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MIIM2002 - 2 > Herpesviridae > Flashcards

Herpesviridae Flashcards

1
Q

Features of herpesviridae

A 
Large viruses (100 - 110nM)
Icosahedral
Enveloped
Double stranded DNA genome
Encode a large variety of proteins
All members can remain latent in the host
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2
Q

Diseases caused by members of Herpesviridae

A

Chickenpox (VZV)
Glandular fever (EBV)
Roseola infantum (HHV-6)
Kaposi’s sarcoma (HHV-8)

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3
Q

Size of herpesvirus genome

A

~300kb

Normal virus genome ~100kb

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4
Q

Herpesviridae causing genital herpes and cold sores

A

Herpes simplex virus serotypes 1 and 2

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5
Q

Features of both herpes simplex viruses 1 and 2

A

Cause cold sores, genital herpes

Can go systemic and cause meningoencephalitis, encephalitis

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6
Q

Target cells of HSV

A

Epithelial cells, fibroblasts, macrophages

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7
Q

How can HSV infect skin?

A

If keratin layer is defective

If skin is damaged

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8
Q

Role of glycoproteins gpB and gpC

A

On HSV envelope surface
Bind receptors on target cell
Not sufficient for entry

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9
Q

Surface glycoproteins on HSV envelope that aid cell entry

A

gpB, gpC

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10
Q

Ligands of gpB, gpC

A

Heparan sulphate

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11
Q

How does HSV enter host cell?

A

gpB and gpC binding to ligands triggers fusion of envelope with host cell membrane
Allows nucleocapsid to enter host cytoplasm

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12
Q 
HSV replication in epithelial cells
1)
2)
3)
4)
5)
6)
7)
8)
A

1) Binding and membrane fusion
2) Release of capsid into cytoplasm, capsid translocation
3) Early genes and mRNA
4) Early proteins (thymidine kinase, DNA polymerase, ICP47)
5) DNA synthesis
6) Late genes and structural proteins
7) Assembly
8) Release

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13
Q

Effects of HSV infection

A

Cell death, virus release

Vesicle, ulcer formation (or asymptomatic)

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14
Q

Diseases caused by HSV-1

A

GsK CHEM

Gingivostomatitis
Keratoconjunctivitis 
Cold sores
Hepatic whitlow
Encephalitis
Meningoenchephalitis
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15
Q

Proportion of the population that are antibody-positive to HSV

A

70-80%

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16
Q

Proportion of population that are asymptomatically secreting at any one time

A

~1%

17
Q

Diseases predominantly caused by HSV-2

A

Genital herpes, neonatal herpes

18
Q

Cross-reactivity between antibodies for HSV-1 and HSV-2

A

Partial

19
Q

Proportion of population antibody positive for HSV-2

A

12.5-25%

20
Q

Proportion of population asymptomatically secreting HSV-2

A

3%

21
Q

Dorsal root ganglia in which HSV-1 normally reside

A

Trigeminal ganglia

22
Q

Dorsal root ganglia in which HSV-2 normally reside

A

Sacral ganglia

23
Q

In what form does HSV exist in the dorsal root ganglia?

A

As an episome

24
Q

How does an HSV infection progress to encephalitis or meningoencephalitis?

A

Migrates to dorsal root ganglia
From here, enters CNS
HSV very effective at killing host cells

25
Q

How does HSV establish latency?

A

Infects epithelial cells, lyses them
Virions infect axons
Virions moved via axonal transport to dorsal root ganglia

26
Q

What does HSV do during latency?

A

Genome circularises to form an episome
Few viral genes are expressed
Latency-activated transcript RNAs are produced, but no gene product
Some products of early genes are seen in human trigeminal cells

27
Q

Does latency stimulate an immune response?

A

Yes

Large numbers of memory CD4 and CD8, chemokines and cytokines associated with infected ganglia

28
Q 
Innate defences induced by HSV infection
1)
2)
3)
4)
A

1) Infected epithelial cells release IFN beta
2) MFs and DCs have PAMP-PRR interations, Release IFN gamma
3) IFN beta and gamma protect uninfected cells from infection, induce influx/activation of NKs
4) NKs lyse infected cells

29
Q

ICP47 role

A

Inhibits presentation on MHCI

30
Q 
Adaptive immune response to HSV infection
1)
2)
3)
4)
A

1) CD4 help activate CD8
2) CD8 lyse infected cells
3) HSV-specific CD8 found clustered around infected ganglia - but no neuronal damage
4) B cell/antibody response of limited effectiveness

31
Q

Why can HSV persist?

A

Lives in CNS cells
Limited immune function here
ICP47 expression inhibits MHCI presentation

32
Q

Diagnosis of HSV infection

A

Grow virus in cell culture

Look for antigens or nucleic acids or antibodies in host

33
Q

When is transmission most common

A

During primary infection, due to high viral load

34
Q

What subdues the primary infection viral load?

A

IgM peak, then IgG peak

35
Q

HSV treatment

A

Acyclovir

Can treat blister formation, but not latent infection

36
Q

Acyclovir mode of action

A

Nucleoside (G) analogue - lacks 3’ OH required to form DNA polymer
Acyclovir has no phosphates. Can’t be phosphorylated by human enzymes, can be phosphorylated by herpes thymidine kinase

MIIM2002 - 2 (12 decks)

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