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CMBM exam 3 > Major DNA viruses > Flashcards

Major DNA viruses Flashcards

1
Q

Molluscum Contagiosum

A

Poxviridae

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2
Q

B19

A

only human parvovirus
ss, linear DNA, naked icosahedral
causes Fifth’s disease - slapped cheek rash
Trans: respiratory and oral secretion

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3
Q

What sort of cells does B19 preferentially infect?

A

mitotically active erythroid precursor cells in the bone marrow
infects proerthyroblast

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4
Q

Describe the lytic phase of B19

A

viremia is established
viral shedding, moves out of bone marrow
flu like symptoms

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5
Q

Describe the non infections immune response of B19

A

circulating immune complexes that cannot fix complement results in erythematous, maculopapular rash, arthralgia, arthritis (last two rare)

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6
Q

What is important for clearing B19?

A

IgG

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7
Q

what causes common rash illness in school aged children?

A

B19

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8
Q

lacy reticular maculopapular rash on trunk and extremities

A

B19

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9
Q

Rash appears with IgM

A

B19

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10
Q

what is the concern with a B19 infection in a sickle cell patient?

A

Aplastic crisis - drop in RBCs

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11
Q

concerns with Intrauterine infection of B19

A

hydrops fetalis or fetal death

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12
Q

Rash appears with IgM

A

B19

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13
Q

How would you treat acute vs. chronic B19?

A

since mild - acute treat with supportive care, ibuprofen for fever and topical anesthetic or antihistamine
For chronic which can be seen in IC pts - IV immunoglobins

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14
Q

Adenovirus

A

DsDNA - linear
non enveloped
respiratory trans. via inhalation of droplets or eye contact
GI trans. - fecal-oral route

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15
Q

Pathogenesis of Adenovirus

A

typically infects where comes in contact with mucoepithelium
commonly infects local lymphoid tissue - conjunctiva, adenoids, tonsils, respiratory, peyer’s patches
*typically not pathogenic

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16
Q

Where can Adenovirus persist?

A

in tonsils and adenoids in childern

in intestines in adults

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17
Q

How does Adenovirus interfere with host defenses?

A

interferes by blocking IFN and T cells

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18
Q

Viral oncogenes of Adenovirus

A

lytic in nature so tumorgenesis is not concern
late proteins E1A and E1B leads to cell growth
E1A inactivates pRB (retinoblasts)
E1B inactivates p53 (mediates cell apoptosis)

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19
Q

What are some clinical manifestations of Adenovirus

A

Acute febrile pharyngitis
Pharyngoconjunctival fever
Acute respiratory disease
cold, laryngitis, croup, bronchiolitis, viral pneumonia
“shipyard eye” -epidemic keratoconjunctivitis
cervicitis and urethritis - rare in women
acute gastroenteritis in infants

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20
Q

With Adenovirus infections in childern, what symptoms would you see in infants and young children versus older children?

A

infants and young - acute febrile - stuffy nose, fever, sore throat
Older children - Pharyngoconjunctival fever - tends to occur in outbreaks. associated with underchlorinated pools

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21
Q

Notice lots of military recruits have Acute respiratory disease. Symptoms include fever, runny nose, cough and pharyngitis. A couple of infected recruits also present with conjunctivitis. What could it be?

A

Adenovirus

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22
Q

papillomaviridae

A

HPV

small, circular (so has own polymerase to make DNA but use host polymerase for RNA), in nucleus, ds, non enveloped

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23
Q

Papilloma

A

benign
squamous epithelial growth
wart
verruca

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24
Q

HPV encodes proteins that promote

A

cell growth
lytic infections in permissive cells
transforming, oncogenic infection in non permissive cells

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25
Q

What does HPV cause?

A

warts, condylomas, papillomas and cervical carcinomas

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26
Q

How long could HPV incubate?

A

2 weeks to 1 year

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27
Q

what strains of HPV could cause Anogenital warts?

A

6 and 11

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28
Q

what strains of HPV could cause Cervical carcinomaL?

A

16 and 18

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29
Q

HPV protein E1

A

binds DNA at ori and promotes viral DNA replication and has helicase activity

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30
Q

HPV protein E2

A

binds DNA
helps E1
and activates viral mRNA synthesis

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31
Q

HPV protein E5

A

oncoprotein that activates the EGF receptor to promote growth

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32
Q

HPV protein E4

A

disrupts cytokeratins to promote release

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33
Q

E6 and E7 of HPV 16 or 18

A

become immortilizing genes
E6 binds to p53, activates telomerase and suppresses apoptosis
E7 binds p105RB

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34
Q

L1 and L2 of HPV

A

late structural (capsid) proteins

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35
Q

describe the development of papilloma

A

infects basal cells of dermal layer via L1 VAP/ integrins
replicates in squamous epithelium of skin(warts) or mucus membranes (genital, oral or conjunctival) -> epithelial proliferation

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36
Q

what is a wart ?

A

virus stimulation of cell growth leads to thickening of basal and prickle layers
epithelial spikes form - papillomatosis
Koilocytes

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37
Q

Koilocytes

A

enlarged keratinocytes with haloes around shrunken nuclei develop

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38
Q

Where is the HPV produced in skin layers?

A

in granular cells near the final keratin layer
not a lytic infection
shed from surface of epithelium

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39
Q

Common warts - HPV

A

benign self limited proliferative lesions

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40
Q

Benign head and neck tumors - HPV

A

usually solitary and rarely reoccur after excision
laryngeal papilloma most common type
causes most common tumor of the oral cavity

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41
Q

Anogenital Warts - HPV

A

condylomata acuminata occur mostly on squamous epithelium of external genitalia/perineum

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42
Q

Cervical dysplasia and Neoplasia - HPV

A

common STD
asymptomatic, may cause slight itching
appear as soft, flesh colored wart that are flat, raised or cauliflower shaped

43
Q

Describe the progression of HPV medicated cervical carcinoma

A

infects and replicates in the epithelial cells
matures and is released as cells progress through terminal differentiation
in some cells, circular genome integrates into host chromosomes inactivating the E2 gene
expression of other genes stimulates the growth of the cell and possible progression to neoplasia

44
Q

What laboratory tests can test for Cervical dysplasia caused by HPV?

A

cytology: koilocytotic cells (vacoulated cytoplasm)
Wart: microscopically view hyperplasia
Papanicolaou stain of exfoliated cervicovaginal squamous epithelial cells
DNA probe anaylsis or PCR (best method)

45
Q

How do you treat HPV?

A

cryotherapy, electrocautery

inteferon, imiquimod or stripping with duct tape to stimulate immune response

46
Q

What sort of vaccinations are available for HPV?

A

Gardasil - Tetravalent (HPV-6, 11, 16, 18)
Cervarix - divalent (HPV 16 and 18)
For girls, boys and women 9-26 years
three doses: initial, 2 month booster, 6 month booster

47
Q

Herpesviruses

“Herpes is forever!”

A

HSV, VZV

Large, ds, enveloped linear

48
Q

What is characteristic of a Herpes infection?

A

lytic, persistent, latent and immortalizing

49
Q

Describe the alpha-herpesvirinae (HSV group)

A

rapid cytolytic growth cycle
commonly destroy the host cell
latent in neuronal ganglia
HSV1 HSV2 VZV

50
Q

Beta-herpesvirinae (CMV group)

A

slow replication
latency non neuronal 1* lymphoreticular cells
CMV HHV6 HHV7
transmitted through saliva
Roseola rash seen on neck, trunk and thighs

51
Q

Gamma-herpesvirinae (lymphoproliferative group)

A

replicate in mucosal epithelia
immortalized in host lymphoid cells
latency established in mucosal epithelia
EBV HHV8
transmitted through saliva and semen
in IC pts, can become opportunistic and cause cancer

52
Q

What is the clinical presentation of HSV1

A

lesion on the oropharynx, cold sores, fever blisters

aquired in early childhood

53
Q

What is the clinical presentation of HSV2

A

lesions on genitalia

2/3 spread from asymptomatic partners

54
Q

Clinical presentation of HSV 1 and 2

A

vesicular lesions and shallow ulcers accompanied by fever, myalgia and malaise

55
Q

What is occuring in the initial stage of HSV infections ?

A

virus replicates at high rates
infection resolves - within two weeks
virus travels axonally to sensory nerve ganglion and produces acute infection at ganglion
leaves episomal (circular) DNA

56
Q

what occurs during HSV reactivation ?

A

stimuli causes the viral episomal DNA to produce LAT which causes the viral DNA to linearize again and to begin producing virus

57
Q

What is the primary manifestion of HSV-1 in children?

A

Gingivostomatitis
primary infx of upper body
fever, malaise, lesions last 3 weeks

58
Q

What is the primary manifestion of HSV-1 in adults?

A

Pharyngitis or tonsillitis

1 week duration

59
Q

What can trigger reactivation of HSV?

A

stress, UV light, infection, menstruation, decreased immunity

60
Q

What can suppress reactivation of HSV?

A

strong cellular immune response

high antibody titer doesnt prevent

61
Q

What are the secondary/recurrent manifestations of HSV?

A

cold sore
keratoconjunctivitis (HSV 1 of the eye) - 2nd MCC of corneal blindness, corneal scarring
Herpetic gladiatorium - wrestlers and burn victims
Herpetic Whitlow - fingers and hands - chiropractors

62
Q

What are the differences in clinical manifestations between HSV 1 and 2?

A

HSV 1 - Keratoconjunctivitis, Gingivostomatitis, tonsilitis, labialis, esophagitis, tracheobronchitis, gladiatorum
HSV 2 - meningitis, perianal, neonatal HSV
both - encephalitis, oral, genital, whitlow

63
Q

Complication of HSV1

A

Encephalitis

64
Q

What is a manifestation of Congenital/perinatal transmission of HSV?

A

CNS (49%), skin, eyes and oral cavity (50%)

asymptomatic

65
Q

Complication of HSV2

A

Meningitis

mostly benign and self limiting with no neurologic

66
Q

Complication of HSV in Immune suppressed pts

A

pneumonia

severe mucocutaneous lesions

67
Q

How would diagnosis of HSV 1/2 be done?

A

clinical appearance
virus isolation from lesions
PCR of CSF for HSV encephalitis
Valacyclovir, acyclovir, famciclovir

68
Q

How is Varicella Zoster virus transmitted?

A

acquired by respiratory droplet inhalation of close contact

69
Q

What are some characteristics of the VZV infections in children and adults?

A

highly contagious, 90% of cases less than 9 years old
97% of adults are seropositive
more severe if primary infection occurs in adults

70
Q

Reactivation of VZV results in ?

A

Shingles/Zoster

triggered by increased age and/or decreased immunity

71
Q

What are complications of VZV?

A

superimposed bacterial infections

Pneumonia

72
Q

what is the clinical presentation of the primary infection of VZV?

A

chicken pox

fever, irritability and lymphadenopathy

73
Q

What is the clincal presentation of a reactivation of VZV?

A

early symptoms: acute pain and redness of dermatome followed by rash
Post herpetic neuralgia

74
Q

VZV receptors

A

4 envelope glycoproteins containing mannose 6 phosphate (Man 6-P) bind Heparan sulphate

75
Q

How is a VZV infection diagnosed?

A

3 types of lesions simultaneously seen:
1. Maculopapular -
Macule: flat discolored area of skin
Papule: small raised bump
Maculopapular: area that is usually red, and has small confluent bumps
2. Vesicular - bump containing clear fluid and when filled with pus = pustule
3. Scabs

76
Q

What are congenital and neonatal complications of VZV?

A

can cross the placenta
ranges from mild to fatal
primary infection during pregnancy leads to pneumonia

77
Q

If infection of VZV during 1st 20 weeks of pregnancy, then ..

A 
3% chance of transmission to fetus = Congenital varicella syndrome 
 scarring of skin
hypoplasia of limbs 
CNS and ocular defects 
Death in infancy is normal
78
Q

If mother is infected with VZV one week before delivery then

A

sufficient immunity transferred to fetus

79
Q

What is treatment for chickenpox?

A

Symptomatic, self limiting
acyclovir may help shorten duration
exclude kids from school until sixth day of rash

80
Q

how is a zoster rash treated?

A

acyclovir

81
Q

How is Zoster post herpatic neuralgia treated?

A

low dose tricyclic antidepressants

82
Q

Who is the VZV vaccine recommended for?

A

live attenuated
for children 12 months of age and seronegative adults
Elderly to prevent zoster (>60 years old)

83
Q

When is VZIG administered?

A

post exposure prophylaxis in individuals at high risk
mother with varicella 5 days before to 2 days after delivery
IC individuals with no reliable history
offers 3 weeks of protection

84
Q

oral HPV vs. oral HSV?

A

Herpes - reddened, vesicular lesions - fluid filled

HPV - flesh colored, papular - skin growing out, skin warping, no fluid

85
Q

Family Poxviridae

A

linear, dsDNA, complex symmetry
brick/box shaped
cytoplasmic replication

86
Q

Transmission of Pox viruses?

A

respiratory droplets or fomites

87
Q

Molluscum Contagiosum infection

A

discrete pustules - smooth dome shaped papules
basophilic inclusion bodies
commonly an STD
primarily seen in children
IC/AIDs pt suffer atypical form and forms tumor like growth

88
Q

Hepadnaviridae

A

Hepatits B virus
ds(partially) DNA
enveloped circular
enters bloodstream and travels to liver to infect hepatocytes

89
Q

Describe the replication of Hep B

A

includes RNA intermediate that serves as template for progeny DNA strands
so encodes reverse transcriptase (RNAd-DNA pol)

90
Q

What liver pathology can results from a Hepatitis infection?

A

Chronic
cirrhosis
hepatocellular carcinoma

91
Q

What is the structure of Hep B?

A

Partially dsDNA with DNA poly at the core
isohedral in shape
surrounded by core antigen which is then surrounded by surface antigen

92
Q

what are the methods of transmission of Hep B?

A

Sexual, parental and perinatal through milk

93
Q

replication of Hep B in the liver leads to ..

A

chronic inflammatory repsonse

CD8 cells kill viral infected cells

94
Q

Clinical manifestations of HBV

A

Hepatitis
Jaundice
multiplies exclusively in liver so continuously seeds blood

95
Q

what is the Hep B incubation period?

A

60-180 days

96
Q

What is characteristic of an acute HBV infection?

A

start with fever, rash, arthritis
Jaundice, dark urine, malaise nausea, RUQ pain
the continuous liver inflammation leads to fibrosis of the liver

97
Q

what is characteristic of a chronic HBV infection?

A

pt did not make surface antibody
so there is constant production of virus
liver cirrhosis

98
Q

Immune tolerant phase of a chronic HBV infection

A

HBeAg positive
very high HBV DNA
ALT is normal

99
Q

Immune active phase of a chronic HBV infection

A

HBeAg positive or negative
ALT is elevated
liver histology shows inflammation and fibrosis

100
Q

What does the active HBV vaccine consist of?

A

recombinant vaccine

HBsAg administered at 0, 1, or 6 months

101
Q

Post exposure of HBV vaccine

A

Passive vaccine
HBIG - serum from person with high titers of antibody of HBsAg
used to prevent exposure in
infants born to infected mothers, spouses of infected patients and HCW following needle stick injury

102
Q

Diagnosis of HBV

A 
liver function test 
-> ALT>AST 
-> aspartate, aminotransferase, alanine aminotransferase 
Jaundice 
RUQ discomfort 
Antibody detection
103
Q

HBV treatment

A

Supportive
HBV immunoglobin (HBIG) post exposure
IFN-alpha
Lamivudine

CMBM exam 3 (24 decks)

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