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Week 7 - microbiology > Antivirals > Flashcards

Antivirals Flashcards

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Biology 101 flashcards
1
Q

What are the 5 key points of the virus life cycle that are targeted with antivirals?

A
  1. Attachment and penetration of the virus to the host cells
  2. Uncoating of the viral genome within the host cell
  3. Synthesis of viral components within the host cell
  4. Assembly of viral particles
  5. Release of the virus to spread and invade other cells
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2
Q

What are the 3 categories of antiviral use?

A
  • Therapeutic
  • Prophylactic
  • Pre-emptive
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3
Q

What are the 5 groups of antivirals?

A
  • Influenza antivirals
  • Herpes antivirals
  • Anti-retrovirals
  • Hepatitis antivirals
  • SARS-coV2 antivirals
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4
Q

What are the 3 main drugs for influenza treatment?

A
  • Adamantanes
  • Baloxavir marboxil
  • Neuraminidase inhibitors
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5
Q

What kind of drugs are adamantanes?

A

M2 ion channel inhibitors

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6
Q

What is the mechanism of action of the adamantanes?

A

•Inhibit the M2 ion channel which is a channel protein that maintains the pH across the viral envelope during cell entry and across the trans-golgi membrane of infected cells during viral maturation

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7
Q

Name 2 adamantanes

A
  • Amantadine

* Rimantadine

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8
Q

Name 3 neuraminidase inhibitors

A
  • Oseltamivir (tamiflu)
  • Zanamivir
  • Peramivir
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9
Q

What kind of influenza are the adamantanes effective against?

A

Influenza A only

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10
Q

What kind of influenza are the neuraminidase inhibitors effective against?

A
  • Influenza A

* Influenza B

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11
Q

What is the mechanism of action of the neuraminidase inhibitors?

A

•Targets the release of new viral particles that are made and released into the extracellular fluid

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12
Q

Explain the issues with resistance and neuraminidase inhibitors

A
  • Issue with oseltamivir in H1N1

* Variable resistance year on year depending on the dominant circulating influenza

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13
Q

What is the definition of complicated influenza?

A
  • Influenza requiring hospital admission
  • and/or signs of lower respiratory tract infection (hyperaemia, dyspnoea, lung infiltrate)
  • Central nervous system involvement
  • and/or a significant exacerbation of an underlying medical condition
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14
Q

Who are the at risks group for influenza?

A
  • Age >65
  • Chronic respiratory/cardiac/renal /liver/neurological conditions
  • diabetes
  • Immunosuppressed
  • Pregnancy
  • Morbid obesity
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15
Q

Who are the severely immunosuppressed groups?

A
  • Solid organ and bone marrow transplant
  • Patients having undergone recent chemotherapy
  • HIV with CD4 less than 200
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16
Q

What is the mechanism of action of Baloxavir marboxil?

A

Hinders mRNA synthesis by inhibiting an endonuclease that cleaves polymeric acid (viral polymerase protein) suppressing viral proliferation

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17
Q

What are the alpha herpes viruses?

A
  • Herpes simplex 1
  • Herpes simplex 2
  • Varicella zoster virus
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18
Q

What are the beta herpes viruses?

A
  • Cytomegalovirus

* HHV 6 and 7

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19
Q

What are the gamma herpes viruses?

A
  • Epstein Barr virus

* Kaposi’s sarcoma herpes virus

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20
Q

What is caused by herpes simplex 1?

A
  • Cold sores
  • Encephalitis
  • Neonatal infection
21
Q

What is caused by herpes simplex virus 2?

A
  • Genital ulcer
  • Meningitis
  • neonatal infection
22
Q

What is caused by the varicella zoster virus?

A
  • Chicken pox

* Shingles

23
Q

What is caused by cytomegalovirus?

A
  • Can just be mild or asymptomatic
  • Congenital infections
  • Severe in immunocompromised
24
Q

What are the antiherpes antivirals?

A
  • Aciclovir
  • Penciclovir
  • Ganciclovir
  • Cidofovir
  • Foscarnet
25
Q

What is the prodrug of aciclovir?

A

Valaciclovir

26
Q

What is the prodrug of Penciclovir?

A

Famciclovir

27
Q

What is the prodrug of ganciclovir?

A

Valganciclovir

28
Q

What is the mechanism of action of aciclovir?

A
  • Aciclovir within the cell is converted into active form using viral kinase (herpes thymidine kinase)
  • Aciclovir triphosphate enters into the nucleus and inserts into viral replication
  • It lacks a free hydroxyl group so viral replication cannot continue
29
Q

when should you use aciclovir?

A

Early, ideally within the prodrome/<24 hours into the illness

30
Q

What is the excretion of aciclovir?

A

Renal

31
Q

What are the toxicities of aciclovir?

A
  • Renal, crystallisation in urine -AKI

* CNS: agitation, confusion, dizziness, drowsiness

32
Q

Explain the use of aciclovir in the first episode of genital herpes

A
  • 7-10 day therapy

* Reduces symptoms and viral shedding (reducing transmission)

33
Q

Explain the use of aciclovir in the suppression of genital herpes

A
  • For 6+ episodes a year
  • Reduces clinical and viral recurrences
  • Reduces risk of transmission between sexual partners
34
Q

When should you treat oral herpes?

A
  • Immunocompromised

* Consider early/suppressive therapy in severe or frequent disease

35
Q

What are the clinical uses of aciclovir?

A
  • Genital herpes HSV 2
  • HSV encephalitis (IV)
  • Eczema herpeticum
  • Varicella zoster virus (chicken pox) if adult presents <24 hours after rash onset, especially if smoker, IV in immunocompromised
  • Herpes zoster (shingles) if<72 hours from rash onset, IV if ophthalmic shingles or secondary CNS infection
36
Q

What is the mechanism of action of ganciclovir?

A

•Competitive inhibition of viral DNA polymerase

37
Q

What is the route of administration of ganciclovir?

A

Intravenous but prodrug can be given orally

38
Q

What is the toxicity of ganciclovir?

A
  • Bone marrow toxicity
  • Carcinogenic/teratogenic
  • May cause hypospermia
39
Q

What are the clinical uses of ganciclovir?

A
  • No need in acute CMV immunocompetent host
  • use in immunocompromised patients with organ invasive CMV (e.g. retinitis, oesophagitis, colitis, pneumonia, encephalitis)
40
Q

Explain resistance to aciclovir

A
  • Alterations in thymidine kinase

* Altered viral DNA polymerase gene

41
Q

Explain resistance to Ganciclovir

A
  • Alteration in UL 97

* Alteration in DNA polymerase gene

42
Q

What is the mechanism of action of cidofovir?

A

•Competitive inhibitor of viral DNA polymerase (doesn’t require viral kinase for initial phosphorylation)

43
Q

What is the route of administration of cidofovir?

A

•IV

44
Q

What is the toxicity of cidofovir?

A
  • Significant renal toxicity
  • Neutropenia
  • May be carcinogenic or teratogenic
45
Q

What is the mechanism of action of foscarnet?

A

•Non competitive inhibitor of viral DNA polymerase

46
Q

What is the route of administration of foscarnet?

A

IV

47
Q

What is the toxicity of foscarnet?

A
  • Significant renal toxicity with electrolyte disturbances common
  • Seizure due to mineral/electrolyte disturbances
48
Q

Which antivirals target the uncoating of the virus?

A

Adamantanes

49
Q

Which antivirals target the synthesis of viral components?

A
  • Aciclovir
  • Ganciclovir
  • Cidofovir
  • foscarnet
  • Baloxavir marboxil

Week 7 - microbiology (12 decks)

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