Herpesvirus and Papilomavirus Flashcards

1
Q

Alphaherpesvirus Genome

A

dsDNA

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2
Q

Alphaherpesvirus Virion

A

Enveloped

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3
Q

Alphaherpesvirus Incubation

A

Anywhere from 2-14 days, but usually 4-5 days

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4
Q

Alphaherpesvirus Strains

A

HSV-1: oral-oral, oral-genial; nearly 2/3 of adults are seropositive
HSV-2: genital-genital, oral-genital; more prevalent with sexual activity, approximately 1/5 of adults

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5
Q

Alphaherpesvirus Replication

A

Nucleus - primarily infect epithelial cells in the skin or mucosa

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6
Q

Alphaherpesvirus Immune inhibition

A

Cell mediated response system is required.

Viral proteins binds antibodies and compliment them, countering the effects of interferons

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7
Q

Alphaherpesvirus Characteristics

A
Variable host range
Short reproductive cycle
Rapid spread in culture
Efficient destruction of infected cells
Capacity to establish latency in sensory ganglia
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8
Q

Alphaherpesvirus Symptoms

A
Flu-like
Localized lesions - virus spreads to neighboring cells
Only 1/3 show symptoms
Can still transmit when asymptomatic
Symptoms last 8-12 days
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9
Q

Alphaherpes virus Transmission

A

HSV-1: oral-oral, oral-genital

HSV-2: genital-genital; oral-genital

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10
Q

Alphaherpes virus Complication

A

Latency

  • Genome circularizes and stays as an episome in the nucleus
  • Peripheral ganglia are a common site of latent infections
  • Can be triggered by sunburn, systemic infections, immune impairment, and stress
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11
Q

Alphaherpesvirus Prevalence

A

HSV-1: 2/3 of adults

HSV-2: 1/5 of adults

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12
Q

Alphaherpesvirus treatment

A

Acyclovir limits virus replication

Will not eliminate latent infection

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13
Q

Alphaherpesvirus Prevention

A

Avoid contact during active herpes recurrence

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14
Q

Betaherpesvirus characteristics

A
Restricted host range
Long reproductive cycle
Slow progress in cell culture
Enlargement of infected cells
Carrier cultures
Latent infection in a variety of tissues
Prototypical member - Cytomegalovirus (CMV)
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15
Q

Gammaherpesvirus charachteristics

A
Restricted hist range
Targets T and B lymphocytes
Lytic infections
Latency in lymphoid tissues
Prototypical member - Epstein-Barr Virus (EBV)
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16
Q

Betaherpesvirus/Gammaherpesvirus Genome

A

dsDNA

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17
Q

Betaherpesvirus/Gammaherpesvirus Virions

A

enveloped

18
Q

Betaherpesvirus/Gammaherpesvirus Replication

A

Nucleus

19
Q

Betaherpesvirus/Gammaherpesvirus Symptoms

A

EBV - Burkett’s lymphoma, Hodgkin’s lymphoma

20
Q

Burkett’s lymphoma

A

Most common childhood cancer in equatorial Africa
Tumor in jaw, eye socket, ovaries
In all cases, tumor cells have monoclonial EBV episome

21
Q

What are the 3 types of Hodkin’s lymphoma

A

NL - nodular sclerosing
MC - mixed cellularity
LD - lymphocyte depletion

22
Q

EBV’s role in Hodkin’s Lymphoma

A

EBV is present in 60-90% of MC and LD tumors
EBV is present in 20-40% of NL tumors
The exact role is not known

23
Q

CMV latency

A

Persists in hematopoietic progenitor cells and macrophages in vitro
Chronic persistent infection, not latency
Controlled by healthy, actime immune system

24
Q

EBV latency

A

Persistence of genome in memory B cells

Virus proteins ensure B cell proliferation and EBV genome replication

25
Q

Betaherpesvirus/Gammaherpesvirus Prevalence

A

Common in the US

26
Q

Betaherpesvirus/Gammaherpesvirus Treatment

A

Infections are usually self-limiting in healthy individuals
Antivirals for immune compromised individuals
Prophylaxis for transplant patients

27
Q

Antiviral therapy for immune compromised individuals for CMV and EBV

A

Glanciclovir, foscarnet, acyclovir

  • Inhibit viral genome replication
  • Resistance can develop
  • Less effective for EBV-induced lymphoproliferation
28
Q

Betaherpesvirus/Gammaherpesvirus Prevention

A

No vaccines

29
Q

HPV Genome

A

circular dsDNA

30
Q

HPV Virion

A

non-enveloped

31
Q

HPV Strains

A

There are many different types associated with different diseases

32
Q

HPV replication

A

Gain access through abrasion of the skin
Virus production in differentiating cells
Cell polymerase required

33
Q

HPV Symptoms

A

Warts at infection sites

Can take moths to manifest, and 50% regress on their own within 2 years

34
Q

HPV Transmission

A

Direct skin-to-skin contact
-Mucous membrane is most susceptible and viruses enter through abrasions
They are hardy to environmental stress, which allows for transmission via fomites

35
Q

HPV Complications

A

Oncogenesis - cervical cancer

Respiratory papollomatosis

36
Q

Respiratory papollomatosis

A

Complication of HPV
Rare
Respired virus
Can be lethal

37
Q

HPV role in cervical cancer

A

HPV requires actively replicating cells to replicate progeny

Actual path to cancer is unknown, either viral transformation or cell proliferation leading to cancer

38
Q

HPV protein E7

A

Blocks retinoblastoma protein (Rb), which leads to continued cell proliferation
May lead to cervical cancer

39
Q

HPV protein E6

A

Blocks the p53 tumor suppressor pathway

May lead to cervical cancer

40
Q

HPV Treatment

A

Most treatments are ablative
Liquid nitrogen, surgical excision, laster, caustic chemicals
Treatments may have to be repeated

41
Q

HPV PRevention

A

Gardasil vaccination - protects against HPV-6, 11, 16, and 18