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Antiviral Treatmen Flashcards

1
Q

How do antivirals work?

A
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2
Q

What are the two approaches of antiviral therapy?

A
  • Approach 1 – Directly Acting Antivirals / Small Molecule Inhibitors
  • Approach 2 – Immunomodulators:
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3
Q

How do the directly acting antivirals/small molecule inhibitors work? What do they target?

A
  • Viruses encode proteins for… cell entry, genomic replication/transcription, assembly and release of progeny
    • E.G. nucleic acid polymerases, proteases, integrase CCR5, terminase
    • These proteins are a target for AV-drugs (e.g. protease inhibitors, polymerase inhibitors, integrase inhibitors)
    • SMIs / DAAs block production/action of the above  inhibit viral replication or action
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4
Q

How do immunomodulators work?

A
  • Viral replication is detected by PRRs (i.e. TLRs, RIG-like receptors)  trigger innate immune responses
  • This antiviral immune response can be boosted by giving immunomodulators
    • E.G. interferon (tx HBV, HCV), IVIG (viral pneumonitis), imiquimod (HPV), steroids (HSE)
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5
Q

What are the limiting factors of antiviral therapy?

A
  • Limiting factors of antiviral therapy:
    • The natural host immune response is critical; difficulties in treating:
      • Transplant patients
      • HIV patients
    • Adherence to treatment
    • Antiviral drug resistance
    • Drug toxicity and interactions
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6
Q

How do we classify herpesvirus?

A
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7
Q

What are the stages of herpes infection?

A
  • Primary infection (e.g. chickenpox)
    • Latency - e.g. in dorsal root ganglia
    • Reactivation e.g. zoster-shingles
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8
Q

What causes chickenpox? What are the complications?

A
  • Caused by primary infection with varicella-zoster virus (VZV)
  • Uncomplicated in children
  • Susceptible to complications in adults (e.g. pneumonitis)
  • Severe disease in immunocompromised
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9
Q

What is zoster? What does it cause I the immuncompetent and immunocompromised?

A
  • •Reactivation of latent infection (dorsal root ganglia)
  • Immunocompetent
    • Dermatomal distribution
    • Complication: Post-herpetic neuralgia
  • Immunocompromised
    • Can experience multidermatomal or disseminated infection with severe complications
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10
Q

What is a prodrug?

A

A prodrug is an inactive precursor of a drug, that is metabolized into the active form within the body.

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11
Q

What antivirals used for the treatment of HSV and VZV?

A
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12
Q

What is the MOA of acyclovir?

A

AKA ‘chain terminators’

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13
Q

What does acyclovir require in order to be activated? How does It have selective activity?

A
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14
Q

How do we treat HSV encephalitis?

A
  • Immediate empirical treatment  IV Aciclovir 10mg/kg TDS (without waiting for test results)
    • I.E. 700mg TDS (for 70kg person)
      • If confirmed, treat for 14-21 days
  • Should do a repeat LP before stopping abx
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15
Q

What are the indications for tx of VZV?

A
  • Chickenpox in adults (risk of pneumonitis)
  • Zoster in adults >50 years (risk of post-herpetic neuralgia)
  • Primary infection or reactivation in an immunocompromised patient
  • Neonatal chickenpox
  • If increased risk of complications (e.g. underlying lung disease, eye involvement)
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16
Q

What are the stages of CMV virus?

A
  • Primary infection → latent in blood monocytes and dendritic cells → reactivated e.g. following immunosuppression
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17
Q

Where would CMV be in asymptomatic patients?

A

Shed in asymptomatic patients via saliva, urine, semen and cervical

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18
Q

What are the consequences of CM infection in the immunocompromised

A
  • Bone marrow suppression
  • Retinitis
  • Pneumonitis
  • Hepatitis
  • Colitis
  • Encephalitis
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19
Q
A

CMV pneumonitis

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20
Q
A

Widespread retinal exudate and haemorrhage - CMV

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21
Q
A

Owl’s eye inclusions - CMV

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22
Q

What are the MCV antiviral drugs? What route are they given by?

A
  • 1st line Gangciclovir (GCV) - IV
    • Prodrug: Valganciclovir (VGC) - PO
  • 2nd line Foscarnet (FOS) - IV/intravitreal
  • 3rd lie Cidofovir (CDV) - IV

Letermovir - recently approved

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23
Q

How does gangciclovir get activated?

A
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24
Q

How do (val/)gangciclovir work? What does it have activity against? How is it excreted? What are the indication? What are the side effects and contraindications?

A
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25
Q

How does foscarnet work? What is it effective against? How is it given? What are the indications? What are the SEs?

A
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26
Q

How does cidofivir work? What is it active against? How is ti administered= What is the indications and side effects?

A
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27
Q

What are the strategies for Treatment of CMV in Transplant Patients?

A
  • (A) TREAT established disease (GCV and reduce immunosuppression) – high mortality in HSCT
  • (B) PROPHYLAXIS with GCV/vGCV
    • Indication: solid organ transplant (i.e. renal)
    • SEs: bone marrow toxicity
  • (C) Best - PRE-EMPTIVE THERAPY with Foscarnet > GCV/vGCV
    • Indication: HSCT
    • Twice weekly monitoring for the appearance of CMV on PCR in the blood
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28
Q

How is maribavir given? What is it effective against? What is it effective against? What are the SEs?

29
Q

How is Letermovir given? What is it effective against? What is it effective against? What are the SEs? What are the interactions?

30
Q

How is EBV transmitted? What illness does it cause? What are the stages? What is it associated with?

31
Q

What is post-transplant Lymphoproliferative disease? What is it associated with? How do we diagnose and manage it?

32
Q
A

IV acyclovir

33
Q

What are the main surface proteins of influenza?

A
  • 2 main surface proteins = haemagglutinin (HA) and neuraminidase (NA)
    • HA = binding and entry into the target cell
    • NA = release of progeny virus particles from the host cell
34
Q

What are the NA inhibitors? What viruses are they effective against? when is it indicated?

A
  • Oseltamivir (Tamiflu) – ORAL
  • Zanamivir (Relenza) – Dry Powder
  • Effective against influenza A and B
  • Indications:
    • Those unwell enough to be admitted to hospital due to influenza virus-related respiratory disease
35
Q

What are the indications for NA inhibitors in the community?

36
Q

What is Peramavir? Hows it given? What is effective against? What is the resistance like to this drug?

37
Q

What is baloxavir? How is it administered? What is the MOA? What are the SEs? What is the resistance like?

38
Q

What drug combination can be used for flu?

39
Q

What does RSV cause? What is it associated with? What are the risk groups?

40
Q

What is used to manage RSV?

41
Q

What is Ribavarin? How is it administered? What does it do? What is it effective against? What re the adverse effects?

42
Q

Describe the role of IVIG in the tx of RSV?

A
  • Derived from pooled donors
  • Often used as an adjunct to treatment of viral pneumonitis in the immunocompromised
43
Q

What is Palivizumab=?What is the indication? How is it given?

44
Q

What is Nirsevimab?

A

Palivizumab-like drug

  • Extended half-wife mAB
  • Require single IM injection to provide protection for the whole winter
45
Q

What tx are used in SARS-CoV-2?

A
  • Antiviral drugs
  • Neutralising monoclonal antibodies (nabs)
  • Immunomodulators
46
Q

What are the antiviral drugs given for SARS-CoV-2?

47
Q

What are neutralising monoclonal Abs-“nMabs”?

48
Q

How do monoclonal antibodies interact with SARS-CoV-2?

49
Q

What are the immunomodulators used for SARS-CoV-2?

51
Q

What is BK Virus? When does infection tend to occur? Who does it cause a problem in?

A

BMT - bone marrow transplant

52
Q

How can hemorrhagic cystitis be treated?

A
  • If significant morbidity  Cidofovir (IV)
  • If nephrotoxicity  Cidofovir (intravesical)
    • Avoids nephrotoxicity if direct into bladder
53
Q

How should BK nephropathy be treated?

A
  • Reduce immunosuppression
  • IVIG
  • NOTE: cidofovir cannot be used because it is nephrotoxic
54
Q

Who does adenovirus cause a problem in? What does it cause? How is it treated?

55
Q

What is Brincidofovir? How is it given? What is the advantage of using it?

56
Q

What is cellular immunotherapy? What are the indications?

A
  • Adoptive immunotherapy, virus-specific cytotoxic T cells, donor lymphocyte infusion
  • Indications: CMV, adenovirus, BK virus, EBV… in transplant recipients
57
Q

What are the causes of treatment failure?

58
Q

What are the mechanisms of drug resistance?

A
  • Selection → selection of pre-existing resistant strains due to inadequate drug levels
  • Diversity → quasispecies (a population of the virus are genetically heterogenous rather than clonal)
59
Q

What are the implications of drug resistance?

A
  • Treatment failure
  • Need to use second-line drugs – less effective and often more toxic
  • Cross-resistance with other antivirals
60
Q

How do we prevents drug resistance?

A
  • Potent combination drug regimens
  • Increase adherence to treatment (i.e. lower pill burden)
61
Q

When should we test for drug resistance?

62
Q

When should we test for drug resistance?

63
Q

What are the different types of drug resistance assays?

A
  • Genotypic assays – sequencing genome  identify known drug resistance mutations:
    • For… HIV, HBV, HCV, CMV
  • Phenotypic assays – culturing in cell monolayers in presence of increasing concentrations of antiviral drugs:
    • AKA: Plaque Reduction Assay
    • For… HSV
64
Q

What causes HSV drug resistance to acyclovir? When does it occur? When should it be suspected? How should it be treated?

65
Q

What causes CMV resistance to Gangcyclovir? Who does it occur in? When should it be suspected? What is the second line for CNV tx?

66
Q

What is the most important mutation conferring resistance in influenza A (H1N1)?

A

Oseltamivir (NA inhibitor) resistance through H275Y mutation

67
Q

What are the different Ig preparations?

Microbiology (19 decks)

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