CSIM 1.19 Herpes Virus 1 Flashcards

1
Q

List the members of the Herpesviridae virus family

A
  • Herpes simplex virus (HSV)
    • Varicella zoster virus (VZV)
    • Cytomegalovirus (CMV)
    • Epstein Barr Virus (EBV)
    • Human Herpes Virus 6, 7 and 8 (HHV6, HHV7, HHV8)
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2
Q

Describe the virology of herpesviridae

A
  • Double-stranded DNA

* Enveloped

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3
Q

What is latency? Which virus family exhibits latency?

What can this lead to?

A

Herpesviridae
• Viral DNA persists in specific cell types lifelong without producing virus

Viral reactivation

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4
Q

Describe viral reactivation

A

Intermittent production of virus from the latent genes which may or may not be symptomatic

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5
Q

Describe the primary infection and latency pathogenesis of HSV

A
  • Herpes infects the mucosal cells lining the insie of the mouth and lips
    • This causes vesicles (PRIMARY ORAL HERPES)
    • As the immune response clears up the infection, some viral particles enter sensory nerve endings
    • The virus travels up the sensory nerve to the cell body, where the viral DNA is stored
    • This allows the virus to reactivate intermittently causing vesicles
    • The immune system will quickly respond, but not quick enough to avoid coldsores in some reactivations
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6
Q

What can cause HSV reactivation?

A
  • Immunosuppression
    • Stress
    • Menstruation
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7
Q

What is the seroprevelance of HSV 1 and 2?

A
  • HSV1 80%

* HSV2 20%

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8
Q

How is HSV transmitted?

A

Mucosal contact
• Oral
• Genital

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9
Q

Which HSV usually causes:

1) Primary oral herpes
2) Oral reactivation
3) Primary genital herpes
4) Genital reactivation

A

1) HSV 1 or 2
2) Usually HSV 1
3) HSV 1 or 2
4) Usually HSV 2

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10
Q

What are the possible complications of HSV?

A
  • Secondary bacterial infection
    • Corneal ulcers
    • Viral meningitis HSV 2
    • Herpes simplex encephalitis HSV1
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11
Q

Who are the HSV risk groups?

A
  • Neonates as there is a high mortality if untreated (dies of primary infection as it spreads from mother’s genitalia during childbirth)
    • Immunocompromised as reactivations are more frequent and severe
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12
Q

If pregnant mother has a primary HSV genital infection during childbirth what is recommended?

A

C-section

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13
Q

What us herpetic whitlow?

A

HSV lesions on fingers after viral entry through wound (e.g. bitten)

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14
Q

What is the difference between primary and initial HSV infection?

A

Primary infection:
• First infection with either HSV 1 or HSV 2

Initial infection:
• First HSV 2 infection in those who have already been infected with HSV 1, or visa versa

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15
Q

How is HSV diagnosed?

A

PCR to detect viral DNA

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16
Q

How is HSV managed?

A

Symptomatic relief

Antivirals
• Aciclovir

17
Q

Aciclovir is a prodrug. What enzyme activated it and where is this enzyme found? How does this enzyme structurally change aciclovir?

Therefore, what is the activated drug?

What does the activated drug do?

A

Thymidine kinase
• Viral enzyme only active in infected cells (thus few side effects)
• Adds a phosphate group to aciclovir
• Cellular kinases can then add 2 more phosphate groups

Aciclovir triphosphate

Inhibits viral DNA polymerase

18
Q

How is aciclovir administered?

A

5 times a day orally (due to poor oral bioavailability)

Can be given IV in severe disease such as encephalitis or in immunocompromised

19
Q

Can HSV be spread through respiratory routes?

A

No

20
Q

Describe the pathogenesis of chickenpox and shingles

A
  • Varicella Zoster Virus infection via respiratory mucosa/conjunctiva
    • Replication in regional lymph nodes
    • Primary viraemia
    • Replication in liver and spleen
    • Secondary viraemia
    • Dissemination to skin causing chickenpox lesions
    • Latency in dorsal ganglion
    • Reactivation in later life as shingles
21
Q

What is the proper name for chickenpox and shingles?

A
Chickenpox = varicella 
Shingles = zoster
22
Q

What is the prodrome of chickenpox?

Describe the distribution of rash

What type of regions are present in chickenpox?

A

Fever

Centripetal distribution (around trunk)

Order: macules->papules->vesicles->pustules

23
Q

How can smallpox lesions be differentiated from chickenpox lesions?

A

Smallpox lesions are all at the same stage, whereas chickenpox lesions are all at different stages along macules->papules->vesicles->pustules

24
Q

How is chickenpox spread?

A

Respiratory (but not with shingles)

Direct contact

25
Q

What is the average incubation of chickenpox and how long are people infectious with it?

A

14 days

Infectious from 2 days before rash to full crusting of vesicles (usually 5 days after rash start)

26
Q

What are the possible chickenpox complications?

A
  • Bacterial sepsis
    • Varicella pneumonia
    • Varicella encephalitis
27
Q

Who are the risk groups for chickenpox?

A
  • Pregnancy
    • Neonates
    • Immunocompromised
28
Q

What are the zoster (shingles) compleications?

What are the zoster risk groups?

A
  • Post herpetic neuralgia
    • Opthalmic zoster
    • Zoster encephalitis/meningitis
    • Immunocompromised patients
29
Q

Which nerve does opthalmic zoster effect?

A

Trigeminal nerve (V1)

30
Q

How is VZV diagnosed?

A

PCR to detect viral DNA

31
Q

How is VZV treated?

A

Children not treated

Adults: aciclovir

32
Q

What form of vaccine is used for varicella?

How does the zoster virus differ?

Who is this given to?

A

Live attenuated vaccine (this still becomes latent)

Identical, but 10x the dose. Given to elderly as it boosts the immunity to prevent reactivation

Given to over 70s

33
Q

Describe post-exposure prophylaxis for VZV

Who is this given to?

A

Intramuscular zoster immunoglobulin in event of

Those who have had
• Face to face contact with infected individual
• >15 mins in the same room
• AND not immune
• AND a high risk group (Pregnant, neonates, immunocompromised)

34
Q

Why do people usually only get shingles once?

A

The reactivation boosts the immune system response to that pathogen