  • Usually two nucleoside/nucleotide reverse transcriptase inhibitors, plus something else. Eg tenofovir + emtricitabine, or abacovir + lamivudine, PLUS a third drug.
  • This third drug might be an integrase inhibitor (raltegravir, elvitegravir, dolutegravir or bictegravir). This is now the preferred option.
  • Or a Protease inhibitor (PI) (darunavir, atazanavir; boosted with ritonvavir, cobicistat).
  • Or a Non-nucleoside reverse transcriptase inhibitor (doravirine, efavirenz, rilpivirine).
40
Q

what combination of anti retroviral therapy can be used if tenofovir nor abacovir can be used

A

if neither tenofovir nor abacovir can be used because of adverse effects or resistance, an integrase inhibitor plus a boosted PI, or a boosted PI plus lamivudine, or an integrase inhibitor plus lamivudine can be used.

41
Q

Name some drugs used in HIV prophylaxis

A
  • Pre-exposure Prophylaxis (PrEP)
42
Q

Who is PrEP used for

A
  • For people with sexual practices likely to expose them to HIV.
43
Q

what anti virals are present in PrEP

A
  • Tenofovir (nucleotide analogue) plus emtricitabine (nucleoside reverse-transcriptase inhibitor) is usually used, combined into single daily pill.
44
Q

what are the steps you should take if you are exposed to body fluids or a needle stick injury

A
  • Infection unlikely. Needlestick most likely, then splash of body fluid onto mucosa, lastly splash of body fluid onto intact skin: this last has never been implicated in transmission.
  • Wash with antiseptic or fluid appropriate to body part.
  • Tenfovir, emtricitabine, PLUS dolutegravir or raltegravir. 28 day course.
45
Q

What antivirals should you take if you have a needle stick injury

A
  • Tenfovir, emtricitabine, PLUS dolutegravir or raltegravir. 28 day course.
46
Q

What kind of anti viral drug is ribavirin

A
  • Guanosine analogue (ie an RNA precursor analogue).

Ribo-nucleoside analogue

47
Q

what does ribavirin (ribo-nuceloside analogue do)

A
  • Inhibitor of viral RNA-dependent RNA polymerase: incorporated into new RNA chain, will not link, terminates chain
48
Q

What viruses does ribavirin treat

A

Effective against RNA viruses including

  • Hep C
  • Viral haemorrhage fevers
  • RSV
  • Influenza
  • some DNA viruses such as herpes viruses
49
Q

what are the adverse effects of ribavirin

A
  • haemolytic anaemia
  • bone marrow suppression,
  • psychiatric side effects - depression
  • cough
50
Q

name drugs that are used in the treatment of influenza

A
  • Neurominidase inhibitors
  • M2 inhibitors
  • Ribavirin
51
Q

how do Neuraminidase inhibitors work

A
  • Viral neuraminidase (on surface of virion) cleaves sialic acid from glycoprotein, allowing release of virion from host cell, prevents aggregation of virions, & reduces viral inactivation by host mucus. Neurominidase inhibitors prevent all this.
52
Q

Give some example of Neuraminidase inhibitors

A
  • Oseltamivir

- Zanamivir

53
Q

What do M2 inhibitors do

A
  • Inhibit M2 protein of virus to decrease hydrogen ion influx.
  • Inhibits uncoating & recoating. – older drugs and not as effective
54
Q

What are drugs used in hepatitis C

A

DAAs - direct acting antivirals

  • Protease inhibitors
  • NS5A inhibitors
  • NS5B inhibitors
55
Q

Describe how protease inhibitors work against Hep C

A

Inhibit viral NS3/4A serine protease.

- Tenofovir is not active against Hepatitis C protease, but it does boost the above drugs by blocking metabolism.

56
Q

Describe how NS5A inhibitors work

A

NS5A is a viral protein which enables assembly - therefore they block this

57
Q

describe how NS5B inhibitors work

A

NS5B is a viral RNA-dependent RNA polymerase - therefore they block this

58
Q

what is first line for Hep C and what is Second line

A

First line = DAAs: protease inhibitors, NS5A and NS5B inhibitors in various combinations.

Second line = Ribavirin is only used as second line therapy if first line fails, and interferon is hardly used at all.

59
Q

how long do you take drugs for Hep C

A

usually 12 weeks

– success rates of over 90% lasting indefinitely

60
Q

what do you have to consider when using treatment for Hep C

A
  • Is there liver damage: deranged LFTs, fibrosis, cirrhosis, carcinoma? Have they had a transplant, or is a transplant being considered?
  • Are there manifestations outside liver, eg cryoglobulinaemia (globins that crystallise in the cold), or kidney damage (glomerulonephritis)?
  • Are they positive for Hepatitis B &/or HIV? – this can affect the treatment you give
  • Are they drinking alcohol? Are they using marihuana or iv recreational drugs? Which genotype do they have (1-6, and 1 is subdivided into 1a & 1b)
  • Have they had previous treatment which failed, either with old drugs (ribavirin plus interferon) or with DAAs?
61
Q

List the types of drugs that are used in the treatment of Hep B

A
  • Reverse transcriptase inhibitors
  • Interferon
  • ## Pegylated interferon
62
Q

describe how reverse transcriptase inhibitors are used

A
  • Lamivudine, tenofovir
  • Virion contains DNA, enters the cell and will be integrated into the genome, transcribed into RNA which is transibed into protein, to make new virions you need more DNA, therefore it reverse transcribes the RNA
63
Q

describe how pegylated interferon works

A
  • Hepatitis B is a hepadnavirus: a DNA virus that uses reverse transcriptase in its fife cycle, hence the usefulness of reverse transcriptase inhibitors.
  • It integrates its genome into host cells’ genomes, thus cannot be completely elimininated.
  • However, can be rendered DNA, surface and core antigen negative.
64
Q

What can you use for treatment of RSV

A
  • Monoclonal antibody against RSV fusion glycoprotein.(Palivizumab)
  • Ribavirine, given by inhalation.
65
Q

What does RSV cause

A
  • RSV causes a wheeze bronchiolitis
66
Q

What is the treatment of Ebola virus

A
  • Monoclonal antibodies blocking docking on are available and effective.
67
Q

What is the treatment of corona virus

A
  • Remdesavir, an inhibitor of RNA-dependent RNA polymerase, possibly has some effect.

Year 3 - Clinical Science and Professionalism (32 decks)

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