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Herpes Virus Cards Flashcards

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Biology 101 flashcards
1
Q

Front

A

Back

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2
Q

What is the genetic material of herpesviruses?

A

DNA virus

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3
Q

What is the incubation period of VZV?

A

10-21 days

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4
Q

Describe how VZV enters and replicates in the body

A

Enters via respiratory tract/conjunctive; local replication in the upper airway and regional lymph nodes; primary viremia nad infection of lymphocytes and nerve cells

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5
Q

Describe how VZV progressed to a skin infection

A

Primary viremia infects lymphocytes and nerve cells; VZV replicates, establishing a secondary viremia (fever) and skin infection (rash)

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6
Q

How does VZV modulate the immune system?

A

VZV infects lymphocytes and inhibits MHC-I expression, thus turning on NK signals

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7
Q

How does interferon-alpha aid in controlling viral infection?

A

IFN-alpha is produced locally in the skin late during a n infection and limits viral spread via blocking viral replication and decreasing virion assembly

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8
Q

How does shingles occur?

A

VZV establishes a latency in ganglia; when anti-VZV memory T cell activity drops with age, VZV re-activates and replicates

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9
Q

How does VZV establish latency?

A

VZV establishes latency in a sensory nerve ganglion which is immunopriviledged

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10
Q

What are possible presentations of disseminated VZV?

A

Hepatitis, pneumonia, encephalitis

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11
Q

What diseases does VZV cause?

A

Varicella (chickenpox) and Zoster (shingles), a reactivation disease

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12
Q

Describe the varicella rash

A

Discrete papules –> vesicles with clear fluid –> cloudy fluid –> crusting at 5-7 days. Pt will have rash including all stages of vesicles at the same time. Involves the entire body. May be 200-500 vesicles!

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13
Q

What is the clinical presentation of shingles?

A

Vesicular rash along dematome, commonly on chest, pain, itching, sensitivity. Doesn’t cross midline.

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14
Q

What are the seasonal/climate associations with Varicella?

A

More often in late winter/spring, in temperate > tropical climates; may affect older individuals in warmer tropical climates, for an unknown reason

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15
Q

How infectious is VZV?

A

Very. 90% secondary attack rate to susceptible household members.

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16
Q

What is the clinical presentation of chicken pox?

A

Itchy vesicular rash, central distribution, with 200-500 vesicles, possibly involving mucous membranes

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17
Q

Describe the epidemiology of zoster

A

Older (>45) or immunocompromised patients

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18
Q

Describe the zoster rash

A

Discrete varicella rash that coalesces; crusts by day 14; painful, does not cross midline and dermatomal

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19
Q

What is the most common complication of varicella?

A

Superinfection of vesicles (scratched open) with Staph aureus or strep pyogenes

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20
Q

Describe post herpetic neuralgia

A

Complication occuring in 20% of pts with zoster, most commonly in elderly. Results in pain that lasts months-years in response to touch and heat.

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21
Q

How is VZV diagnosed?

A

VZV is usually a clinical diagnoses based on symptoms and rash progression. May do PCR on vesicular fluid if atypical (e.g. varicella in previously immunized patient).

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22
Q

How are VZV antibody tests interpreted?

A

IgG indicates previous infection or immunization. If IgG antibodies rise 4x, suggests recent acute infection (in non-immunized pt)

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23
Q

What is the basic treatment for VZV?

A

Prevention of secondary infection; antivirals in adults or immunocomromised patients

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24
Q

What antiviral is used to treat VZV?

A

Acyclovir (at a higher dose than for HSV) or Famciclovir as an alternative

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25
Q

What is the mechanism of action and resistance for acyclovir?

A

Acyclovir inhibits viral DNA polymerase; virus may mutate thymidine kinase

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26
Q

What is the treatment of zoster?

A

Antivirals (acyclovir) to speed resolution of rash and decrease post-herpetic neuralgia, plus pain management

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27
Q

What type of vaccine is the varicella vaccine?

A

Live attenuated

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28
Q

How is the varicella vaccine given?

A

Primary immunization at 1 year old and booster at 4-6 years old

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29
Q

What type of vaccine is the zoster vaccine?

A

Live attenuated, with a higher concentration of varicella virus than in the varicella vaccine

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30
Q

How is the zoster vaccine given?

A

Routine immunization at 60yo or greater; most effective in 60-69yo

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31
Q

How can you prevent/treat VZV in an immunocompromised host?

A

Immunoglobulins (VariZIG) for post-exposure management + acyclovir early in infection

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32
Q

Describe the HSV rash

A

Vesicular and crusting rash, localized or in small groups, painful

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33
Q

Describe the variola virus rash

A

Vesicular and pustular rash on the entire body; lesions will be all at the same stage of progression

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34
Q

Describe the coxsackie virus rash

A

Combination of papules, pustules and vesicles localized on the hand, foot, mouth, and buttocks (hand food mouth disease); possibly with fever

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35
Q

Describe the etiology and characteristics of bullous impetigo

A

Etiology: Staphylococcus aureus; rash: fluid-filled bullae, non-itchy

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36
Q

What are the characteristics of alpha-herpesviruses? Name three alpha-herpesviruses

A

HSV1, HSV2, VZV. These have short reproductive cycle, rapid culture growth, latency in sensory ganglia, and destruction of infected cells.

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37
Q

What are the characteristics of beta-herpesviruses? Name three.

A

CMV, HHV6, HHV7. These have a long reproductive cycle, slow culture spread, non-ganglionic latency, and enlargement of infected cells.

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38
Q

What is the presentation of roseola?

A

Highmulti-day fever, fussiness, diarrhea, lymphadenopathy followed by erythematous morbiliform rash on the trunk, spreading to face/extremities

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39
Q

Which subgroup of HHV6 causes most disease?

A

HHV-6B

40
Q

What property allows HHV6 to be transmitted vertically?

A

In latency, HHV6 may integrate into telomeres and become germ-line

41
Q

What are the neurological symptoms of HHV6?

A

HHV6 infects astrocytes and glial cells, causing seizures in primary illness and encephalitis in reactivation disease

42
Q

What are common complications of HHV6?

A

Usually no complications; may have febrile seizures (in pts 6mo-6yo)

43
Q

Which patients are most likely to have HHV6 reactivation?

A

Bone marrow and solid organ transplant patients

44
Q

What is the treatment for HHV6?

A

Sympomatic treatment in healthy patients; antivirals (acyclovir) in immunocompromised

45
Q

What cells does HHV7 infect?

A

CD4+ T cells and other tissues

46
Q

How is HHV7 transmitted?

A

Respiratory secretion (persistent salivary infectious burden) from asymptomatic people

47
Q

What is the clinical presentation of HHV7?

A

Similar to HHV6 (high fever –> rash) but febrile seizures may be more severe

48
Q

Where is body temperature regulated?

A

Thermoregulatory center in the hypothalamus

49
Q

Name four endogenous pyrogens

A

IL-1, IL-6, TNF-alpha, IFN

50
Q

What are adverse effects of a fever?

A

Induction of sepsis, increase in oxygen demand/consumption, stress on CV and neurological tissue

51
Q

What are beneficial effects of a fever?

A

Recruitment of Increased antigen presentation, antibody production, cytokine production, lymphocyte proliferation; inhibition of pathogen growth and increased antimicrobial susceptibility

52
Q

What causes diurnal variation in temperature?

A

Serum cortisol release from the adrenal glands in a diurnal pattern

53
Q

What is the definition of FUO?

A

Temperature above 38.3/101.0 on multiple occasions for >3 weeks, with no diagnosis after >1 week evaluation

54
Q

What are the characteristics of gamma herpesviruses? Name two.

A

EBV, HHV8. These replicate in lymphoblastoid cells. Latency sites are lymphoid tissue (EBV) or monocytes/B lymphocytes (HHV8)

55
Q

Describe the microbiology (shape, surface markers, etc) of EBV

A

dsDNA genome, enveloped, with multiple surface glycoproteins

56
Q

Name the three EBV-specific antigens

A

Viral capsid antigen, early antigen, and nuclear antigens

57
Q

How does EBV suppress the immune system?

A

In the lytic phase, it produces an IL-10 homologue that inhibits Th1 response/release of IFN-gamma and macrophage activation

58
Q

What are reactive/atypical lymphocytes?

A

Large reactive lymphocytes that appear in EBV, CMV, and viral hepatitis

59
Q

How is EBV transmitted?

A

Saliva, infecting epithelium of oropharynx

60
Q

What immune response leads to the symptoms of primary EBV infection?

A

CD8+ T cell proliferation

61
Q

What is the clinical triad of mononucleosis?

A

Fever, pharynitis, adenopathy

62
Q

What are possible causes of mononucleosis syndrome?

A

EBV, but also CMV, HIV, viral hepatitis, rubella, parvovirus, influenza, secondary syphilis, bacteremia, rickettsia, coccidiomycosis, malaria, toxoplasmosis. Also drug reaction, malignancy, drug reaction. Basically everything!

63
Q

How does EBV establish infection?

A

It infects epithelial cells and B cells via binding the CD21 receptor. It then enters a lytic or latent phase.

64
Q

What occurs during an EBV lytic phase?

A

Linearization of circular EBV genome and production of infectious virions using viral DNA polymerase.

65
Q

When does EBV lytic phase occur?

A

In epithelium, this occurs right after entry. In B cells, this occurs usually after reactivation from latent phase (a small % are immediately in the lytic phase).

66
Q

What occurs in the EBV latent phase?

A

Viral circular DNA is integrated into the host cell; few proteins are expressed (immune evasion); uses host cell DNA polymerase; cell aquires the capacity to proliferate indefinitely

67
Q

How is EBV latency maintained during host c ell division?

A

Epstein-Barr Nucleic Acid-1 binds viral episome to host chromosome to maintain virus in nucleus of B cell

68
Q

What occurs during an EBV reactivation phase?

A

Viral gene expression using host DNA polymerase; apparently unlimited and unregulated growth

69
Q

Describe T cell activity during different stages of EBV

A

T cells control EBV infection not only in lytic/reactivation but also during latency. T cell disorders are associated with lymphoproliferative syndromes.

70
Q

What are 6 EBV-associated malignancies?

A

Burkitt lymphoma, nasopharyngeal lymphoma, Hodgkin’s lymphoma, CNS lymphoma, post-transplant lymphoproliferative disease, and oral hairy leukoplakia

71
Q

Which EBV genes are associated in EBV malignancies?

A

Latent genes; no lytic genes are expressed

72
Q

Describe clinical presentation of endemic Burkitt lymphoma

A

Jaw, facial bones, GI, GU involvement

73
Q

Describe the epidemiology of endemic Burkitt lymphoma

A

Associated with EBV, appears in malaria endemic regions (malaria = reduced resistance to EBV)

74
Q

What is the common genetic mutation in endemic Burkitt lymphoma?

A

8:14 or 8:22 translocation of c-myc

75
Q

Describe sporadic Burkitt lymphoma

A

Rare lymphoma, not associated with EBV, more commonly in the ileocecal region

76
Q

Describe the histology of Burkitt lymphoma

A

Intracytoplasmic lipid droplets or “starry sky”

77
Q

What is the epidemiology of nasopharyngeal carcinoma?

A

More common in Southern China, native North Americans

78
Q

What genes are expressed in nasopharyngeal carcinoma?

A

EBNA-1, LMP-1 (latent EBV genes)

79
Q

Does EBV play a role in Hodgkin lymphoma?

A

Maybe. EBV antibodies or DNA may be present, especially in aggressive Hodgkin lymphoma

80
Q

What are the clinical symptoms of CNS lymphoma?

A

Headache, focal neurological deficits, seizure, neuropsychiatric symptoms

81
Q

What is the MRI finding in CNS lymphoma?

A

1+ homogenously enhancing lesions in periventricular white matter

82
Q

What is the CSF finding in CNS lymphoma?

A

Elevated intracranial pressure, elevated protein, high WBC, predominantly lymphocytes

83
Q

In which patients is CNS lymphoma most common?

A

Pts with HIV/AIDS (DC4

84
Q

What is the histology of CNS lymphoma?

A

Neoplastic lymphoid cells (pale, with mitoses) that are 3-4x larger than normal lymphocytes, arranged in a perivascular distribution; may have EBV genomes

85
Q

How does post-transplant lymphoproliferative disease develop?

A

Following organ transplant, immunosuppression and T cell depletion prevent control and lead to B cell proliferation

86
Q

What is oral hairy leukoplakia?

A

Cutaneous lesion involving lingual epithelium commonly found in HIV patients; It is not premalignant; results from over-replication of EBV (not cell dysfunction due to infection)

87
Q

How do you tell oral thrush apart from oral hairy leukoplakia?

A

OHL is firm and will not scrape off, usually affecting the lateral tongue; thrush is candida and will scrape off, usually affecting buccal mucosa. Both are associated with immunosuppressed states, although OHL is more specific for HIV infection.

88
Q

How do you treat OHL?

A

Antiviral therapy to target excessive EBV replication or HAART to target underlying HIV immunosuppression

89
Q

What is the “monospot” diagnostic test?

A

An IgM heterophile antibody (induced by external antigen) with an affinity for sheep and horse RBC. Positive after 1 week and up to 3-6 months, but not positive during the incubation period.

90
Q

How is acute EBV infection diagnosed?

A

Mononucleosis syndrome plus positive monostop heterophile antibody test

91
Q

What is the specificity/sensitivity of the monospot test?

A

High specificity (rule in). False negatives during incubation, but 4yo) than in teens and adults (>80%). False positives may occur in HIV, lymphoma and lupus.

92
Q

Describe the pattern of antibodies to EBV viral capsid antigen

A

Anti-VCA present during illness; IgM appears first and disappears after 3 months; IgG appears second but persists

93
Q

Describe the pattern of antibodies to EBV early antigen

A

IgG to EA may appear early in clinical illness (not always) and dispapears after recovery; may be present in reactivation

94
Q

Descibe the pattern of antibodies to EBV nuclear antigens

A

Anti-NA are expressed during latency (6-12 weeks) and persist indefinitely

95
Q

What is the antibody pattern of EBV reactivation?

A

Negative IgM VCA; Positive IgG VCA, EA, NA

Microbiology (9 decks)

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