Herpes Flashcards

1
Q

Classify the herpesviruses

A

family: herpesviridae. enveloped. dsDNA icosahedral capsid

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2
Q

How many herpesviruses are there?

A

8

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3
Q

HSV-1 does what?

A

cold sores

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4
Q

HSV-2 does what?

A

genital herpes

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5
Q

VZV

A

Chickenpox, zoster

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6
Q

EBV

A

mono, oral hairy leukoplakia, B cell lymphoma, nasopharyngeal carcinoma

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7
Q

CMV

A

post transplant infections, retinitis

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8
Q

HHV-6

A

exanthem subitum or roseola infantum

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9
Q

HHV-7

A

no associated disease

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10
Q

HHV-8

A

Kaposi’s Sarcoma

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11
Q

What virus and what is herpetic gingivostomatotis

A

vesicular lesions on the oral mucous memranes that rupture and leave yellowish-gray ulcers or plaques. usually HSV-1

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12
Q

Herpes labialis

A

cold sores, fever blisters. vesicles at localized sites in the orofacial area that rupturea nd leave shallow ulcers or dry and form a scab.

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13
Q

genital herpes

A

HSV2. genital vesiceles that rupture forming ulcers in the genital region

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14
Q

neonatal herpes

A

infection of the newborn during delivery usually HSV2

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15
Q

herpes keratitis

A

acute necrotizing viral encephalitis usually HSV1

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16
Q

Describe pathogenesis of HSV

A

HSV is transmitted by direct contact of mucosal surfaces. Virus infects the epithelial cell and spreads causing primary lesion. Virus encounters sensory neuron ending where it binds and enters. It travels up via retrograde transport to the cell body and just hangs out there in a period of latency expressing LAT. Because there is no protein expression, it is not killed by a CTL response. At a later time, it will travel back down the neuron causing reactivation

17
Q

What is the prevalence of HSV1

A

70% in the US. 90% in the developing world

18
Q

What is the prevalence of HSV2

A

17% in the US. 50-80% in developing countries

19
Q

Describe pathogenesis of VZV

A

VZV is inhaled as respiratory aerosols. Virus replicates in epithelial cells, then leads to the regional lymph nodes and infects T cells. Viremia then occurs in the blood. Leading to infection of liver and spleen. Infected mononuclear cells spreads then to the skin and mucousal membranes leading to pocks. Virus spreads to the dorsal root ganglia establishing latency there. Reactivation will then occur again along the dermatome usually on the body trunk.

20
Q

Describe pathogenesis of EBV

A

transmitted by saliva. virus infects pharyngeal epithelial cells where it replicates and is shed in throat and saliva. EBV then infects the B cells (esp. those in the tonsils). EBV gene products stimulate proliferation of random B-cells which is why you can detect via monospot.

21
Q

What drugs do we use to inhibit HSV

A

Acyclovir

22
Q

Is there a vaccine for HSV?

A

No, but there is one in the pipelines

23
Q

Is there a vaccine for VZV?

A

Yes

24
Q

What actually causes the mono sx

A

T cell response to EBV

25
Q

Does EBV persist?

A

Yes. It persists in the B cells in latent form

26
Q

What are the sx of mono?

A
  1. enlarged lymph nodes
  2. sore throat
  3. fatigue
27
Q

What are the lab results for mono?

A

heterophile antibodies react to antigens from animal RBC’s and thus agglutinate

28
Q

What is a bad outcome of EBV infection?

A

enlarged spleen and potential rupture

29
Q

What can happen long-term with EBV?

A

cancer

30
Q

How is CMV spread?

A

ubiquitous virus that usually leads to asymptomatic sx, CMV is established from mother to child congenitally (transplacetally). Can also be with breast milk

31
Q

HHV-6 does what?

A

Childhood disease that causes exanthum roseola, fever and rash. Can come back with bone marrow transplant recipients

32
Q

What does HHV-8 do?

A

Kaposis Sarcoma which creates complex angioproliferative and inflammatory lesions.

33
Q

how does acyclovir work?

A

It is a nucleoside analog which is incorporated in the DNA, but then lacks a special side chain moiety that prevents chain elongation and blocks viral DNA synthesis