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Infectious Disease Unit 1 > Herpes Viruses > Flashcards

Herpes Viruses Flashcards

1
Q

What are the three subclasses of herpes virus and which viruses are in each?

A

Alpha:
HSV1
HSV2
VZV

Beta:
CMV
HHV6&7

Gamma:
EBV
KSHV (HHV8)

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2
Q

What are the latency reservoirs for the alpha herpes viruses?

A

HSV1 - Trigeminal Ganglion
HSV2 - Sacral Sensor Ganglion
VZV - Dorsal Root Ganglion

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3
Q

What are the characteristic diseases for the alpha herpes viruses?

A

HSV1 - Oral lesions
HSV2 - Genital lesions
VZV - Chickenpox (primary), Zoster (Reactivation)

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4
Q

What are the latency reservoirs for the beta herpes viruses?

A

CMV - CD34+ myeloid cells

HHV6&7 - B cells/myeloid progenitor cells/T cells

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5
Q

What are the characteristic diseases for the beta herpes viruses?

A

CMV - Primary: mild disease or Mononucleosis-like syndrome. Immune Compromised: systemic disease with end organ damage
HHV6&7 - Infant: Roseola. Immune Compromised: End organ damage like encephalitis, pneumonitis

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6
Q

What are the latency reservoirs for the gamma herpes viruses?

A

EBV - B cells

KSHV (HHV8) - B cells

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7
Q

What are the characteristic diseases for the gamma herpes viruses?

A

EBV - Mononucleosis, EBV associated malignancies

KSHV(HHV8) - Karposi’s sarcoma, B-cell Lymphomas

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8
Q

How stable are herpes viruses, and how do they spread?

A

Labile and easy to decontaminate or kill in the environment = spread requires close contact.

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9
Q

What is the genetic and protein structure of herpes viruses?

A

Linear DsDNA
Spherical, enveloped visions
DNA surrounded by tegument (viral proteins with some RNAs and cellular proteins used to reprogram newly infected host cell.)
In the host cell, the genome is delivered to the NUCLEUS and forms an episome (circle).

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10
Q

Where does the herpes virus gain its envelope from, and what properties does the envelope provide?

A

Envelope derived from host Golgi, coated with 10-12 surface glycoproteins important for:
cell binding,
cell-cell spread,
and immune evasion.

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11
Q

What are the three stages of viral gene expression during lytic replication?

A 
1st immediate early (IE) genes-set up environment conducive for viral replication and needed for expression of E and L genes.
2nd Early (E) genes-encode replication enzymes and nonstructural viral proteins.
3rd Late (L) genes- encode viral structural proteins needed for packaging a new virion and egress from infected cell.
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12
Q

Where in the cell does herpes DNA replication occur, what proteins are involved, and what diagnostic feature does this produce?

A

Herpesvirus DNA replication occurs in the nucleus using viral-encoded DNA polymerase and accessory viral proteins. Encapsidation of genome occurs in the nucleus. Thus, intranuclear inclusions (accumulated viral capsid proteins) are often diagnostic on histopathology for herpesvirus infection.

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13
Q

What are differences between primary and reactivation herpes infections common to all herpes viruses?

A

Most primary infections have a clinical presentation different than the disease associated with reactivation.
Primary infection results in LATENT infection in specific cells in the host.
Reactivation can be subclinical (shedding) or cause clinical disease. Both may result in spread of infection to new hosts.
Disease from reactivation is usually less severe than disease from initial infection.
Herpesvirus infection is more severe in patients with Tcell defects.

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14
Q

Describe latency in all herpesviruses

A

Small subset of viral genes expressed but no infectious particles produced

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15
Q

What is the purpose of viral glycoproteins?

A
  1. mediate cellular tropism (determines which cells the virus enters)
  2. Targets of the adaptive immune response
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16
Q

What do we use Acyclovir for?

A

Alpha herpesvirus

17
Q

What do we use gancyclovir for mainly?

A

Beta herpesviruses

18
Q

How does Acyclovir work?

A

chain terminator

Must have a thymidine kinase (betas dont)

19
Q

Inclusion bodies

A

Indicative of Herpesviral infection

Intranuclear:
HSV, VZV: Cowdry type A
CMV: owl eyes

Intranuclear and intracytoplasmic :
HHV6, CMV

20
Q

Host immune response to herpesvirus

A

Innate immune response: INF/cytokine production and NK cell activities

Adaptive immune response: neutralizing Ab, CD4+ and CD8+ t-cell functions

21
Q

How does herpesvirus evade the innate immune response?

A

Block induction of type I interferons and other cytokines

Block dendritic cell maturation

Prevent complement activation

alter NK cell functions

22
Q

How does herpesvirus evade the adaptive immune response?

A

Cytokine and chemokine mimetics and decoy receptors

Fc receptor binding proteins

Interfere with antigen presenting to t cells

23
Q

What are two important complications of HSV1 int he normal host?

A

Herpetic keratitis

HSV encephalitis

24
Q

Complications of genital herpes

A

Urethritis
Meningitis
Yeast superinfection
Perianal/perirectal disease

25
Q

HSV in the immunocompromised host

A

Severe local disease (oral or genital)
Neonatal (severe/fatal)
Important role for antiviral

26
Q

What’s the diagnostic test of choice for HSV?

A

PCR

27
Q

How is VZV transmitted and what disease does it cause?

A

Through the air: respiratory secretions
Goes to lymph node, blood, liver, spleen, skin

Chickenpox

28
Q

What population do we really worry about CMV with and give prophylaxis to?

A

transplant pts

29
Q

Diagnostic tests for CMV

A

IgM
PCR
Tissue histology

30
Q

Severe CMV in an immunocompromised host

A

Severe end organ disease + viremia

31
Q

How do we treat disseminated CMV?

A

gancyclovir

If resistant- foscarnet

32
Q

Congenital CMV infection (in utero)

A

90% are mild

10% severe: jaundice, microcephaly, enlarged liver/spleen, decreased platelets; moratlity (10-20%)

33
Q

Roseola

A

HHV6 and HHV7

Beta herpesviruses

High fever for 3-7 days
Rash appears as fever end abruptly
Rash starts on trunk and goes to face, neck, extremities

Complications: febrile seizures, end organ disease in immune compromised

Treat immunocompromised with gancyclovir

34
Q

EBV

A

Ebstein Barr Virus

gamma-herpesvirus

35
Q

EBNA1 and EBNA2

A

NA1: links viral genome to cellular chromosome
NA2: turns on other viral latent genes and cellular-activation associated genes including c-myc

36
Q

Mononucleosis

A 
EBV
Fever
Adenopathy
Pharyngitis 
Hepatosplenomegaly
Atypical lymphocytes
Heterophil antibodies (tested in monospot test)
37
Q

Anti-EBNA

A

Negative during acute infection

Positive during latency

38
Q

KSHV

A 
HHV8
Causes kaposi's sarcoma
Gamma-herpesvirus
HIV
Spread sexually

Infectious Disease Unit 1 (19 decks)

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