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MIMM 324 > 18. Herpesvirus 2 > Flashcards

18. Herpesvirus 2 Flashcards

1
Q

oncogenic EBV - 3 types

A
  1. many animal herpesviruses are oncogenic
  2. African Burkitt’s lymphoma
  3. Nasopharyngeal carcinoma in East Asian people
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2
Q

example of oncogenic animal herpesvirus

A

Marek’s disease virus in chickens –> must vaccinate chickens

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3
Q

indication of burkitt’s lymphoma and nasopharyngeal carcinoma

A

both are positive for episomal EBV DNA and EBV-specific antigens

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4
Q

is EBV infection required for malignancy?

A

yes, but infection alone will not cause malignancy

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5
Q

what 2 other things contribute to malignancy of EBV

A
  1. genetics
  2. Malaria
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6
Q

what happens in infectious mono?

A

polyclonal increase in both B and T lymphocytes

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7
Q

what happens early in mono?

A

B/T ratio = 4:1

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8
Q

why are there more B cells early in mono?

A

EBV infects and transforms B cells which become immortal in vitro and can produce human monoclonal antibodies

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9
Q

what happens later in mono?

A

T/B ratio = 4:1

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10
Q

why are there more T cells later in mono?

A

cytotoxic lymphocytes kill EBV-infected B cells

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11
Q

what happens normally with EBV-induced infectious mononucleosis?

A

normally, polyclonal B cell lymphocytic leukemia lymphoma which can be controlled by immune system

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12
Q

what happens with EBV infection in ppl with severe T cell defects or organ transplant patients?

A

can manifest as progressive B cell lymphoproliferative disease which behaves like lymphomas

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13
Q

when does EBV infection occur in organ transplant patients and treatment

A

normally occurs long after transplant –> can only treat by stopping immunosuppressive drugs

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14
Q

describe attachment of HSV to cell surface

A

NON-SPECIFIC btwn proteoglycans of cell surface and virus glycoprotein C

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15
Q

how does HSV enter the cell?

A

fusion

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16
Q

what happens once HSV fuses into cell?

A

viral capsid migrates to nuclear pores along cellular microtubules with cellular transport machinery

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17
Q

how does HSV genome enter nucleus?

A

viral DNA is injected thru a pore while capsid proteins remain in cytoplasm

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18
Q

does HSV encode its own RNA pol?

A

yes, part of late gene

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19
Q

are herpes viruses old or young? age?

A

OLD –> 400 million years old

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20
Q

where are herpes virus found?

A

EVERYWHERE! and many different types

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21
Q

do herpes viruses insert their genome into host genome?

A

normally no, but very few can!

22
Q

what is herpes virus integration called?

A

STRATEGIC SOMATIC GENOME INTEGRATION

23
Q

what is strange about herpes virus?

A

that we haven’t found an endogenous herpes virus

24
Q

describe primary infection

A

infection is seen in lips
- virus can then travel thru sensory neurons with long axis to trigeminal ganglion

25
Q

describe recurrent infection

A

reactivation of virus, travels retrograde along axon to initial site of infection

26
Q

where does latent infection and reactivation occur?

A

in sensory neurons

27
Q

describe how virus becomes latent (5 steps)

A
  1. virus enters neurons at periphery and genome travels up axon to neuronal nucleus
  2. virus replications and destroys some neurons, but most neurons survive
  3. viral genome as an EPISOME becomes associated with host histones and forms MINI-CHROMOSOMES
  4. viral gene expression remains absent during latent infection
  5. some latent infected neurons express a HSV transcript
28
Q

what is LAT?

A

Latency Associated Transcript –> encoded in repeat regions of genome

29
Q

describe how LAT contributes to latency

A
  • LAT domain transcribed to RNA
  • 2kb intron is spliced
  • this intron is stable in nucleus of neuron and persists as circular RNA (lariat)
30
Q

does LAT involve expression of protein?

A

no

31
Q

describe the experiment with rabbits about the function of LAT

A

compared trigeminal ganglia of rabbits infected by WT HSV1 vs rabbits infected by HSV1 without LAT
- no LAT = lots of apoptosis!

32
Q

describe the experiment with introducing LAT gene in cells

A

in primary human lung cells, monkey kidney cells, murine neuroblastoma cells –> introducing LAT protects cells from apoptosis

33
Q

does the reactivation event involve killing neurons?

A

unknown

34
Q

how does the frequency of reactivation change with time?

A

most evidence suggests it decreases

35
Q

does chromosomal integration always happen?

A

no –> rare event, only in <0.1% of infected cells

36
Q

describe integration in HHV6

A

normally hard to detect chromosomal integration, but in HHV6, integrated virus is transmitted thru gametes so offspring have viral copy in every cell

37
Q

what do we know about consequences of herpesvirus integration?

A

unknown

38
Q

what directly AND indirectly affect latency and reactivation?

A

cytokines and inflammatory state of host

39
Q

effects of IL-4/IL-13 and IFN

A

transcription factors downstream of these cytokines may have direct effects on ORF 50 of MHV68

40
Q

3 other ways that immune system may affect reactivation/latency?
how?

A
  1. altered autophagy in macrophages
  2. altered HOIL-1 expression
  3. M2 expression in B cells

by affecting host inflammation

41
Q

how can other infections change the latency/reactivation of herpesvirus?

A

if there’s a co-infection that changes inflammatory state, this might affect latency/reactivation

42
Q

what happens when KSHV-infected cell line was treated with IL-4

A

IL-4 treatment of KSHV-infected cell induced production of viral genome and lytic transcripts

43
Q

what is HOIL-1 deficiency associated with?

A

hyper inflammation and mild immunodeficiency

44
Q

what happens when HOIL-1-deficient mice are infected with MHV68?

A

hyperinflammation

45
Q

what does latent infection with MHV68 in HOIL-1-deficient mice lead to?

A

latent MHV68 protects the HOIL-1-deficient mice from otherwise lethal bacterial infection

46
Q

describe how herpesvirus infections affect disease caused by HOIL-1 deficiency

A

disease caused by HOIL-1 deficiency may be modified by presence of chronic herpes infection –> therefore there is variability btwn ppl with same immunodeficiency and diff ppl

47
Q

what is unknown about herpes and inflammation?

A

is the systemic inflammation induced by herpes really inflammation or is it the normal, basal state of the immune system?

48
Q

how can inflammation induced by herpes indicate a basal level of inflammation?

A

if >90% of the human population is infected with herpesvirus, the inflammation caused by virus may reflect the basal inflammation level

49
Q

3 treatments for herpesvirus

A
  1. acyclovir
  2. famiciclovir
  3. valacyclovir
50
Q

how do herpesvirus treatments work? 3 steps

A
  • mimic GUANOSINE
  1. drug gets phosphorylated in cells with HSV thymidine kinase
  2. but host kinases cannot phosphorylate it
  3. acts as chain terminator and binds more tightly to DNA pol to inhibit it

MIMM 324 (37 decks)

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