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x virology term 2 quiz 4 > spreadsheet > Flashcards

spreadsheet Flashcards

1
Q

flaviviruses (virus types)

A

hep C; St louis encephalitis virus; west nile virus; yellow fever virus; dengue virus

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2
Q

flaviviruses (subclasses)

A

hepacivirus and arboviruses

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3
Q

arboviruses

A

st. louis encephalitis virus; west nile virus; yellow fever virus; dengue virus

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4
Q

arboviruses - enveloped?

A

enveloped

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5
Q

arboviruses - nucleic acid/structure

A

+ssRNA

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6
Q

arboviruses - virion structure

A

icosahedral

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7
Q

St. Louis encephalitis virus - transmission route

A

arthropods (mosquitoes; urban/rural habitat), wild/domestic birds

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8
Q

west nile virus - transmission route

A

arthropods (mosquitoes; urban/rural habitat), wild/domestic birds

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9
Q

dengue virus - transmission route

A

Aedes aegypti mosquito, humans

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10
Q

yellow fever virus - transmission route

A

humans, Aedes aegypti mosquito (jungle yellow fever can infect tree mosquito and monkeys…tree mosquito infects human, which then is bitten by Aedes aegypti)

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11
Q

st. louis encephalitis virus - diseases caused

A

encephalitis

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12
Q

west nile virus - diseases caused

A

encephalitis

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13
Q

yellow fever virus - diseases caused

A

yellow fever

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14
Q

dengue fever virus - diseases caused

A

Classical Dengue (“bone-break fever”), dengue hemorrhagic fever (fatal)

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15
Q

st. Louis encephalitis - general epidemiology
how long are the two incubation periods?
Are human’s dead end hosts?

A

requires multiplication in arthropod host (usually 2 incubation periods; intrinsic 7 days in humans; extrinsic 14 days in arthropod), humans are dead-end hosts b/c not high enough viremia

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16
Q

west nile virus - general epidemiology
How long are the two incubation periods?
Are humans dead end hosts?

A

requires multiplication in arthropod host (usually 2 incubation periods; intrinsic 7 days in humans; extrinsic 14 days in arthropod), humans are dead-end hosts b/c not high enough viremia

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17
Q

yellow fever virus - general epidemiology

Where is this virus endemic?

A

only in rural tropical Africa and South America

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18
Q

dengue fever virus - general epidemiology
Where is this virus endemic?
Are humans dead end hosts?

A

found in tropics/subtropics, esp in S.E. Asia and Caribbean islands, humans are not dead-end hosts

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19
Q

st. louis encephalitis - epidemiology
How old are the usual infected patients?
What percentage of cases are fatal?
Where is this virus endemic? Where is this virus found?

A

Generally infects adults over 50yo, 10% cases fatal (mostly in elderly), many subclinical infections, St Louis from N America, West Nile from N Africa and Middle East

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20
Q

west nile virus - epidemiology
What age are the infected patients?
What percentage of cases are fatal?
Where is this virus endemic? Where is this virus located?

A

Generally infects adults over 50yo, 10% cases fatal (mostly in elderly), many subclinical infections, St Louis from N America, West Nile from N Africa and Middle East

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21
Q

yellow fever virus - epidemiology
What is the mortality rate?
Are there ever subclinical infections?

A

High mortality, some subclinical infections

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22
Q

dengue virus - epidemiology
is this virus fatal?
how many subtypes of this virus exist?

A

severe but not usually life-threatening disease, 4 antigenic types

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23
Q

st. louis encephalitis virus - pathogenesis
how long is the incubation period?
Where does the virus first multiply during viremia?
What are the prodromal symptoms?
What are the full infection symptoms?

A

Encephalitis after 7 day incubation period, viremia from multiplication in vascular endothelium, prodromal febrile malaise followed by encephalitis with paralysis/coma/death

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24
Q

west nile virus - pathogenesis
Where does the virus first multiply during viremia?
What are the prodromal symptoms?
What are the full infection symptoms?

A

Encephalitis after 7 day incubation period, viremia from multiplication in vascular endothelium, prodromal febrile malaise followed by encephalitis with paralysis/coma/death

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25
Q

yellow fever virus - pathogenesis
Where is the primary infection?
Where are the secondary infection sites?

A

Primary infection in vascular endothelial cells, then viremia, then secondarily infects liver and other organs (spleen, kidney)

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26
Q

dengue fever virus - pathogenesis

Explain dengue hemorrhagic fever development

A

dengue hemorrhagic fever from massive macrophage infection –> cytokine storm (after sequential infections w/2 diff antigentically cross-reacting dengue viruses)

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27
Q

arboviruses - incubation period in humans?

A

about 7 days

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28
Q

st. louis encephalitis virus - signs and symptoms?

A

fever, malaise

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29
Q

west nile virus - signs and symptoms

A

fever, malaise

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30
Q

yellow fever virus - signs and symptoms

A

fever, nausea, jaundice

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31
Q

dengue virus - signs and symptoms

A

fevere, severe headache, muscle and joint pains, rash… dengue hemorrhagic fever causes patient to vomit blood/hemorrhage/go into shock (most often in native pop)

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32
Q

yellow fever virus - What kind of vaccine?

How long is protection?

A

live-attenuated vaccine (17-D vaccine) gives lifelong protection

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33
Q

togaviruses - subclasses

A

1) arboviruses (zoonoses)

2) nothing (Rubella is a Togavirus, but not an arbovirus)

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34
Q

togaviruses - virus types

A

western equine encephalitis virus; eastern equine encephalitis virus; rubella

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35
Q

togaviruses - enveloped?

A

enveloped

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36
Q

togaviruses - nucleic acid/structure

A

+ssRNA

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37
Q

togaviruses - virion structure

A

icosahedral

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38
Q

western and eastern equine encephalitis virus - transmission route

A

wild birds, mosquitoes (humans and horses dead-end hosts)

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39
Q

rubella virus - transmission route

A

airborne

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40
Q

western and eastern encephalitis virus - diseases caused

A

encephalitis

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41
Q

rubella virus - diseases caused

A

Rubella (German Measles), congenital rubella

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42
Q

western equine encephalitis virus - general epidemiology

What is the habitat of this virus?

A

mosquito habitat - rural

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43
Q

eastern equine encephalitis virus - general epidemiology
How dangerous is this virus?
How old are the usual infected patients?
In what habitat is this virus found?

A

most deadly arbovirus encephalitis in US, mostly infects children in swampy/wetland areas (mosquito habitats)

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44
Q

rubella virus - general epidemiology
how is this virus spread?
Where in the body does the virus multiply?
Does viremia occur?
Is rubella more or less contagious than measles?

A

airborne
after multiplies in respiratory epithelium
viremia develops
less contagious than measles

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45
Q

western equine encephalitis virus - epidemiology
What percentage of cases are fatal?
Are there subclinical infections?
What age groups (name two) are the infected patients?

A

10% clinical cases fatal
many subclinical infections
infects infants and adults over 50 yo

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46
Q

eastern equine encephalitis virus - epidemiology
What percentage of cases are fatal?
Are there subclinical infections?
What age group are the usual infected patients?

A

75% clinical cases fatal, some subclinical infections, generally infects children under 10 yo

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47
Q 
rubella virus - epidemiology
Are there subclinical infections?
How severe in adults?
What is a common symptom?
How long is immunity after infection?
A

sometimes subclinical infection
can be more severe in adults
can cause transient arthritis
all infections produce lifelong immunity

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48
Q

western equine encephalitis virus - pathogenesis
Who are dead-end hosts?
Who are the vectors?

A

humans and horses are dead-end hosts, virus maintained by birds and mosquitoes

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49
Q

eastern equine encephalitis virus - pathogenesis
Who are the dead end hosts?
Who are the vectors?

A

humans and horses are dead-end hosts, virus maintained by birds and mosquitoes

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50
Q

rubella virus - pathogenesis
Where does this virus multiply?
Is there vertical transmission? If so, what type of vertical transmission?

A

multiplies in respiratory epithelium… can cross placenta during pregnancy to cause congenital rubella (earlier infectied, more likely to have defects -esp 1st trimester)

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51
Q

eastern and western equine encephalitis virus - incubation period in humans?

A

7 days

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52
Q

rubella virus - incubation period in humans?

A

18 days

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53
Q

rubella virus - signs and symptoms

A

rash lasts 3 days with fever/lymphadenopathy…
congenital rubella can cause cataracts/heart defects like patent ductus arteriosus/deafness/retardation of child (also spontaneous abortion)

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54
Q

rubella virus - vaccines
What type?
How many doses?

A

live-attenuated vaccine (MMR; 2 doses)

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55
Q

parvovirus - virus type

A

parvovirus B-19

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56
Q

parvovirus B-19- enveloped?

A

non-enveloped

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57
Q

parvovirus B-19 - nucleic acid/structure

A

linear ssDNA

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58
Q

parvovirus B-19 - virion structure

A

icosahedral

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59
Q

parvovirus B-19 - transmission route

A

airborne

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60
Q

parvovirus B-19 - diseases and symptoms caused

A

Transient aplastic crisis
erythema infectiosum (childhood rash = slapped cheek)
hydrops fetalis if infected in first or second trimester

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61
Q

parvovirus B-19 - general epidemiology
Are there subclinical infections?
What is the most common symptom?
What is effect of infection during pregnancy?

A

often subclinical infection, can cause acute arthritis (most common symptom), infection during pregnancy can cause fetal death via edema (hydrops fetalis)

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62
Q

parvovirus B-19 - epidemiology

Who is affected most severely?

A

Patients with pre-existing RBC deficit (anemia, sickle cell anemia) have more severe infection = Transient Aplasic Crisis

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63
Q

parvovirus B-19 - pathogenesis
What cells does paro B-19 infect?
Why are certain patients more susceptible to consequences?

A

infects RBC precursors (inhibits RBC production during incubation)
patients with either anemia or sickle cell anemia are susceptible due to their already low RBC counts.

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64
Q

parvovirus B-19 - incubation period

A

7 days

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65
Q

parvovirus B-19 - signs and symptoms

A

normal people have asymptomatic infection OR ///fever, malaise, rash (erythema infectiosum caused by immune complexes)… keratitis presents with red eye/irritation/photophobia (can cause blindness)

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66
Q

parvovirus B-19 - chemotherapy ie what is treatment?

A

Passive immunization with pooled IgG for people with immunological defects that result in prolonged anemia

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67
Q

papovaviruses - subclasses

A

Polyomavirus (now its own family apart from Papovaviruses but this is not in our notes)

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68
Q

papovaviruses

What viruses are part of papovirus class?

A

papilloma virus (HPV); JC virus

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69
Q

papovaviruses - enveloped?

A

non-enveloped

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70
Q

JC virus - nucleic acid/structure

A

circular dsDNA

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71
Q

papovaviruses - virion structure

A

icosahedral

72
Q

JC virus - transmission route

A

aerosols

73
Q

JC virus - diseases caused

A

progressive multifocal leukoencephalopathy (PML)

74
Q

JC virus - general epidemiology
Who does this illness occur in?
(ie, this is a slow virus and is present for a long time before becoming an illness)

A

Occurs in immunocompromised, slow virus

75
Q

JC virus - pathogenesis
What is the progression of the illness?
How long before death once the illness begins?

A

Demyelinating disease of brain that infects oligodendeoglia
no inflammation!
reactivation of JC virus causes PML that progresses to blindness/dementia/coma/death within 6 months
Note: progressive multifocal leukoencephalopathy (PML)

76
Q

kuru - transmission route

A

consuming brains

77
Q

creutzfeld-jakob disease (CJD) - transmission route

A

inherited mutations, spontaneous mutations, corneal transplants + GH preparations (iatrogenic)

78
Q

variant CJD (mad cow) - transmission route

A

Consuming beef from infected cows (who were fed brains/bone marrow of cows/sheep)

79
Q

prions - diseases caused

A

kuru
creutzfeld-jakob disease (CJD)
variant CJD (mad cow)

80
Q 
kuru - epidemiology
What group of people does this effect?
What was its peak mortality rate?
What is the transmission route?
What is the rate now?
A

limited to stone-age tribe in New Guinea (Fore tribe), caused 1/2 total mortality at peak, transmissible via brain products, low incidence now with reduced cannibalism

81
Q

CJD - epidemiology
How common is this illness among prions?
Who are the hosts?
What are the causes?

A

Most common human spongiform encephalopathy
transmitted to primates
Causes:
can be result of inherited mutation (most spontaneous)
some iatrogenic via corneal transplants and GH preparations

82
Q

vCJD - epidemiology

What started this illness?

A

Outbreak in England linked to eating beef from infected cows

83
Q

Kuru - pathogenesis

What is the progression of this illness?

A

Progressive degenerative disorder of CNS (especially cerebellum), causes spongiform encephalopathy

84
Q

CJD - pathogenesis

A

Spongiform encephalopathy

85
Q

vCJD - pathogenesis
What illness?
What is the cause of this illness?

A

Spongiform encephalopathy of cows (mad cow disease) from using brains/marrow of cow/sheep for bovine food

86
Q

herpesviruses - virus types

A

HSV-1, HSV-2, VZV, CMV, EBV, HHV-6, HHV-7, HHV-8/KSHV

87
Q

herpesviruses - enveloped?

If so, which ones?

A

1-5 are enveloped

88
Q

herpesviruses - nucleic acid/structure

A

1-5 are linear dsDNA

89
Q

herpesviruses - virion structure

A

1-5 icosahedral

90
Q

herpesviruses - how virus multiplies

A

1-5: virion adsorbs to cell, fuses with PM, nucleocapsid goes to nucleus, synthesis of proteins/DNA/mRNA, progeny nucleocapsids assembled in nucleus (nuclear inclusion bodies), glycoproteins inserted into nuclear membrane that nucleocapsids bud through, glycoproteins in PM can result in cell fusion (multinucleate giant cells like measles), also has tegument proteins btw envelope and nucleocapsid

91
Q

HSV-1 - transmission route

A

saliva

92
Q

HSV-2 - transmission route

A

sex, perinatal infection

93
Q

VZV - transmission route

A

airborne, contact with lesions

94
Q

CMV - transmission route

A

close contact, nasopharyngeal fluid, semen, urine, vaginal secretions

95
Q

EBV - transmission route

A

first-basing (kissing, duh!), close oral contact, shared items

96
Q

HSV-1 - diseases caused

symptoms

A

herpes, cold sores, herpes simplex encephalitis/keratitis

97
Q

HSV-2 - diseases caused

symptoms

A

genital herpesm neonatal herpes simplex (perinatal infection, 6 days after birth)

98
Q

VZV - diseases caused

A

chickenpox (primary infection), zoster/shingles (recurrent disease), congenital varicella syndrome

99
Q

CMV - diseases caused

A

mononucleosis-like, most frequent viral congenital infection

doesn’t this also cause some degradation of the brain if there is an nervous system infection?

100
Q

EBV - diseases caused

A

mononucleosis, oral hairy leukoplakia or tumor (in immunocompromised), Burkitt’s lymphoma (esp African boys), nasopharyngeal carcinoma,hepatitis, fatal lymphoproliferative disease in pts w/mutation that blocks cell-mediated immunity

101
Q

HHV-6 - diseases caused

A

roseola infantum (system infection w/rash in infants), MS, CFS, epilepsy

102
Q

HHV-7 - diseases caused

A

none known

103
Q

HHV-8/KSHV - diseases caused

A

Kaposi’s sarcoma

104
Q

HSV-1 - general epidemiology
Are there subclinical infections?
Are primary or secondary infections worse?

A

primary infection often subclinical… often recurrent infections
Primary is worst

105
Q

HSV-2 - general epidemiology
When is this virus most fatal and to whom?
What is the major disruption caused?

A

most fatal perinatal infection is acute primary infection around time of delivery
hepato-adrenal necrosis in neonates

106
Q

VZV - general epidemiology
When do epidemics occur?
Who is most affected?

A

winter-spring epidemics every few years

patients with impaired immune response get severe/fatal chickenpox

107
Q

CMV - general epidemiology
What are the cellular feature of a CMV infection?
During what age in life are infections subclinical?
how common is this infection in newborns?

A

infected cells large with nuclear inclusion
primary infections before puberty often subclinical and
infection of nursing infants is asymptomatic
most frequent viral congenital infection

108
Q

EBV - general epidemiology
What illness does EBV usually cause?
What age group of people usually see a clinical infection?
How does EBV affect the immune system?
Where in the body does the virus reproduce/shed?

A

most common cause of infectious mononucleosis
disease of teenagers and young adults
immortalizes B-cells
virus found in saliva and produced by lymphoid cells in oro-pharynx

109
Q

HHV-6 - general epidemiology

What is the prevalence? in human populations?

A

90% prevalence worldwide, 1% have HHV-6 integration

110
Q

HHV-8 - general epidemiology

What co-infection is HHV-8 usually found with?

A

most frequent neoplasm in persons with AIDS

15-20% AIDS patients develop KS

111
Q

HSV-1 - epidemiology
What brings an latent infection into clinical infection?
Where in the body is the virus latent? Where does it travel to become clinical?
What is the prevalence of infection in adults?

A
  • latent infections activated by…
    fever, UV light, emotion
  • virions transported down axon to site of initial infection, produce cold sores
  • 80% seroprevalence in adults
112
Q

HSV-2 - epidemiology
Are infections once and done or recurrent?
What percentage of the U.S. population is sero-positive?
What precautions during birth should be taken if the mother has an active infection?

A

can cause recurrent infection
20% of US population seropositive
vaginal lesions before delivery indication for C-section

113
Q

VZV - epidemiology
What age group is most affected by Zoster clinical infection? Why?
What other type of patients is at risk for Zoster infection?

A
  • zoster risk increases after 50 yo (decline in cell-mediated immunity)
  • immunosuppressed pts at risk for disseminated zoster (spread by viremia)
114
Q

CMV - epidemiology
What similarities and differences exist between CMV and mononucleosis?
* Where is infection common (age group and external location?
* Do recurrent infections occur?

A

appears like mononucleosis with negative heterophile test

  • transmission common in nursery schools
  • can be post blood transfusion complication
  • recurrent disease only in immunocompromised
115
Q

EBV - epidemiology
What cancer does this cause?
What is the prognosis for young males, if untreated?
What are the different illnesses that this virus causes (aside from mono)?

A

Burkitt’s lymphoma most frequent childhood tumor in Africa, boys at greater risk, if untreated will die in 6 months… can also cause nasopharyngeal carcinoma, Hodgkin’s disease, gastric carcinoma, AIDS patients tumors

116
Q

HSV-1 - pathogenesis
Where (body part) does this virus first infect?
Where does this virus remain as a latent infection?

A

primarily infect nose/eyes/fingers/mouth… travels into sensory ganglia for latent infection

117
Q

HSV-2 - pathogenesis

Where does this virus remain as a latent infection?

A

primarily infect sensory ganglia in genital region (sacral ganglia)

118
Q

VZV - pathogenesis
Where (in the body) does the virus initially infect?
Where is the virus latent?
What immune feature is present in the latent virus location?

A

infection in respiratory tract followed by viremia, latency established in sensory ganglia, monocyte infiltration of involved ganglion

119
Q

CMV - pathogenesis

How does vertical infection occur?

A

virus can cross placenta to cause congenital disease, latent infected cell type unknown

120
Q

EBV - pathogenesis
What cells are infected?
What is the process by which the cancer causes infection?

A

infects B-cells (attacked by CTLs)… for Burkitt’s lymphoma, often involves translocation placing c-myc protoncogene under Ig promoter

121
Q

HHV-8 - pathogenesis

What growth factor does this virus cause to be expressed?

A

tumor cells express high cellular VEGF (for vascularization)

122
Q

HSV-1 - incubation period

A

7-14 days

123
Q

HSV-2 - incubation period

A

7-14 days

124
Q

VZV - incubation period

A

14-21 days

125
Q

CMV - incubation period

A

3-12 weeks

126
Q

EBV - incubation period

A

4-6 weeks

127
Q

HSV-1 - signs and symptoms

A

cold sores, stomatitis (with vesicles in mouth), encephalitis (temporal lobe), keratitis (red eyes)

128
Q

HSV - 2 - signs and symptoms

A

lesions on genitalia, primary infection - bilateral lesions or asymptomatic, recurrent disease - fewer lesions that are unilateral

129
Q

VZV - signs and symptoms

A

fever, rash, lesions… congenital varicella can result in limb atrophy/scarring of skin… post-herpetic neuralgia (pain after zoster lesions heal), zoster lesions have unilateral, dermatomal distribution

130
Q

CMV - signs and symptoms

Also, if the patient has a co-infection with AIDS, what symptoms are common?

A

congenital CMV can result in microcephalic mental retardation with intracerebral calcifications, neuro-sensory deafness, jaundice, enlarged liver/spleen, anemia// immunosuppressed get generalized infections, AIDS pts have high incidence of retinitis and gastroenteritis caused by CMV

131
Q

EBV - signs and symptoms

A

fever, sore throat, lymphadenpathy… oral hairy leukoplakia (white patches on tongue/buccal mucosa)

132
Q

HHV-6 - signs and symptoms

A

systemic infection with rash in infants, high fever

133
Q

HHV-8 - signs and symptoms

A

multiple, pigmented, highly-vascularized nodules on skin

134
Q

HSV-1 - lab diagnostics

A

PCR detection in CSF for herpes simplex encephalitis

135
Q

CMV - lab diagnostics

A

mononucleosis with negative heterophile test, owl’s eye inclusion bodies

136
Q

EBV - lab diagnostics

Also, do antibodies neutralize EBV?

A

heterophile test (antigenic cross-reactivity of Abs to EBV and sheep RBCs), Ab does not neutralize EBV

137
Q

VZV - vaccines

A

live-attenuated (reduces clinical infecions by 85%, reduces severe infections by 97%, elderly should receive booster

138
Q

CMV - vaccines

A

experimental live virus vaccine

139
Q

HSV-1 - chemotherapy

A

trifluridine for recurrent keratitis
adenine arabinoside for encephalitis
acyclovir for systemic infection and for encephalitis

140
Q

HSV-2 - chemotherapy

A

acyclovir

141
Q

VZV - chemotherapy

A
  • Passive immunization with IgG (VZIG)
  • acyclovir (can reduce risk of post-herpetic neuralgia too)
  • foscarnet
142
Q

CMV - chemotherapy

A

ganciclovir, Foscarnet (PPi analogue)

143
Q

papovaviruses - virus types

A

papilloma virus (HPV)

144
Q

HPV - enveloped?

A

non-enveloped

145
Q

HPV - nucleic acid/structure

A

circular dsDNA (10 genes so relies greatly on host proteins)

146
Q

HPV - virion structure

A

icosahedral

147
Q

HPV - how virus multiplies

A

has early and late (capsid) genes… early gene can bind promoter to recruit DNApol for genome replication, all genes essential for virus growth,

148
Q

HPV - transmission route

A

direct contact, sexual contact, perinatal

149
Q

HPV - diseases caused

A

Papillomas (plantar genital, and anogenital warts), cervical carcinoma, condylomas, association w/H&N cancers

150
Q

HPV - general epidemiology
what is the prevalence in college-aged women?
What is a common disease caused by HPV?

A
  • 1/3 college women have HPV in cervix
  • 80-90% of cervical carcinomas have HPV integrated into host genome
  • other cofactors like smoking can cause cervical carcinoma
151
Q

HPV - epidemiology
What illnesses are caused by HPV 6b and HPV 11?
What illnesses are caused by HPV 16 and HPV 18?

A

condylomas (from nononcogenic HPV 6b and 11), >75% cervical carcinomas from HPV16 and HPV18

152
Q

HPV - pathogenesis
Is there virus integration in warts?
Is there virus integration in cervical cancers?
What is the mechanism of uncontrolled cell proliferation?

A
  • in warts the viral genome is not integrated
  • in cervical tumors, early genes are integrated
  • early genes E6 binds p53 to inactivate it and E7 binds Rb to inactivate it (both tumor suppressors)
153
Q

HPV - lab diagnostics

A

Pap smears

154
Q

HPV - vaccines

A

recombinant vaccine based on viral capsid protein

155
Q

retroviruses - virus types

A

human T-cell Leukemia virus-1 and 2 (HTLV 1/2) and HIV

155
Q

retroviruses - virus types

disregard, repeated question

A

disregard, repeat

156
Q

retroviruses - subclasses

A

oncoviruses and lentiviruses

156
Q

retroviruses - subclasses

A

oncoviruses and lentiviruses

157
Q

oncoviruses - virus types

A

HTLV 1 and 2

157
Q

oncoviruses - virus types

A

HTLV 1 and 2

158
Q

HTLV-1 and 2 - enveloped?

A

enveloped

158
Q

HIV - enveloped?

A

enveloped

159
Q

HTLV-1 and 2 - nucleic acid structure

A

+ssRNA, two identical copies

159
Q

HIV - nucleic acid structure?

A

+ssRNA, two identical copies

160
Q

HTLV-1/2 - how virus multiplies

A

RT makes DNA from RNA, DNA integrates into host genome

160
Q

HTLV-1/2 - how virus multiplies

A

RT makes DNA from RNA, DNA integrates into host genome

161
Q

HTLV-1/2 - transmission route

A

sexual contact, blood, breast milk (horizontal transmission)

161
Q

HTLV-1/2 - transmission route

A

sexual contact, blood, breast milk (horizontal transmission)

162
Q

HTLV-1/2 - disease caused

A

adult T-cell leukemia (ATL; from HTLV-1), cutaneous T-cell lymphoma

162
Q

HTLV-1/2 - disease caused

A

adult T-cell leukemia (ATL; from HTLV-1), cutaneous T-cell lymphoma

163
Q

HTLV-1/2 - general epidemiology

A

endemic in southern Japan, central Africa, Caribbean… 0.025% incidnece in US

163
Q

HTLV-1/2 - general epidemiology

A

endemic in southern Japan, central Africa, Caribbean… 0.025% incidnece in US

164
Q

HTLV-1/2 - epidemiology

A

ususally asymptomatic, 0.1% infected individuals develop ATL after 10-30 year latency

164
Q

HTLV-1/2 - epidemiology

A

ususally asymptomatic, 0.1% infected individuals develop ATL after 10-30 year latency

165
Q

HTLV-1/2 - pathogenesis

A

viral tax protein is transcription factor that induces IL-2 and receptor for autocrine loop for transformation

165
Q

HTLV-1/2 - pathogenesis

A

viral tax protein is transcription factor that induces IL-2 and receptor for autocrine loop for transformation

x virology term 2 quiz 4 (6 decks)

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