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Virology > Lecture 18 - Herpesviruses > Flashcards

Lecture 18 - Herpesviruses Flashcards

1
Q

Passive immune evasion strategies of persistent infections 1) 2) 3) 4)

A

1) Cell tropism is nonreplicating cells
2) Replicates in sites not exposed to the immune system (blood brain barrier, eye, luminal surface of ducts)
3) Replicates in MHC negative cells (such as neurons)
4) Can spread by cell-cell fusion

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2
Q

Active immune evasion strategies of persistent infections 1) 2) 3) 4) 5) 6)

A

1) Limit expression of viral genes
2) Non-cytopathic infection (DNA genome integration)
3) Blockade of specific immune defences (block MHC, IFN, decoy cytokine receptors)
4) Blockade of apoptosis mechanisms
5) Rapid genetic evolution
6) Immunosuppressive, anergic epitopes

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3
Q

Anergy

A

When an epitope doesn’t elicit an immune response

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4
Q

Latent infection

A

Persisting infection with long periods without any detectable infectious virus or disease

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5
Q

How many herpesviruses lead to latent infection?

A

All

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6
Q

Breadth of species that can be infected by herpesviruses

A

Virtually all species

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7
Q

Structure of herpesvirus virion 1) 2) 3) 4) 5)

A

1) gB, gN glycoproteins on envelope
2) Enveloped
3) Tegument
4) Nucleocapsid
5) Circular dsDNA genome

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8
Q

Number of herpesviruses establishing life-long latency in humans

A

Eight

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9
Q

Broad types of herpesviruses 1) 2) 3)

A

1) Alphaherpesviruses
2) Betaherpesviruses
3) Gammaherpesviruses

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10
Q

Alphaherpesviruses 1) 2)

A

1) Herpes simplex (HSV-1 and
2) Oropharyngeal and genital infections
2) Varicella-zoster virus Chickenpox and shingles

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11
Q

Betaherpesviruses 1) 2)

A

1) Cytomegalovirus Mild fever Pneumonia, chorioretinitis in immunocompromised patients
2) Human herpesvirus 6 (HHV-6) Mild rash in infants (roseola infantum)

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12
Q

Gammaherpesviruses 1) 2)

A

1) Epstein-Barr virus Infectious mononucleosis Burkitt’s lymphoma Nasopharyngeal carcinoma Immunodeficiency-related lymphoproliferative disease
2) Kaposi sarcoma virus (HHV-8)

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13
Q

Where are alphaherpesviruses persistent?

A

In neurons

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14
Q

Where are betaherpesviruses persistent?

A

Maybe in monocytes or secretory glands

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15
Q

Where are gammaherpesviruses persistent?

A

In lymphocytes

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16
Q

Length of herpesvirus genomes

A

120-240kb

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17
Q

Number of proteins that herpesviruses encode

A

Normally around 80 proteins

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18
Q

Common early genes for herpesviruses

A

Enzymes (HSV thymidine kinase) and regulatory genes (HSV host shut-off gene product)

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19
Q

What does HSV produce during latency?

A

Latency Associated Transcripts (LATs).

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20
Q

What does EBV produce during latency?

A

EBNA 1-6 proteins

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21
Q

HSV1 prevalence

A

70-90% adults seropositive

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22
Q

HSV2 prevalence

A

20-60% adults seropositive

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23
Q

CMV prevalence

A

40-100% prevalence

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24
Q

EBV prevalence

A

90% adults seropositive

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25
Q

How do herpesvirus genomes persist in cells?

A

As a circular, non-integrated DNA (episome)

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26
Q

EBV genome origins of replication 1) 2)

A

1) Ori-P (Origin of plasmid maintenance) - Used to replicate genome during latent infection of dividing B cells
2) Ori-Lyt - Used to replicate genome during lytic infection

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27
Q

Ori-P

A

EBV origin of plasmid maintenance. Used to replicate EBV genome during latent infection of dividing B cells. Binding site of EBNA-1 protein (a latent gene product).

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28
Q

HSV genome origins of replication.

A

Has both Ori-P and Ori-Lyt, which are both inactive during latency, and both active during lytic infection.

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29
Q

How do herpesviruses replicate their genomes?

A

Fork replication, rolling circle.

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30
Q

Rolling circle replication

A
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31
Q

How are concatemers formed during herpesvirus genome replication?

A

ssDNA from rolling replication has discontinous strand formed on it.

32
Q

EBV Ori-P driven infection

A

Latent replication in replicating B cells. Needs EBNA-a

33
Q

EBV Ori-L driven infection

A

Active, lytic infection

34
Q

Why doesn’t HSV need to express latent proteins, as EBV does?

A

HSV lies latent in non-replicating cells (neurons). Therefore, the episome won’t be diluted out with replication.

35
Q

Number of HSV infections that are asymptomatic

A

85-90%

36
Q

Number of HSV infections that result in lesions

A

10-15%

37
Q

Number of HSV infections that enter blood and distant organs (EG: brain)

A

Under 1%

38
Q

HSV CNS disease 1) 2) 3) 4)

A

1) Very rare (1-3000 cases per year)
2) Most common during disseminated infection of a newborn
3) 70% mortality rate. Under 2.5% achieve normal neurological function after infection.
4) Diagnosed by PCR of CSF, confirmed by viral culture.

39
Q

Where on the lip does HSV-1 normally recur?

A

Mucocutaneous junction

40
Q

Dorsal root ganglia that HSV will be latent in if initial infection is of the lip

A

Trigeminal ganglia

41
Q

Dorsal root ganglia that HSV will be latent in if initial infection is of the genitals

A

Sacral ganglia

42
Q

Size of HSV latent genome

A

150kb

43
Q

Number of people who harbour latent HSV genome

A

20%

44
Q

Number of HSV episomes per cell

A

10-100’s

45
Q

Size of HSV LATs

A

~2kb

46
Q

Type of axonal transport used by re-emerging HSV

A

Anterograde transport

47
Q

LATs 1) 2) 3)

A

1) Stable, non-translated HSV RNA transcripts 2) ~2kb 3) Processed into viRNAs

48
Q

Potential role of LATs

A

Suppress apoptosis, to maintain latency

49
Q

How is primary viremia of VZV spread?

A

In DCs

50
Q

How is secondary viremia of VZV spread?

A

In T lymphocytes

51
Q

Timeline of VZV infection

A

Day 0 - Infection of conjunctiva and/or mucosa of URT - Viral replication in regional lymph nodes Day 4-6 - Primary viremia in bloodstream (DC spread) - Further viral replication in liver and spleen - Secondary viremia (T cell spread) Day 10 - Appearance of infectious vesicular rash

52
Q

Most effective response to herpesvirus infections

A

T cell response

53
Q

Where does VZV reemerge as shingles?

A

The dermatome where the virus initially infected

54
Q

How can shingles be treated?

A

Acyclovir or other antivirals. Passive VZV MABs

55
Q

Demographic at risk of shingles

A

Elderly (associated with immune decline). Children under 5 (from incomplete T cell immunity)

56
Q

Human VZV vaccine 1) 2) 3)

A

1) Live attenuated 2) Recommended for all seropositive children after 12 months of age, booster at 10 years 3) Recommended for those at risk - teachers, health care workers

57
Q

How is EBV transmitted?

A

Direct contact with infected saliva with oropharynx

58
Q

Where does EBV-1 predominate?

A

Australia, Europe, USA

59
Q

Where is EBV-2 found?

A

EBV-1 and -2 are equally prevalent in Africa

60
Q

Where does EBV establish a productive infection?

A

Epithelial cells of the salivary glands and oropharynx

61
Q

Site of EBV latency

A

B cells

62
Q

What might EBV cause in transplant recipients?

A

B-lymphoproliferative disease

63
Q

Is EBV initial infection lytic?

A

Yes

64
Q

Does primary EBV cause a large immune response?

A

Yes

65
Q

EBV proteins expressed during latency 1) 2)

A

1) Epstein-Barr virus Nuclear Antigens (EBNA). 6 Of these proteins. 2) Latent membrane proteins (LMP). 2 of these.

66
Q

Protein involved in replication of EBV genome

A

EBNA-1

67
Q

Three types of EBV latency

A

1) 9 latent antigens expressed 2) 3 latent antigens expressed 3) Only EBNA-1 expressed during latency

68
Q

Disease associated with type 1 EBV latency

A

B-lymphoproliferative disease

69
Q

Disease associated with type 2 EBV latency

A

Hodgkins disease

70
Q

Disease associated with type 3 EBV latency

A

Burkitts lymphoma

71
Q

Type of EBV mRNA that 90% of adults have in B cells

A

EBV LMP2a mRNA present in memory B cells

72
Q

Malignancies associated with EBV reactivation

A

Hodgkins lymphoma, Burkitts lumphoma, nasopharyngeal carcinoma

73
Q

What can congenital CMV infection lead to?

A

Deafness, chorioretinitis, microencephaly

74
Q

Leading infectious cause of stillbirth

A

CMV

75
Q

How does CMV infect a foetus?

A

~30% chance of crossing placenta form mother to foetus

Virology (29 decks)

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