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MICBI - Clinical MICBI > L36 Herpesvirus > Flashcards

L36 Herpesvirus Flashcards

1
Q

Herpesviridae persists in host for life. T/F?

Briefly describe/

A

T
Primary infection > asymptomatic/symptomatic
> Latent infection (Nervous/Lymphoid)
> Reactivation (symptomatic/asymptomatic)

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2
Q

Herpesviridae has oncogenic property. Give 3 examples.

A
  1. Nasopharyngeal carcinoma HHV4 (EBV)
  2. Burkitt’s lymphoma HHV4 (EBV)
  3. Kaposi’s sarcoma HHV8 (KSV)
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3
Q

Herpesviridae can be eliminated by alcohol rub?

A

Yes, Enveloped virus
- damage by soap and water, alcoholic rub due to lipid capsule

VS
non-enveloped: adenovirus

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4
Q

Among 9 types of HHV (Human herpesviruses), which of them are of high prevelance?

A

All except
HHV2 (Herpes simplex virus type 2) and
HHV 8 Kaposi’s sarcoma-associated herpesvirus (KSHV)

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5
Q

Among 9 types of HHV (Human herpesviruses), which of them are dermatotrophic? (tend to infect the skin and cause rashes)

A

All except
HHV4 (Epstein-Barr virus)
HHV5 Human cytomegalovirus (CMV)

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6
Q

Among 9 types of HHV (Human herpesviruses), which of them are with neurolatency?
(use nerves as site of latency)

A

All except
HHV4 (Epstein-Barr virus),
HHV5 (Human cytomegalovirus,
HHV 8 Kaposi’s sarcoma-associated herpesvirus

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7
Q

Among 9 types of HHV (Human herpesviruses), which of them are with lympholatency?
(use lymphs as site of latency)

A

HHV4-HHV8

// all except 1-3

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8
Q

Herpes simplex virus 1 - Primary infection
A. Early childhood >95%
B. Transmitted by kissing - shed virus in saliva
C. Usually asymptomatic
D. Causes gingivostomatitis
E. Causes rash typically

A

E is wrong
D: in children
- Pharyngitis and tonsilitis in older
- resolves in 2-3 weeks

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9
Q

After primary infection in Herpes simplex virus 1, what happens in

  1. Latency - reside at?
  2. Reactivation - Trigger? Causes? Complication?
A
  1. Latency - reside at
    - local sensory dorsal root ganglion
    - trigeminal ganglia, brain
  2. Reactivation
    - Trigger: Stress, UV light, injury to innervated tissue, immunosuppression and non-specific triggers
    - 40-50% had herpes labialis
  • Cx: Herpes simplex encephalitis (actively damage brain)
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10
Q

Mode of transmission of Herpes simplex 2 virus?
What are the typical symptoms? (5)
Complications? (2)

A

Sexually transmitted
- more severe than oral infection

S/S

  • Fever, dysuria, pain (vesicular lesions at genitalia area)
  • Perianal, proctitis

Cx

  • aseptic meningitis
  • radiculomyelitis
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11
Q

After primary infection in Herpes simplex virus 2, what happens in

  1. Latency - reside at?
  2. Reactivation - compared to primary infection?
A
  1. Latency - reside at
    - local sensory dorsal root ganglion
    - sacral ganglia
  2. more frequent than oral infection (vesicular lesions at genitalia area);
    but fever vesicles, less painful than primary infection
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12
Q

Cause of neonatal herpes?

A

Primary HSV-2 infection or reactivation at mother > vaginal delivery

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13
Q

What is the name for HHV-3?

What infection does it cause?

A

Varicella zoster virus

- Chicken pox

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14
Q

Mode of transmission of Varicella zoster virus (HHV-3)?

A

Airborne

- only this and measles are imp airborne viruses

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15
Q

What is the clinical course of VZV primary infection? (3)

A

Chickenpox

  1. Vesicular rash starts on face > trunk > limbs (Central to peripheral)
  2. Pus due to bacterial infection
  3. More complications in adults, e.g. pneumonia, encephalitis
  • subside after 1 week
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16
Q

For Varicella Zoster virus, there is life-long latency in ______________ (site where it resides)?

What happens in reactivation Zoster?
- Chance of reactivation increases sharply after >60 years old

A

Posterior root ganglia (trigeminal, thoracic)

Reactivation zoster = Shingles

  • affects area of nerve supply
  • pain/ numbness before rash
  • severe pain may persist after healing (post-herpetic neuralgia)
17
Q

Where are the common sites for VZV reactivation - shingles/zoster (3)?

A
  1. Thoracic and lumbar T5-L2
  2. Trigeminal nerve (ophthalmic branch)
  3. Ramsay-Hunt syndrome: facial nerve palsy, geniculate ganglion VII nerve
18
Q

How can we prevent Varicella Zoster Virus infection?

A
  1. Vacccine
    - Live-attenuated vaccine, alone or combined with MMR
    - Zoster: prevent reactivation by
    > Live-attenuated/ recombinant subunit
    > recommended for >50/60 years old
  2. Immunoglobulin (HNIG, VZIG)
    - post-exposure prophylaxis for high risk patients:
    a) susceptive pregnant women/
    b) immunocompromised/
    c) neonate
19
Q

Which of the following are correct regarding the diagnosis for HSV and VZV?
A. Typical clinical presentation thus seldom requires lab investigations
B. Viral nucleic acid detection by PCR is used in CSF
C. Viral antigen detection by immunofluoresence is used
D. A good skin scrap sample is collected for IF
E. Serology is not useful due to cross-reaction between HSV and VZV

A

All of the above

EM is not used too

20
Q

Name for HHV-4?

A

Epstein-Barr virus

21
Q

Epstein-Barr virus
A. Common in young children, transmitted via saliva and genital secretions
B. Mostly asymptomatic
C. Infectious mononucleosis - fever, enlarged cervical LN is a complication
D. Primary infection can be in teenagers
E. Persistence and latency has frequent shedding at feces

A

All except E

  • Frequent shedding at oropharynx
  • Latency in B lymphocytes
22
Q

For presistence and latency in Epstein-Barr virus, reactivation will occur in which 2 groups of patients?

Malignant diseases related?

A
  1. Immunocompromised
  2. Lymphoproliferative disorder

Malignancies

  • NPC
  • Burkitt’s lymphoma
  • HL
  • Gastric carcinoma
  • NHL
23
Q

How is EBV diagnosed in:

  1. Infectious mononucleosis in primary infection
  2. Lymphoproliferative disease in immunocompromised
  3. NPC ?
A
  1. Infectious mononucleosis in primary infection
    - EBV VCA (viral caspid Ag) IgM
    - Monospot test: heterophile Ab test
  2. Lymphoproliferative disease in immunocompromised
    - Histology (definitive)
    - EBV DNA viral load
  3. NPC
    - Histology (definitive)
    - EBV IgA
    - Plasma EBV DNA
24
Q

HHV-5 name?

A

Cytomegalovirus

25
Q

Primary CMV infection in infants:
A. Very common
B. Contact at vaginal delivery, breast milk, saliva, urine
C. Always asymptomatic
D. Causes hepatomegaly, hepatitis, pneumonitis in adults
E. In-utero infection may cause hearing and eye sight problem

A

D is wrong: should be in pre-mature infants
Adults: mostly asymptomatic, occasionally with infectious mononucleosis

E: outcome depends on primary infection/ reactivation in mother

26
Q

CMV persistence: frequent shedding from?

Latency at?

A

Salivary glands and kidneys ;
Latency: hematopoietic progenitors

> transmission: blood transfusion, organ transplant
reactivation: opportunistic infection in immunocompromised

27
Q

CMV causes serious diseases in immunocompromised patients.
What patients?
What disease?

A

AIDS, transplant recipients, autoimmune disease, immune-suppressive therapy

  • Retinitis, enteritis, hepatitis, pneumonitis
28
Q

What is the problem of CMV-status mismatch in transplant/transfusion?
e.g. CMV IgG+ donor to CMV IgG- recipient

How to prevent?

A

Primary infection in immunocompromised: more severe disease than reactivation

  • Should do CMV- to -, + to +
  • should use leukocyte depleted blood
29
Q

CMV infection = CMV disease? T/F?

A

F

  • isolation of CMV does not mean suffering from disease
  • from tissue with pathology gives a better correlation but still not definitive
30
Q

In pregnant women and immunocompromised patients, primary infection is more serious than reactivation. T/F?

A

T

  • there is no reliable test to differentiate the 2
  • CMV IgM and 4 fold rise in Ab occur in both
  • A prior serum to prove CMV IgG-ve to confirm primary infection

(Appreciate the difficulty to diagnose CMV, dont jump to CMV + conclusion and give treatment, as it is quite toxic)

31
Q

HHV-6 = human herpesvirus type 6
A. affected 90% of us from 6 months to 2 years old
B. transmitted via saliva
C. Exanthem subitem: high fever > rash
D. Febrile convulsion, hepatitis, lymphadenitis
E. Persistence and Latency at B lymphocytes

A

E is wrong
T lymphocytes and brain

EBV is B lymphocytes

32
Q

HHV-7
A. Infection occurs later than HHV-6
B. Symptoms similar to HHV-6 to less frequently symptomatic
C. Less well-defined association with reactivation in immunocompromised patients
D. Similar epidemiology and clinical picture

A

All of the above

33
Q

HHV-8
A. T-lymphotrophic
B. KS (Kaposi’s sarcoma) in AIDS is more common in MSM
C. KS in HIV-ve are more common in Mediterranean elderly men, immunosuppression in transplant
D. All KS subtypes are associated with HHV-8
E. Virus is found in breast milk and saliva in endemic areas

A

All except A

should be B lymphotrophic

34
Q

In endemic area: HHV-8
A. Has both sexual and non-sexual route of transmission
B. infection occurs in adults

A

B is wrong (should be non-endemic area)

infections occurs in early age, slowly increase with age

35
Q

Persistence = presence of virus in the body

Latent VS chronic?

A

Latent: presence of virus in an inactive site
Chronic: presence of virus with active replication

MICBI - Clinical MICBI (19 decks)

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