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Pharmacology (Semester 6) > 9.1 Anti-virals > Flashcards

9.1 Anti-virals Flashcards

1
Q

Label 1-6 of a virus lifecycle

A
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2
Q

Antiviral drugs shows the best response in which type of patients?

A

In patients with competent immune systems ➞ a healthy immune system works synergistically with drug to eliminate or suppress viral activity

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3
Q

Give 4 DNA viruses treated with anti-viral agents

A
  1. Herpes simplex I & II
  2. Varicella-zoster virus
  3. Cytomegalovirus
  4. Hepatitis B
  5. Epstein Barr Virus
  6. Human Herpes-virus 8
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4
Q

Give 4 RNA viruses treated with anti-viral agents

A
  1. Influenza
  2. Human Immunodeficiency Virus (HIV)
  3. Hepatitis C
  4. Respiratory Syncitial Virus (RSV)
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5
Q

Give 2 drugs used to treat Influenza

A
  1. Oseltamivir
  2. Zanamivir
  3. Amantadine
  4. Rimantadine
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6
Q

Give 4 Influenza-related complications

A
  1. bronchitis
  2. pneumonia
  3. sinusitis
  4. exacerbation of underlying disease
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7
Q

Give the 3 types of Influenza virus and give a feature of each

A

1) Influenza A: has multiple host species and does antigenic drift and shift
2) Influenza B: has no animal reservoir and lower mortality
3) Influenza C: common cold like flu

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8
Q

Give the 3 main surface antigens of Influenza and explain how each causes damage

A

1) Neuraminidase: glycoprotein that hydrolyses mucus on respiratory epithelia, then digests sialic acid on cell surface. Allows entry and exit of influenz into host cell
2) Hemagglutinin: attachment + membrane fusion with endosome.
3) Matrix 2: viral uncoating which releases viral RNA and proteins

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9
Q

Which part of the influenza lifecycle do vaccines target?

A

Attachement and entering of host cell

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10
Q

Give the MoA of M2 ion channel blockers

A

Blocks the ion channel function of the M2 protein of influenza A virus which Inhibits viral uncoating ➞ interferes with corresponding steps in viral life cycle

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11
Q

Give an example of an M2 ion channel blocker and which type of influenza these target

Which drug family do these belong too?

A

Amantadine and Rimantadine ➞ active against influenza A

Belong to the Tricyclic primary amines class

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12
Q

Give an example of a neuraminidase inhibitor

A

Zanamavir and Oseltamivir

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13
Q

Zanamavir is a ________. It has a ______ bioavailability and is detectable in ______ up to 24 hours post dosing. Following metabolism it is excreted ______.

A

Neuraminidase inhibitors, low, sputum, renally

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14
Q

How is Zanamivir administered and what types of influenza does it treat?

Give 2 adverse effects

A

Given via inhalation

Spectrum: Uncomplicated influenza A and B, some strains of avian influenza, H5N1

Adverse effects: nasal and throat discomfort, bronchospasm

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15
Q

What is Oseltamivir and which type of influenza does this treat

Give 2 adverse effects

A

Oseltamivir is a neuraminidase inhibitor which is a pro-drug and has 80% bioavailability

Spectrum: Infuenza A and B in children and adults, avian influenza and H5N1

Adverse effects: Nausea and vomitting, headache

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16
Q

Give the MoA of Oseltamivir

A

Cleaves terminal sialic acid residues on glycoconjugates and destroys receptors

Newly formed virions adhere to cell surface because they cannot digest sialic acid which limits spread

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17
Q

Resistance is emerging against what neuraminidase inhibitor and why?

Which drug are viruses still sensitive too?

A

Oseltamivir H1N1 resistance due to H274Y mutation around active site

Viruses generally remain zanamivir sensitive

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18
Q

Give 2 oral agents again Herpes simplex and Varicella zoster

A
  1. Aciclovir
  2. Valaciclovir
  3. Famciclovir
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19
Q

Give 2 topical agents again Herpes simplex and Varicella zoster

A

Aciclovir and Penciclovir

20
Q

Aciclovir is uptaken by infected cell where ________ phosphorylates it to acyclovir ________

Cellular enzymes then convert it to acyclovir triphosphate which competes with ________ for viral DNA polymerases

When acyclovir triphosphate incorperates into DNA it results in _________ due to the absence of a ________ group

This prevents attachment of additional nucleosides and Inactivates the viral DNA polymerase

A

VSTK (virus-specific thymidine kinase), monophosphate, dGTP, chain termination, 3’ hydroxyl

21
Q

What are the 2 types of Herpes virus?

A

HSV-1: Oral Herpes
HSV-2: Genital Herpes

22
Q

Give 2 consequences of HSV

A

Herpes encephalitis and Herpes Meningitis

23
Q

What is Mollaret’s meningitis?

A

Recurrent Herpes Meningitis

24
Q

Giveve 3 ways resistance against Aciclovir may occur

A

1) reduced or absent thymidine kinase
2) altered thymidine kinase activity resulting in decreased acyclovir phosphorylation
3) altered viral DNA polymerase with decreased affinity for acyclovir triphosphate

25
Q

Give 2 drugs used to treat Cytomegalovirus

A
  1. Ganciclovir
  2. Valganciclovir
  3. Foscarnet
  4. Cidofovir
26
Q

Does CMV always require treatment? Explain your answer

A

Primary CMV infection rarely requires treatment in immunocompetent host

However, in immunocompromised hosts re-activation of CMV can be dangerous hence requires treatment

27
Q

Compare presentation of primary vs reactivated CMV

A

Primary: usually asymptomatic or flu-like symptoms (usually goes undiagnosed)

reactivation: CMV retinitis, CMV colitis, etc…

28
Q

What is ART and explain simply what it does

What is HART?

A

Antiretroviral Treatment- aims to suppress the virus and may help to reverse some damage to the immune system. Acts by halting viral replication at various places throughout the HIV life cycle

HART: Highly active antiretroviral therapy

29
Q

What are the 3 main drugs used in ART and what is the “basic recipe”?

A

1) nucleoside reverse transcriptase inhibitors (NRTI)
2) protease inhibitors
3) Integrase inhibitors

Basic recipe = two NRTIs + one drug from a different class

30
Q

Genotypic testing is done when a new diagnosis of viral infection is made, why?

A

To test for resistance through mutations

31
Q

Give a drug used to treat Hepatitis B

A
  1. Lamivudine
  2. Entecavir
  3. Interferons
32
Q

Compare the need for treatment of acute Hep B vs chronic Hep B

A

Acute Hepatitis B rarely requires treatment

Chronic Hepatitis B may require treatment

33
Q

Give the MoA of Interferons

A

Not directly virucidal or virustatic

Induces changes in the infected or exposed cell to promote resistance to the virus and Induces several enzyme activities that promote an antiviral state

34
Q

What is SVR in terms of Hep C treatment and how is it defined?

A

SVR = Sustained virologic response

Defined as an undetectable RNA level 12 weeks following the completion of therapy

35
Q

Give 4 targets to promote an anti-viral state

A
  1. Proteins that inhibit synthesis of RNA
  2. Proteins that cleave viral DNA
  3. Proteins that inhibit mRNA
  4. Alterations of the cell membrane that inhibit the release of replicated virions
36
Q

Give a drug used to treat Hepatitis C + a new drug class used in treatment

A
  1. Drug = Ribavirin
  2. Pegylated interferon

New drug class ➞ Novel DAA’s

37
Q

What is Ribavirin?

A

A purine nucleoside analog used in the treatment of Hep C

38
Q

The MoA of Ribavirin is unclear but it is though to do what 4 things?

A
  1. causes alterations to cellular nucleotide pools
  2. inhibits viral RNA synthesis
  3. lethal mutagenesis of certain RNA viral genomes
  4. possibly acts as an analog of guanosine or xanthosine
39
Q

Explain the targets of new DDAs in treatment of Hep C

A

When inside the cell, viral polyproteins are synthesised on ER and then processed by protease such as NS3-4A which cleaves proteins (target for DDAs)

2 of these proteins are also impt targets of DDAs

  • NS5A which regulates Hep C viral RNA
  • NS5B which serves as the RNA dependant RNA polymerase
40
Q

Give the 4 classes of DDA’s

A
  1. NS3-4A protease inhibitors
  2. NS5B nucleoside polymerase inhibitors
  3. NS5B non-nucleoside polymerase inhibitors
  4. NS5A inhibitors
41
Q

Give 2 advantages of NS3-4A protease inhibitors + an example

A

low barrier to resistance and high potency varies c genotype

Example ➞ Simeprevir

42
Q

Give an example of NS5A inhibitor

A

Daclatasvir

43
Q

Give an example of NS5B nucleoside polymerase inhibitor + 2 advantages of this

A

Sofosbuvir

Advantages: moderate to high efficacy across all six genotypes and high barrier to resistance

44
Q

Give an example of NS5B nucleoside polymerase inhibitor

Give one advantage and one disadvantage of this

A

Dasabuvir

Advantages: low barrier to resistance

Disadvantage: potency varies among c genotype

45
Q

Give 2 examples of fixed dose combinations

A
  1. Elbasvir-grazoprevir
  2. Glecaprevir-pibrentasvir

Pharmacology (Semester 6) (17 decks)

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