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Arjun's PM copy-Microbiology and Infection > MI: Antivirals > Flashcards

MI: Antivirals Flashcards

1
Q

Describe two approaches to antiviral treatment.

A
  • Drugs targetting viral proteins
  • Drugs that modulate host immune response (e.g. interferon)
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2
Q

How are viral infections normally detected by the immune system?

A

Viral genetic material and proteins are detected by pattern-recognition receptors which trigger an innate immune response leading production of anti-viral cytokines (e.g. interferon)

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3
Q

List some limiting factors for antiviral therapy.

A
  • Impaired host immune response
  • Adherence to treatment
  • Antiviral drug resistance
  • Drug toxicity
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4
Q

What is a possible complication of shingles?

A

Post-herpetic neuralgia

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5
Q

How might shingles present differently in immunocompromised patients?

A

Multi-dermatomal distribution or invasive disease

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6
Q

What is the main treatment option for VZV infection?

A

Aciclovir (PO or IV)

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7
Q

Outline the mechanism of action of aciclovir.

A

It is a nucleoside (guanosine) analogue inhibits viral DNA polymerase and also blocks strand elongation (lacks 3’ OH group)

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8
Q

In which 2 ways is aciclovir specific in targeting viruses?

A
  • Requires activation by viral thymidine kinase (which is only present in host cells that are infected by the virus)
  • Has a higher affinity for viral DNA polymerase than host DNA polymerase
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9
Q

What is the prodrug of aciclovir? How does it differ from aciclovir?

A

Valaciclovir - can only be adminstered orally

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10
Q

What are two 2nd line treatment options for aciclovir-resistant HSV/VZV infection?

A
  • Foscarnet - viral DNA polymerase inhibitor
  • Cidofovir - cytidine analogue
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11
Q

HSV encephalitis is a medical emergency. How should it be treated?

A
  • IMMEDIATE treatment with IV aciclovir 10 mg/kg TDS on clinical suspicion without waiting for test results
  • If confirmed, treat for 14-21 days
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12
Q

What are symptoms of HSV encephalitis

A

Fever + confusion, seizures, altered consciousness

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13
Q

What is HSV meningitis and how should it be treated?

A

Usually self-limiting

Immunocompromised patients and those who are unwell enough to require hospital admission require treatment

  • IV aciclovir for 2-3 days followed by oral aciclovir for 10 days
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14
Q

List some indications for treatment of VZV.

A
  • Infection in adults (high risk of pneumonitis)
  • Shingles in > 50 years (risk of post-herpetic neuralgia)
  • Infection in immunocompromised patients
  • Neonatal infection
  • If increased risk of complications (e.g. underlying lung disease)
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15
Q

What is CMV?

A

Beta-herpesvirus that causes opportunistic infection in immunocompromised patients

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16
Q

In which cells does CMV lie dormant?

A

Monocyte and dendritic cells

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17
Q

List some consequences of CMV infection in immunocompromised patients.

A
  • Bone marrow suppression
  • Retinitis
  • Pneumonitis
  • Hepatitis
  • Colitis
  • Encephalitis
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18
Q

What is a characteristic histological feature of CMV infection?

A

Owl’s eye inclusion

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19
Q

What is the 1st line treatment option for CMV infection?

A

Ganciclovir (IV) and reduce immunosuppression

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20
Q

Which patient group is given ganciclovir as prophylaxis?

A

Solid-organ transplant patients

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21
Q

Describe pre-emptive therapy for CMV

A

Used for HSCT transplant patients

  • Monitoring with weekly blood CMV PCR
  • Gancicolvir/valganciclovir initiated when viral load reaches certain threshold e.g. 1000 c/ml
  • This threshold is a reached a week before the onset of disease
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22
Q

What is the mechanims of action of ganciclovir? How is it activated?

A
  • Nucleoside analogue that inhibits viral DNA polymerase and also halts chain elongation
  • Activated by viral UL97 kinase
23
Q

What is the pro-drug of ganciclovir?

A

Valganciclovir (given PO)

24
Q

What are 2nd line treatments for CMV?

A
  1. Foscarnet (IV/intravitreal)
  2. Cidofovir
  3. Maribavir
25
What is the mechanism of action of foscarnet?
* Non-competitive inhibitor of viral DNA polymerase ## Footnote NOTE: does not require activation
26
What is a major side-effect of foscarnet?
Nephrotoxicity
27
What is the mechanism of action of cidofovir?
Cytidine analogue that competitively inhibits viral DNA synthesis ## Footnote NOTE: does not require activation
28
What is a major side-effect of cidofovir?
Nephrotoxicity (requires hydration and probenecid)
29
How is CMV pneumonitis treated?
Ganciclovir with IVIG
30
What are three strategies for the treatment of CMV in transplant patients?
1. TREAT established disease 2. PROPHYLAXIS (mainly in solid organ transplant patients) 3. PRE-EMPTIVE THERAPY (for bone marrow transplant patients)
31
What is the mechanism of action of maribavir?
Inhibits viral kinase UL97 | Effective *in vitro*, currently undergoing clinical trials
32
What is the mechanism of action of letermovir? What is it used for?
- CMV DNA terminase inhibitor - Used for CMV prophylaxis in IgG-positive HSCT patients
33
In which cells does EBV cause continuous low-grade viral replication?
B cells
34
What is post-transplant lymphoproliferative disease (PTLD)?
* Polyclonal expansion of B cells associated with immunosuppression used in organ transplant * This is due to breakdown of immunosurveillance keeping the B cells and EBV in check * This predisposes to lymphoma
35
How is post-transplant lymphoproliferative disease diagnosed and treated?
Diagnosis: EBV viral load >10^5 c/ml in blood + positive biopsy Treatment * Reduce immunosuppression * Rituximab (anti-CD20)
36
What are the roles of haemagglutinin and neuraminidase in the influenza virus?
* Haemagglutinin - mediates viral binding and entry into target cell * Neuraminidase - allows release of progeny virus particles from the host cell to infect neighbouring cells
37
Name two examples of neuraminidase inhibitors.
* **Oseltamivir (Tamiflu)** - oral * Zanamivir (Relenza) - dry powder
38
What is the most common cause of bronchiolitis?
RSV
39
List three treatments for bronchiolitis and their mechanism of action
* **Ribavirin** - guanosine analogue * **IVIG** - often used as adjunct to treatment of viral pneumonitis in immunocompromised patients * **Palivizumab** - monoclonal antibody against RSV F (fusion) protein. Used for **prophylaxis** against serious infection in high-risk infants (e.g. BPD) ## Footnote No real drug against active RSV.
40
What drug is used to treat monkeypox? When is it used?
**Tecoviromat** - Severe disease - >100 lesions, encephalitis, sepsis - Anatomical concern - eye lesions, dysphagia, urinary retention - High-risk patient - immunocompromised, pregnant, paediatric
41
What is BK virus? What diseases can it cause and in which groups of patients?
A ubiquitous virus that is asymptomatic - Can cause haemorrhagic cystitis in HSCT patients - Can cause BK nephritis and ureteric stenosis in renal transplant patients
42
Outline the treatment of BK haemorrhagic cystitis.
* Bladder washouts * Reduce immunosuppression * **Cidofovir IV** (may consider intravesical)
43
Outline the treatment of BK nephropathy.
* **Reduce immunosuppression** * IVIG ## Footnote NOTE: cidofovir cannot be used because it is nephrotoxic
44
In which subgroup of patients is adenovirus a major issue?
Paediatric transplant patients - can cause disseminated disease ## Footnote Adenovirus is very common and usually causes self-limiting respiratory, GI, and conjunctival infection
45
Outline the treatment of adenovirus infection in transplant patients.
* Cidofovir IV * IVIG
46
Describe how cellular immunotherapy may be used to treat viral infection
Patient CD8 T cells are isolated then exposed to specific viral antigens, and then reinfused ## Footnote Now increasingly used as second line therapy for a range of viral infections in transplant recipients.
47
What is the main cause of antiviral drug resistance?
Inadequate drug levels
48
How can antiviral drug resistance be prevented?
* Combination drug therapy * Increasing adherence (e.g. therapies with lower pill burden) * Sequencing to identify baseline drug resistance
49
Describe two types of drug resistance assays.
* **Genotypic assay** - identify drug resistance mutations - used in **HIV** * **Phenotypic assay** - grow the virus in monolayers in the presence of increasing concentrations of antiviral drugs (plaque reduction assay) - routinely used for **HSV**
50
What are most cases of HSV drug resistance caused by?
Mutations in viral thymidine kinase
51
What are most cases of CMV drug resistance caused by?
Mutations in UL97 protein kinase gene
52
What are the main treatment options for drug resistant HSV and CMV infection?
Foscarnet and cidofovir
53
How does oseltamivir resistance occur?
Neuraminidase mutation
54
Name some pre- and post-exposure uses of antibodies?
Pre-exposure - Palivizumab - RSV bronchiolitis Post-exposure - HBV Ig - neonate - Rabies Ig - risky bite in unvaccinated - VZIG - pregancy

Arjun's PM copy-Microbiology and Infection (26 decks)

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