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MIMM 324 > 17. Herpesvirus 1 > Flashcards

17. Herpesvirus 1 Flashcards

1
Q

when did publications about herpesvirus start to increase?

A

1960s

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2
Q

what type of genome does herpesvirus have? size?

A

dsDNA –> 125,000-229,000 bp

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3
Q

shape of herpesvirus capsid?

A

icosahedral

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4
Q

is herpesvirus enveloped or naked?

A

enveloped

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5
Q

where does herpesvirus envelope come from?

A

come from nuclear membrane from budding

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6
Q

how many capsomeres are there?

A

162

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7
Q

what surrounds the capsid?

A

tegument

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8
Q

is herpesvirus a complex virus?

A

yes –> over 100 transcripts and over 70 ORFs

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9
Q

all human herpesviruses have identical ___________

A

all human herpesviruses have identical EM morphology

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10
Q

are herpesviruses ubiquitous or rare?

A

ubiquitous –> infect a majority of all humans

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11
Q

can herpesviruses be latent?

A

yes, ALL remain latent lifelong and may reactivate

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12
Q

8 human herpesviruses:

A
  1. HSV1 (HHV1)
  2. HSV2 (HHV2)
  3. Varicella-zoster virus (HHV3)
  4. EBV (HHV4)
  5. Cytomegalovirus (CMV, HHV5)
  6. HHV6
  7. HHV7
  8. Kaposi sarcoma-associated virus (KSHV, HHV8)
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13
Q

a) What cell does HSV1/HHV1 target?
b) Pathophysiology of HHV1
c) Site of HHV1 latency
d) Means of spread

A

a) Mucoepithelial cells
b) Oral and/or genital herpes, usually orofacial
c) Latent in neurons
d) Spread by close contact –> oral or sexual

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14
Q

a) What cell does HSV2/HHV2 target?
b) Pathophysiology of HHV2
c) Site of HHV2 latency
d) Means of spread

A

a) Mucoepithelial cells
b) Oral and/or genital herpes
c) Latent in neurons
d) Spread by close contact –> oral or sexual

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15
Q

a) What cell does Varicella zoster virus/HHV3 target?
b) Pathophysiology of HHV3
c) Site of HHV3 latency
d) Means of spread

A

a) Mucoepithelial cells
b) Chicken pox, shingles
c) Latent in neurons
d) Spread by respiratory and close contact

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16
Q

a) What cell does EBV/HHV4 target?
b) Pathophysiology of HHV4 (4)
c) Site of HHV4 latency
d) Means of spread (4)

A

a) B cells/epithelial cells
b) - Infectious mononucleosis
- Burkitt’s lymphoma
- Hodgkin’s lymphoma
- post-transplant lymphoproliferative disease
c) Latent in B cells
d) Spread by:
- close contact
- transfusions
- tissue transplant
- congenital transmission

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17
Q

a) What cell does Cytomegalovirus/HHV5 target?
b) Pathophysiology of HHV5
c) Site of HHV5 latency
d) Means of spread

A

a) Monocytes and epithelial cells
b) Infectious mononucleosis-like syndrome, retinitis
c) Latent in monocytes
d) Spread by saliva, urine, blood, breast milk

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18
Q

what type of people are infected with cytomegalovirus/HHV5?

A

immunocompromised people
(ex. AIDS patients)

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19
Q

what 2 type of disease does cytomegalovirus cause in immunocompromised ppl?

A

hematologic disease and solid organ cancer

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20
Q

4 locations of CMV infections in immunocompromised ppl

A
  1. Brain –> encephalitis
  2. Eye –> retinitis
  3. Lung –> pneumonia
  4. Stomach/intestines –> gastroenteritis
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21
Q

treatment for CMV infection? and most common type

A

treat with biologic modifying infections, most commonly Mab

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22
Q

downside of Mab?

A

all have complications –> relative immunosuppression, infections, etc.

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23
Q

a) What cell does Roseolovirus/HHV6 target?
b) Pathophysiology of HHV6
c) Site of HHV6 latency
d) Means of spread

A

a) T cells
b) Sixth disease, Roseola infantum, exanthem subitum
c) Latent in T cells
d) Respiratory, saliva, close contact

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24
Q

a) What cell does Roseolovirus/HHV7 target?
b) Pathophysiology of Roseolovirus/HHV7
c) Site of Roseolovirus/HHV7 latency
d) Means of spread

A

a) T cells
b) pathophysiology not well-defined
c) latent in T cells
d) unknown means of spread

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25
Q

what type of ppl does roseolovirus typically infect?

A

immunocompromised ppl

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26
Q

what disease do infants infected with primary roseolovirus infection get? how is it spread?

A

infants get EXANTHUM SUBITUM –> spread by people’s saliva when they kiss the baby, etc.

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27
Q

a) What cell does Kaposi’s sarcoma-associated herpesvirus/HHV8 target?
b) Pathophysiology of HHV8
c) Site of HHV8 latency
d) Means of spread

A

a) Lymphocytes
b) Kaposi’s sarcoma, primary cavity lymphoma
c) B cell
d) close contact, saliva

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28
Q

what strength of therapies do patients with KSHV/HHV8 need? why?

A

need very toxic therapies bc virus can infect internal organs

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29
Q

describe HSV1/HSV2 membrane glycoproteins

A

HSV1 and HSV2 have serologically distinct membrane glycoproteins

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30
Q

do HSV1/HSV2 cause similar symptoms?

A

yes, when infecting identical sites

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31
Q

do HSV1/HSV2 have the same epidemiological pattern?

A

different but converging epidemiological pattern

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32
Q

describe Herpes B virus

A

found in Macaques and only found in ppl who interact with Macaques –> leads to fatal encephalitis

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33
Q

HSV1 or HSV2 more common in urogenital infection?

A

HSV2

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34
Q

HSV1 or HSV2 more common in labial infection?

A

HSV1

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35
Q

HSV1 or HSV2 more common in ocular keratitis?

A

HSV1

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36
Q

HSV1 or HSV2 more common in Whitlow/Hand infection?

A

equal

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37
Q

HSV1 or HSV2 more common in encephalitis?

A

HSV1

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38
Q

HSV1 or HSV2 more common in meningitis?

A

HSV2

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39
Q

why is HSV2 more common in meningitis?

A

HSV1 is latent in nerve ganglia and travels to brain along axons, but HSV2 does not have access to brain bc it only travels thru blood

40
Q

HSV1 or HSV2 more common in neonatal infection? why?

A

HSV2 –> mothers with genital infection pass it on

41
Q

HSV1 commonly causes:

A

HSV1 commonly causes Herpes labialis

42
Q

HSV2 commonly causes:

A

HSV2 commonly causes Herpes genitalis

43
Q

what percent of the population is infected with HSV1/2 by age 5?

A

30-100%

44
Q

what is a factor that affects which ppl are infected with HSV1/2?

A

class –> 30-50% of middle class children get infected while 80-100% of poorer populations get infected

45
Q

describe primary HSV1/2 infection

A

usually asymptomatic but may present as SEVERE gingivostomatitis

46
Q

why are some primary HSV1/2 infections symptomatic but most are asymptomatic?

A

everyone has different immune systems that work differently

47
Q

how long is HSV1/2 incubation period?

A

2-12 days (i.e. time from infection to symptoms)

48
Q

what can happen at the same time as primary HSV1/2 infection?

A

eye, hand, or other sites can be infected de novo or auto-innoculation

49
Q

describe primary HSV1/2 infection in ppl who are not immunocompromised

A

usually no serious symptoms and treatment is optional

50
Q

where does HSV1/2 sit latent?

A

sensory ganglia

51
Q

where does recurrent HSV1/2 infection occur?

A

in same site as primary infection

52
Q

what causes recurrent HSV1/2 infection?

A
  1. concurrent infection, fever
  2. stress, menses, exposure to UV light
53
Q

describe asymptomatic recurrent HSV1/2 infection

A

small quantities of HSV1/2 can periodically be shed asymptomatically

54
Q

do asymptomatic men or women spread virus more?

A

asymptomatic women spread the virus more bc lesions less visible

55
Q

describe herpes infantum

how do we prevent this?

A

infected at birth from mother with latent genital herpes
- baby develops herpes encephalitis with herpes all over the skin

  • pregnant person is continually checked for herpes if previously had herpes and treated with antiviral
56
Q

describe whitlow

A

scratch herpes lesions –> get infection on finger

57
Q

are STDs caught on public toilets? why?

A

NO

herpes is enveloped so it is very fragile
- envelope disintegrates in non-aqueous state
- virus need body temp to survive

58
Q

2 types of VZV

A
  1. Varicella –> chicken pox
  2. Zoster –> shingles
59
Q

describe varicella/chicken pox

A

PRIMARY infection throughout body

60
Q

describe zoster/shingles

A

LOCAL recurrence of latent infection

61
Q

does primary infection cause immunity?

A

yes there is absolute immunity to reinfection

62
Q

how does shingles occur if primary infection causes immunity?

A

immune to NEW infection but virus can sit latent in sensory ganglia and reactivate

63
Q

difference in distribution of chicken pox and HSV1/2 lesions

A

chicken pox mainly on trunk, head, and fewer lesions on extremities

64
Q

chicken pox in children vs adults vs pregnant ppl

A

more vicious infection in adults –> more symptoms + more lesions

in pregnant ppl can cause viral pneumonia

65
Q

difference in distribution of chickenpox and smallpox lesions

A

smallpox mainly extremities and head, chicken pox mainly torso and head

66
Q

4 types of ppl that varicella/chicken pox usually occurs in:

A
  1. returnees from subsaharan africa
  2. non-vaccinated children
  3. non-vaccinated adults
  4. farm workers
67
Q

describe the 6 types of spinal nerves

A
  1. 12 pairs cranial nerves
  2. 8 pairs cervical nerves
  3. 12 pairs thoracic nerves
  4. 5 pairs sacral nerves
  5. 5 pairs lumbar nerves
  6. 1 pair coccygeal nerves
68
Q

how does shingles latency occur relative to nerves?

A

occurs unilateral of various nerves

69
Q

describe shingles at trigeminal nerve + what is trigeminal nerve

A

trigeminal nerve = cranial nerve that is the main sensory nerve

lesions at one of 3 branches (V1, V2, V3)

70
Q

how can you diagnose shingles that has very few lesions?

A

by culturing virus

71
Q

chicken pox vaccine name?

A

zostavax

72
Q

shingles vaccine name?

A

shingrix

73
Q

describe CMV infection

A

very common but inapparent

74
Q

Canadian city with highest rate of CMV?

A

Montreal –> 74%

75
Q

city with highest rate of CMV?

A

Burkina Faso –> 99.5%

76
Q

how many infants infected with CMV?

A

30-50% of infants infected during 1st year of life

77
Q

how do infants get infected with CMV?

A

VERTICAL TRANSMISSION - intrauterine and neonatal

bc CMV present in maternal blood and breast milk

78
Q

how many ppl at reproductive age get infected with CMV?

A

20-50% infected during 2nd and 3rd decades of life

79
Q

where is CMV present in ppl of reproductive age?

A

in saliva and genital secretions

80
Q

where do ppl asymptomatic for CMV have infectious virus? (7)

A
  1. urine
  2. saliva
  3. WBC
  4. semen/vaginal secretions
  5. breast milk
  6. CSF
  7. tissue
81
Q

why is CMV found in many tissues despite having serum antibodies?

A

serum antibodies don’t prevent it from replication

82
Q

who does SYMPTOMATIC CMV infect?

A

immunocompromised ppl

83
Q

is symptomatic cmv new infection or reactivation of virus?

A

can be either!

84
Q

what 3 symptoms of CMV are common in transplant patients?

A
  1. fever
  2. hepatitis
  3. pneumonia
85
Q

what 4 symptoms of CMV are common in AIDS patients?

A
  1. retinitis
  2. pneumonia
  3. esophagitis
  4. disseminated infection
86
Q

what is the fovea?
what is the optic disk?

A

fovea –> highest concentration of retinal cells

optic disk –> where optic nerve enters retina from brain

87
Q

what does a pale area in the retina indicate?

A

retinal necrosis from CMV

88
Q

how many ppl in North America carry EBV by age 5?

by age 30?

A

50%

90-95%

89
Q

proportion of oropharyngeal shedding of virus in seropositive healthy adults?

A

10-25%

90
Q

proportion of oropharyngeal shedding of virus in recent transplant recipients?

A

50-75%

91
Q

proportion of oropharyngeal shedding of virus in acute infectious mononucleosis?

A

50-100%

92
Q

proportion of oropharyngeal shedding of virus in acute leukemia/AIDS?

A

85-100%

93
Q

what happens to the mouth with Mono

A

uvula is engorged, tonsils increased, inflammation everywhere!

94
Q

describe lymphocytes found in Mono

A

big and floppy and can get indented by RBCs

95
Q

what happens to spleen with mono?

A

can increase in size, can split open and hemorrhage

96
Q

why should you not engage in contact sports for at 3m after infection?

A

the main cause of death is hemorrhage!

MIMM 324 (37 decks)

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