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Micro 2023 > 35 - Virology DNA Viruses > Flashcards

35 - Virology DNA Viruses Flashcards

1
Q

what produce eruptive skin pustules called pocks or pox that leaves scars

A

poxviruses

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2
Q

what is the largest and most complex animal virus

A

poxvirus

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3
Q

what has the largest genome of all human viruses

A

poxvirus

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4
Q

describe structure of poxvirus

A

single linear dsDNA molecule of 130-300 kb with
hairpins at either end

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5
Q

where do poxvirus multiply

A

cytoplasm in factory areas

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6
Q

what does poxvirus have specificity for

A

cytoplasm of epidermal cells and subcutenaous CT

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7
Q

what are human pox viruses

A
  1. orthopoxvirus
  2. molluscipoxvirus
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8
Q

what is variola virus (smallpoxl monkeybox)

A

orthopoxvirus

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9
Q

what is molluscum contagioscum virus

A

molluscipoxvirus

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10
Q

cytopathology of pox

A
  • extremely cytopathic
  • inhibit DNA, RNA, and protein synthesis
  • replication occurs in cytoplasmic factories
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11
Q

what is first disease eliminataed by vacc

A

smallpox

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12
Q

how does smallpox exposure occur

A

inhalation of skin contact

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13
Q

incubation period of smallpox

A

5-17 day

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14
Q

what other symptoms do smallpox pt have

A

high fever, headache, malaise, prostruation, rash

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15
Q

infections associated with smallpox

A

variola major and minor

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16
Q

variola major or minor:

highly virulent, caused toxemia, shock, and intravascular coagulation

A

major

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17
Q

variola major or minor:

less mirulent

A

minor

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18
Q

when was smallpox eradicated? when did routine vacc end

A

1977; 1972

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19
Q

when was the vaccine for small pox reintroduced for who

A

2002 - military and certain medical personnel

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20
Q

what is this:

Primarily an infection of children
in endemic areas.
Transmitted by direct contact and
fomites.
In U.S., most commonly an STD.

A

molluscum contagiosum

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21
Q

what does molluscum contagioscum look like

A

Lesions are 2-5 mm small,
smooth macules in genital area
and thighs.
Pearly papules with a central
depression whose core may be
expressed, producing a white
cheesy material.

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22
Q

symptoms of molluscume contagiosm

A

AIDS patients suffer an atypical
form which attacks the skin of
the face and forms tumor-like
growths.

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23
Q

treatment of molluscum contagioscum

A

freezing, electric cautery, chemical agents

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24
Q

how is monkeypox transmit

A

Transmitted by direct contact with lesions or contaminated surfaces
(bedding/towels).
Commonly intimate contact (sexual).
Also by contact with respiratory secretions.

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25
Q

incubation period of monkeypox

A

3-17 day

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26
Q

what is considered milder form of small pox (including pock-like rash)

A

monkeypox

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27
Q

what is this:

Lesions are firm or rubbery, well-circumscribed, deep-seated, and often
develop umbilication (resembles a dot on the top of the lesion).
Often painful until healing phase.
Typically not disseminated; commonly genital, anorectal, oral.

A

monkeypox

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28
Q

symptoms of monkeypox

A

Fever, lymphadenopathy (diagnostic from smallpox), malaise, headache, etc… may occur before or after lesion appearance

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29
Q

how is animal poxvirus transmitted

A

direct contact with lesions (ocupations, wild animals, cow sheep_

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30
Q

what do animal poxvirus look like

A

single nodular lesion forms at point of contact. lesion resolves after 4-5 weeks without scarring

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31
Q

vaccines against poxvirus

A
  • vaccinia (ACAM2000)
  • JYNNEOS
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32
Q

what vaccine:

Live virus used to vaccinate against Smallpox.
Distinct species of Orthopoxvirus.
Administered by variolation (skin pricking)

A

Vaccinia against POXVIRUS NOT SMALLPOX

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33
Q

clinical features of poxvirus vaccine

A

Localized pustular lesion at site of inoculation
Swelling of draining lymph nodes
Secondary lesions are atypical
Immunocompromised individuals
Mechanical transfer from primary inoculation site
Large number of Contraindications & Complications:
Progressive vaccinia (immunocompromised individuals)
Eczema vaccinia
Encephalitis (rare)

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34
Q

what vaccine:

Live-attenuated virus delivered by sub-cutaneous injection.
2 dose vaccination, 14-day interval.
Considered protective 14 days after second dose.
Unknown efficacy (immunity comparable to ACAM2000)

A

JYNNEOS for poxvirus

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35
Q

types of alpha herpesvirus

A

HSV-1
HSV-2
VZV

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36
Q

types of beta herpesvirus

A

CMV
HHV-6 (Roseola)
HHV-7

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37
Q

types of gamma herpesvirus

A

EBV
HHV-8 (Kaposi’s
sarcoma)

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38
Q

what is a common, persistent human virus

A

herpesvirus

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39
Q

what is this:
All members show latency and cause recurrent infection; viral DNA forms episome.
Clinical complications of latency and recurrent infections become more severe with advancing age, cancer chemotherapy, or other conditions that compromise the immune defenses.

A

herpesvirus

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40
Q

what is this:

Common and serious opportunists among AIDS patients.
Large enveloped icosahedral dsDNA.
Replicates within nucleus.

A

herpesvirus

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41
Q

humans are susceptible to whwat HSV

A
  1. HSV-1
  2. HSV-2
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42
Q

what HSV:

usually lesions on the oropharynx, cold sores, fever blisters Typically acquired in early childhood.

A

HSV-1

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43
Q

epidemiology of HSV

A

Lifelong infection.
Transmitted by secretions
and close contact.

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43
Q

what HSV:

lesions on the genitalia, possibly oral
Typically acquired in ages 14-29. Can be spread without visible lesions.

A

HSV-2

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44
Q

how do you get HSV-2

A

sexual of birth

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45
Q

what is ubiquitous HSV

A

HSV-1 is ubiquitous. World-wide estimate is 67% of the population has HSV-1. Estimated prevalence in
the Americas is 40-50%.

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46
Q

pathogenesis is similar for what HSV? what is the difference tho

A

HSV-1 and 2

1 is associated with above the waist
2 is below

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47
Q

how is HSV 1 and 2 transmited

A

Transmission by direct exposure to secretions containing the virus; active lesions most significant
source; genital herpes can be transmitted in the
absence of lesions.

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48
Q

where does HSV infection initiate

A

mucoepithelial cells

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49
Q

T/F: In HSV 1 and 2, local viremia and establishment of latent infection in innervating neurons.

A

TRUE

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50
Q

how does HSV 1 travel

A

retrograde transport to ganglia
Trigeminal (HSV-1) or Sacral (HSV-2)

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51
Q

what cells are inomportant for maintaining latency in HSV1 and 2

A

CD8 T-cells and gamma-interferon are
important for maintaining latency.

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52
Q

what can reactivate HSV

A

various stimuli

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53
Q

what happens when HSV is reactivated

A

Upon reactivation the virus returns to initial site of infection.
Inapparent.
Vesicular lesions.
Generally are less severe than original infection.

54
Q

tissue damage results from what in HSV? how do lesions heal

A

Tissue damage results from both viral and cellular
(immune) induced damage.
Lesions generally heal without scarring.

55
Q

what herpes, specific type

fever blisters, cold sores; most
common recurrent HSV-1 infection; vesicles
occur on mucocutaneous junction of lips or
adjacent skin; itching and tingling prior to vesicle
formation; lesion crusts over in 2- days and
heals within 14 days.
Can occur throughout the mouth: palate, pharynx,
gingivae, tongue.

A

herpes labialis - type 1

56
Q

what herpes, specific type

infection of
oropharynx in young children; fever, sore throat,
swollen lymph nodes.

A

herpetiv gingivostomatitis, type 1

57
Q

what herpes, specific type
- ocular herpes
inflammation of eye; gritty feeling in the eye,
conjunctivitis, sharp pain, and sensitivity to light.

A

Herpetic keratitis, type 1

58
Q

what herpes and type

herpes genitalia starts with malaise,
anorexia, fever, and bilateral swelling and tenderness in the groin; clusters of sensitive vesicles on the genitalia, perineum, and buttocks; urethritis, painful urination, cervicitis, itching; vesicles ulcerate.

A

genital herpes type 2

59
Q

where does latency occur in type 2

A

sacral ganglia

60
Q

are recurrent bouts more or less severe in type 2 herpes? triggered by what

A

LESS - triggered by menstruation, stress, and concurrent bacterial infection

61
Q

herpes of newborn 1 vs 2

A

HSV-1 (rare) and HSV-2 (typical)

62
Q

is neonatal herpes fatal

A

yes in neonate and fetus

63
Q

how can newborn get herpes

A

Infant contaminated by mother before (in
utero) or during birth; or after birth by contact
transmission to infant.
Infection of mouth, skin, eyes, CNS, or
disseminated disease.

64
Q

if pregnant women are positive for HSV, how are babies delivered

A

C-section at time of birth

65
Q

what infection:

HSV-1 or HSV-2 can
Infection of skin through a cut or
abrasion.
Extremely painful and itchy.
Whitlow is common in healthcare
workers treating HSV patients
(dentists!)
Gladiatorum is associated with
wrestling.

A

herpetic whitlow and gladiatorum

66
Q

___ rare complication but most common sporadic form of viral encephalitis in the U.S.

A

HSV-1 encephalitis

67
Q

how to diagnose herpes simplex

A
  1. Vesicles and exudate are typical diagnostic signs.
  2. PCR of lesions, CSF or blood is preferred method.
  3. Scrapings from base of lesions showing giant cells.
  4. Direct fluorescent antibody tests also used.
68
Q

what meds to tx herpes simplex

A
  1. acyclovir
  2. famciclovir/penciclovir
  3. valacyclovir
  4. abreva/docosanol
  5. topical medications
69
Q

what med:

Specifically activated by HSV
induced thymidine kinase
enzyme
Inhibits HSV viral polymerase as a
competitor of dGTP, causing DNA chain
termination

A

acyclovir (nucleoside analog)

70
Q

what med:

Acyclyic nucleoside analog of
guanosine
Less potent than Acyclovir; but better
uptake & half-life

A

Famciclovir/Penciclovir

71
Q

what med:

L-valyl ester of acyclovir

A

Valacyclovir

72
Q

what med:

Thought to act by blocking fusion of the
virus with the host cell.

A

Abreva/Docosanol

73
Q

chicken pox and shingles are what type of virus

A

varicella-zoster virus

74
Q

only natural host of VZV? is it highly contagious

A

humans; yes!

75
Q

how is VZV transmitted

A

Transmitted by contact, aerosolized virus and possibly respiratory dróplets.
- Airborne infection is initiated in respiratory tract.
- ~14 day incubation period.
- Contagious 1-2 days prior to appearance of rash.

76
Q

pathology of VZV

A

Chickenpox - characterized by itchy rash, progresses
rapidly from macules to papules to vesicular lesions which
crust.
Children typically exhibit 2-3 days of fever.

77
Q

what is breakthrough varicella

A
  • VZV infection of vaccinated individuals.
  • Typically afebrile illness with < 50 lesions.
78
Q

T/F: VZV primary infection does NOT give you life long immunity

A

FALSE! primary infection confers life-long immunity

79
Q

in VZV, does virus enter neuron and remain laten

A

yes

80
Q

what:

Reactivation of the virus results in
shingles with vesicles localized to distinctive
areas, dermatomes.
Commonly in older patients

A

Zoster

81
Q

complictions of zoster

A
  • postherpetic neuralgia
  • opthalmic involvement
  • bacterial superinfectino
  • nerve palsies
82
Q

what zoster complication:

Persistent pain at rash site after resolution.
Risk increases with age.

A

postherpetic neuralgia

83
Q

tx for VZV

A

treat symptoms in uncomplicated
infections; acyclovir, famciclovir, interferon for
systemic disease.

84
Q

vaccine for VZV

A
  1. varicella (zostavax)
  2. zoster (shingrix)
85
Q

most infections in ___ are asymptomaticc

A

cytomegalovirus

86
Q

is CMV mostly asymp?

A

yes

87
Q

what:

Ubiquitous in the population
70 - 90% of adults are infected
Produce giant cells with nuclear
and cytoplasmic inclusions.

A

cytomegalovirus (CMV)

88
Q

how is CMV transmitted

A

Transmitted in saliva, respiratory
mucus, breast milk, urine, semen,
cervical secretions.
Commonly latent in various
tissues.

89
Q

what groups develop a virulent form of disease in CMV

A
  1. fetuses
  2. newborns
  3. immunodeficient adults
90
Q

newborn complicatins of CMV

A

Newborns may exhibit enlarged liver and spleen, jaundice,
capillary bleeding, microcephaly, and ocular inflammation;
may
be fatal.
Babies who survive develop neurological sequelae, hearing,
visual disturbances and mental retardation

91
Q

perinatal complications of CMV

A

Perinatal CMV infection
mostly asymptomatic, but can
cause pneumonitis, or a mononucleosis-like symptoms.

92
Q

AIDS pt complications of CMV

A

AIDS patients - CMV mononucleosis, disseminated CMV,
retinitis.

93
Q

complications of CMV for transplant patients

A

Transplant patients - pneumonitis, hepatitis, myocarditis,
meningoencephalitis.

94
Q

what disease:

Etiologic agent of “Mono” or “Kissing
Disease.” “Ultimate B-cell parasite.”
Ubiquitous Worldwide distribution. ~90% of adults have antibodies.

A

EBV

95
Q

how is EBV transmitted

A

spread by body fluids especially saliva

96
Q

pathogenesis of EBV

A

Viremia spreads virus throughout the body via lymphatic system and blood.
Latency occurs with infection
of B-cells that differentiate into
B-memory cells.
1 B-cell/milliliter

97
Q

where does EBV infection intitiate

A

Infection initiates in epithelial cells in oropharynx or nasopharynx.
B-cells in tonsils.
Virus shedding into saliva.

98
Q

EBV drive _-cell activation and proliferation with spurious production of ___

A

B-cell, antibodies

99
Q

what cells response to proliferation of B cells in EBV? what happens?

A

T-cell response to proliferation of B and limit outgrowth.
“Civil war” between B- & T-cells.
Lymphocytosis- 10-80% of WBC
count.
Symptoms result from immune
system “fight”.

100
Q

EBV complications

A
101
Q

how to diagnose EBV

A
  1. Differential blood count shows lymphocytosis, neutropenia, and large atypical lymphocytes; cervical lymphadenopathy.
  2. Serological assays to detect antibodies and antigen. Immunoassays / PCR
102
Q

treatment of EBV

A

Treatment directed at relief of
symptoms of fever and sore
throat.
Acyclovir can block EBV
replication, but does not affect
clinical symptoms of AIM.
Disseminated disease
may be
treated with IV gamma globulin,
interferon, acyclovir, and
monoclonal antibodies.

103
Q

what this:

Originally known as human B-
lymphotropic virus.
1 of 5 classic exanthems.
Transmitted by close contact with
saliva and other secretions; very
common.

A

HHV 6 and 7

104
Q

what:

Causes roseola, an acute febrile
disease in babies 2-12 months;
begins with fever, followed by a
faint maculopapular rash; usually
self-limited (1-2 days).
High seroprevalence.

A

HHV 6 and 7

105
Q

symptoms of HHV 6 and 7

A

Adults may
get mono-like
symptoms, lymphadenopathy and
hepatitis.

106
Q

what:

present in Kaposi sarcoma, primary effusion lymphoma and multicentric Castleman disease Endemic in Africa. Assoc. w/ AIDS patients in US.

A

HHV-8

107
Q

how does HHV-8 spread

A

Spread primarily as a sexually transmitted disease, direct contact with infected secretions, including saliva.

108
Q

primary target of HHV-8

A

B-cell primary target, also
endothelial cells, monocytes,
epithelial cells, and sensory
nerve cells.

109
Q

where is latency in HHV-8? incubation period

A

blood lymphocytes and lymphoid tissue
incubation period unknown

110
Q

what type of virus is hep B

A

hepadnavirus

111
Q

what is an inflammatory disease of liver cells that may result from several viruses.

A

Hepatitis

112
Q

what interferes with liver’s excretion of bile pigments, bilirubin accumulates in blood and tissues causing jaundice, a yellow tinge in skin and eyes.

A

hepatitis

113
Q

3 principal viruses in hep

A

Hepatitis B, hepatitis A (RNA virus), hepatitis C (RNA virus)

114
Q

why has incidence of hep plummeted

A

Incidence has plummeted in US due to
surveillance, and vaccines for A & B.

115
Q

structure of HBV

A
  • Small, enveloped DNA virus; 42 nm.
  • Genome is circular and partially dsDNA3200 bases.
116
Q

what does HBV encode

A

Encodes a reverse
transcriptase and replicates
through an RNA
intermediate.
During late step of infection.

117
Q

T/F: in HBV, defective particles of HBsAg outnumber infectious virions. May be spherical or filamentous.

A

TRUE

118
Q

how does HBV replicate

A
119
Q

transmission of hep B

A
120
Q

pathogenesis of hep B

A
121
Q

latency of HBV

A
122
Q

diagnosis of Hep B

A

Typically picked up by clinical symptoms/elevated liver enzymes.
Serological tests to detect viral antibodies or antigen.

123
Q

treatment of acute and chronic hep b

A
  • Post-exposure prophylaxis with anti-HB immunoglobulin for persons exposed, or possibly exposed, including neonates born to infectedmothers
  • Acute Infection= Supportive therapy.
  • Chronic Infection (Interferon alpha, pegylated interferon and Nucleoside analogs)
124
Q

nucleoside analogs for tx of chronic hep b

A
  1. tenofovir (HIV reverse transcriptase inhibitors)
  2. entecavir (deoxyguanosine analog)
125
Q

prevention against hep B

A
126
Q

what is this:

Only B19 and bocavirus are
parvoviruses known to cause human
disease.
B19= Fifth disease-#5 childhood
exanthem (rash)
Boca = mild respiratory infection

A

parvovirus

127
Q

what is smallest human DNA virus

A

parvovirus

128
Q

structure of parvovirus

A

Linear ssDNA molecule.
(+) and (-) strands can be packaged into
virions.

129
Q

where does parvovirus replicated and how do they exit

A

Replicate only in mitotically active
cells.
Erythroid lineage
Requires S phase for complementary
strand synthesis.
Exit by lysis

130
Q

describe fifth disease

A
131
Q

what is worst complicatin of fith disease

A

hydrop fetalis

132
Q

what is infection of seronegative mother and virus can infect fetus and kill erythrocyte precursors resulting in anemia and congestive heart failure

A

hydropfetalis

Micro 2023 (7 decks)

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