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IHO Week 6 (EH) > Viruses (Skildum) > Flashcards

Viruses (Skildum) Flashcards

1
Q

Colorado Tick Fever - family

A

reoviridae

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2
Q

Colorado Tick Fever - genome

A

dsRNA, segmented

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3
Q

Colorado Tick Fever - Envelope

A

no

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4
Q

Colorado Tick Fever - Capsid

A

icosahedral

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5
Q

Colorado Tick Fever - Baltimore

A

III (dsRNA)

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6
Q

Colorado Tick Fever - Tropism

A

pro-erythroblasts (marrow) –> and then present in mature RBCs

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7
Q

Colorado Tick Fever - pathologies

A

Colorado Tick Fever: Saddleback fever pattern (days of high fever, normal, and then maybe again), travel to mountain West

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8
Q

Colorado Tick Fever - tx

A

supportive

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9
Q

Colorado Tick Fever - vector

A

Dermacenter andersoni tick

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10
Q

Colorado Tick Fever - geography and season

A

March – November

Mountainous western regions

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11
Q

CTFV uses the __________________ strand of its genome for transcription and as a template for replication of the ________________ strand.

A

-RNA (transcribe to +strand = mRNA)

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12
Q

Cytomegalovirus is same as

A

HHV5 (CMV)

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13
Q

CMV - family

A

herpes (beta)

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14
Q

CMV - genome

A

dsDNA

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15
Q

CMV - envelope

A

yes

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16
Q

CMV- capsid

A

icosahedral

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17
Q

CMV - baltimore

A

I

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18
Q

CMV - tropism

A

systemic (variety of cells); latent in CD34+ cells (monocyte –> macrophage)

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19
Q

CMV - pathologies

A

CMV infectious mononucleosis: heterophile Ab negative, Owl’s eyes cells
Congenital systemic CMV: deafness

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20
Q

CMV- tx

A

supportive; ganciclovir for immunocompromised patients

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21
Q

HHV-6 HHV-7 - family

A

herpes

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22
Q

HHV-6 HHV-7 - genome

A

dsDNA

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23
Q

HHV-6 HHV-7 envelope

A

yes

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24
Q

HHV-6 HHV-7 capsid

A

icosahedral

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25
Q

HHV-6 HHV-7 baltimore class

A

HHV-6 HHV-7

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26
Q

HHV-6 HHV-7 tropism

A

CD4+ T cells, others: PBMNCs, epithelial cells

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27
Q

HHV-6 HHV-7 pathologies

A 
exanthem subitum (roseola) = rash taht develops after fever resolves,
heterophile Ab negative mononucleosis
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28
Q

EBV aka

A

HHV4

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29
Q

EBV family

A

herpes

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30
Q

EBV genome

A

dsDNA

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31
Q

EBV envelope

A

yes

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32
Q

EBV capsid

A

icosahedral

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33
Q

EBV baltimore

A

I

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34
Q

EBV tropism

A

acute: epithelial cells of oropharynx (supports lytic life cycle)
latent: B cells

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35
Q

EBV pathologies

A

EBV infectious mononucleosis: Heterophile Ab positive mono
Burkitt lymphoma: t(8:14)
Hodgkin & non-Hodgkin lymphoma
nasopharyngeal lymphoma
X-linked lymphoproliferative disease: inherited mutation in SAP adaptor

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36
Q

tx ebv

A

supoortive (mono)

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37
Q

Kaposi Sarcoma aka

A

HHV-8

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38
Q

Kaposi Sarcoma family

A

herpes

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39
Q

Kaposi Sarcoma genome

A

dsDNA

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40
Q

Kaposi Sarcoma envelope

A

yes

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41
Q

Kaposi Sarcoma capsid

A

icosahedral

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42
Q

Kaposi Sarcoma baltimore

A

I

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43
Q

Kaposi Sarcoma tropism

A

epithelial cells, b cells

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44
Q

Kaposi Sarcoma pathology

A

in immunocompromised patients only: Kaposi sarcoma, primary effusion lymphoma, multifocal castlemans disease

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45
Q

Kaposi sarcoma tx

A

Ganciclovir, cidofir, foscarnet

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46
Q

Parvovirus B19 family

A

parvovirus

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47
Q

Parvovirus B19 genome

A

ssDNA (+ or -)

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48
Q

Parvovirus B19 envelope

A

no

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49
Q

Parvovirus B19 capsid

A

icosahedral

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50
Q

Parvovirus B19 baltimore

A

II

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51
Q

Parvovirus B19 tropism

A

erythroid progenitor cells

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52
Q

Parvovirus B19 pathologies

A

erythema infectiosum: fiery red rash on cheek. Transient aplastic crisis: in patients with underlying anemia

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53
Q

tx Parvovirus B19

A

support

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54
Q

Human T Lymphocyte virus-1 family

A

Retrovirus

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55
Q

HTLV-1 genome

A

ssRNA +

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56
Q

HTLV-1 envelope

A

yes

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57
Q

HTLV-1 capsid

A

icosahedral

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58
Q

HTLV-1 baltimore

A

VI

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59
Q

HTLV tropism

A

T cells
HTLV-1 >CD4
HTLV-2>CD8

60
Q

HTLV-1 pathologies

A

Acute T cell lymphoma / leukemia (ATL): Viral transcription factor Tax drives proliferation; blocks apoptosis.
HAM/TSP: Inflammation on the spine

61
Q

HTLV treatment

A

chemotherapy/BMT

62
Q

HIV family

A

retrovirus

63
Q

HIV genome

A

ssRNA +

64
Q

HIV envelope

A

yes

65
Q

HIV capsid

A

icosahedral

66
Q

HIV baltimore

A

VI

67
Q

HIV tropism

A

CD4+ T cells (also CD4+ monocytes & macrophages, others)

68
Q

HIV pathology

A

Acquired immunodeficiency syndrome: depletion of CD4 T cells allows opportunistic infections

69
Q

HIV tx

A

Multiple anti-retroviral agents

70
Q

Ebola family

A

filovirus

71
Q

ebola genome

A

ssRNA -

72
Q

ebola envelope

A

yes

73
Q

ebola capsid

A

helical/complex

74
Q

ebola baltimore class

A

V

75
Q

ebola tropism

A

macrophages

76
Q

ebola pathologies

A

hemorrhagic fever

77
Q

ebola tx

A

supportive, working on it

78
Q

what does Parvovirus B19 require to gain entry to host cell and establish infection

A

P blood antigen = B19V receptor, found on erythroid progenitor cells

79
Q

How does parvovirus replicate

A

Enters nucleus, folds ssDNA back on itself in hairpin loop structure (self priming)

80
Q

What is the relationship between viral protein NS1 and B19V pathogenesis?

A

NS1 affects cellular DNA and induces apoptosis of erythroid progenitor cells leading to a decrease in the production of erythrocytes (promotes NFkB binding site to IL-6 – activation of polyclonal B cells to cause inflammation?)

81
Q

How to dx parvovirus (beyond clinical signs)

A

serology for anti-pv IgG and IgM. IgM at time of rash, 3rd day of TAC. PCR could be used - but will be positive even in healthy individuals.

82
Q

typical clinical presentation erythema infectiosum

A

Fever 7-10 days after exposure

Then a Slapped cheek appearance and lacy exanthem rash for a few days, may spead

83
Q

When does Transient aplastic crisis occur?

A

Parvovirus B19 in individuals already at risk for anemia –> disastrously low blood counts

84
Q

Other conditions caused by B19V

A

Hydrops fetalis, meningitis, encephalitis, neuropathy

ARthritis, arthralgia (NS-1 hyperinflammatory may lead to autoimmune antibodies)

85
Q

how is CTFV infection diagnosed?

A

Virus isolated from whole blood by inoculation of cell cultures. RT-PCR can detect viral RNA in red blood cells and in plasma. Specific neutralizing antibodies appear in the 2nd wk of illness and can be detected by plaque reduction tests. Can also do ELISA or fluorescent antibody tests.
Usually clinical.

86
Q

Malignancies associated with EBV

A 
Nasopharyngeal carcinoma
Burkitt lymphoma
Hodgkin disease
Non-Hodgkin lymphoma
X-linked lymphoproliferative disease (extremely rare and severe--occurs with a certain an inborn error of metabolism)
87
Q

How does EBV gain entry to B cells and establish infection

A

Viral envelope proteins gp350/220 bind the C3d complement receptor (aka CD21) –> endocytosis
Genome circularizes and immediate early, then early then late genes are expressed.
Viral particles then bud through cell membranes to make infectious particles.

88
Q

EBV oncogene LMP1 function

A

The EBV oncogene LMP-1 functions as a constitutively active CD40. CD40 is normally responsible for CD4+ T-cell dependent activation of B cells.

89
Q

What transcription factors does LMP-1 activate?

A

NF-kB

90
Q

EBV oncogene LMP2 function

A

constitutively active B cell receptor, promoting MAPK activation and transcription of fos/jun (et a) regulated genes. Normally responsible for antigen dependent B cell activation.

91
Q

What transcription factors are activated by LMP2?

A

fos/jun (et al) transcription factors

92
Q

EBV oncogene EBNA3C function

A

The EBV oncogene EBNA3C functions to bind and activate cyclin D1 complexes, resulting in:
Hyperphosphorylation of retinoblastoma protein (Rb)
De-repression (i.e. activation) of E2F family transcription factors
Expression of genes that control DNA replication
Cell cycle progression

93
Q

EBNA3C affects control what checkpoint

A

G1–> S

94
Q

Classic triad of infectious mononucleosis

A

pharyngitis, lymphadenopathy, fever

95
Q

What test is diagnostic for EBV IM

A

monospot

96
Q

what does monospot detect

A

heterophile Abs produced by polyclonal expansion of B cells

97
Q

presence of VCA-IgM in a blood indicates (EBV)

A

acute infection

98
Q

presence of VCA-IgG in blood indicates (EBV)

A

previous infection

99
Q

appearance of what in a blood smear is diagnostic for EBV

A

atypical lymphocytes

100
Q

X linked lymphoproliferative disease presents as

A

Fuliminant infectious mononucleosis (FIM)
Median age for FIM is 3 years old; average survival after FIM is 1-2 months
Patients who survive FIM develop lymphoproliferative disorders and dysgammaglobulinemias

101
Q

Molecular basis for X linked lymphoproliferative disease

A

mutation that results in non-functional SAP protein (SAP adapter protein that recruits kinases to immunological synapse)
SAP depletion results in deficiency of IL-4 production by T cells.

102
Q

IL-4 normally signals

A

CD4 TH2 differentiation and regulates B cell class switching

103
Q

How are HTLV-1 and HTLV-2 different?

A

HTLV-1: >CD4+; HTLV-2: >CD8+

HTLV-1 causes Adult T-cell leukemia, and both 1 and 2 cause HTLV-associate myelopathy

104
Q

What does Ebola virus bind and how to get into cell

A

attachment factors and receptors on the cell surface through the viral spike protein, glycoprotein (GP)

105
Q

what happens after binding of ebola virus to outside of cell

A

The virus is then internalized into a macropinosome (step 2) and trafficked to an endosomal compartment containing the cysteine proteases cathepsin B (CatB) and CatL (step 3).

106
Q

What do catB and catL do to ebola

A

These proteases digest GP to a 19 kDa form, which is then triggered to initiate fusion between the viral and endosomal membranes (step 4).

107
Q

what happens after fusion of ebola membrane and endosomal membrane?

A

After fusion, the viral nucleocapsid is released into the cytoplasm, where the genome is replicated (step 5) and transcribed (step 6) with the aid of the viral proteins VP35, VP30 and L, and viral mRNAs are then translated (step 7).

108
Q

GP protein production in ebola life cycle

A

mRNAs encoding GP are brought to the endoplasmic reticulum (ER) (step 8), where GP is synthesized, modified with N-linked sugars and trimerized. GP is further modified in the Golgi and delivered to the plasma membrane in secretory vesicles (step 9).

109
Q

final assembly ebola life cycle

A

At the plasma membrane the ribonucleoprotein complex (RNA plus nucleoprotein (NP)) and associated viral proteins assemble with the membrane-associated proteins (matrix proteins VP24 and VP40, and GP), and the resultant virions bud from the cell surface (step 10). Non-structural forms of GP, including soluble GP (sGP), are also secreted (step 11).

110
Q

pathogenesis ebola w/ tropism

A

First in DCs, monocytes and macrophages. Neutrophils see viral antigen and are activated (degranulate). As more virus, lymphocytes apoptose, see failure of immune response. (upregulate inhibitory molecules, PD1) infection spreads to many cells, ie hepatocytes. Too many cytokines.

111
Q

Early signs of ebola infection

A

incubation: 2-21 days
Fever, fatigue, muscle pain, headache, sore throat
vomit, diarrhea, rash, kidney/liver issues, internal and external bleeding

112
Q

Cause of death for patients who die of ebola

A

organ failure

113
Q

How is HIV-2 different?

A

Less easily transmitted, period between infection and presentation is longer.
West africa, viral loads lower than HIV-1

114
Q

Normal number CD4
Below what is Immunocompromised
Below what is AIDS

A

600-1200 normal
Below 500 IC
Below 200 AIDS

115
Q

Role of CD4 T cells

A

combat viruses, bacteria, fungi, parasites, cancer

116
Q

If CD4 positive T cells are depleted (HIV)

A

increased viral, fungal, and bacterial functions

Increased risk for some malignancies (ie kaposi sarcoma)

117
Q

What does HIV ELISA measure

A

Direct - antibody

Indirect - antigen for p24 protein (encoded by gag)

118
Q

Positive HIV-1 ELISA confirmed by

A

Wester blot - measures ab in pt serum with sample antigen separated by size

119
Q

what tests are used to monitor health of people with hiv-1

A

CD4+ flow cytometry

viral load

120
Q

where is HTLV-2 more common

A

HTLV-2 endemic to American Indian tribes in North, Central and South America as well as Central African pygmies. Hyperendemic among injection drug users in NA and europe.

121
Q

What molecular interaction allows HTLV to enter a cell?

A

HTLV binds host gp46 and fuses w/ host cell membrane → integrates into DNA → TAX-induced (affects CREB, CREm, NFkB, and NSF) viral gene transcription and REX induced translation or viral mRNA

122
Q

How does HTLV become a provirus?

A

Once in cell, Reverse transcriptase (from virus) transcribes viral RNA into dsDNA. dsDNA (cDNA) is transported to nucleus (as a complex w/ p24 capsid protein and integrase and RT). Integrase helps insert DNA into host genome → lifelong infection.
LTRs (integration sites where provirus attaches to cellular DNA, regulatory)

123
Q

What host genes are upregulated in HTLV-1 Tax?

A

21-bp enhancer, ***NF-kB binding site, serum-response element → cellular genes such as IL-2, IL-2R, fos, erb…
Overproduce IFN-gamma →inflammation

124
Q

What host genes are downregulated by HTLV-1 Tax?

A

beta-polymerase gene = required for genomic stability (does base excision repair)

125
Q

How does Tax contribute to T lymphocyte transformation in HTLV-1?

A

Upregulate proteins for cell growth → proliferation but downregulate pol B which leads to more genetic instability –> malignancy

126
Q

clinical presentation ATL

A

Generalized lymphadenopathy, visceral involvement, hypercalcemia, cutaneous involvement (localized or diffuse, papules, nodules, plaques or patches or erythemoderma, w/ infiltration of malignant lymphocytes, pautrier’s microabscesses, lytic bone lesions, peripheral blood involvement (flower cells).

127
Q

clinical presentation HTLV-1 Associated Myelopathy (HAM)

A

Chronic progressive demyelinating disease that affects spinal cord or white matter of the CNS.
May be associated with blood transfusion, or familial.
Mainly adults (females), some children younger than 10.
Subtle onset - Stiff gait, progressing to increasing spasticity and lower extremity weakness, back pain, urinary incontinence, impotence (men). Tingling, pins and needles, burning.

128
Q

Malignancies associated with Kaposi Sarcoma virus

A

aposi
sarcoma, primary effusion lymphoma,
multifocal Castlemans disease

129
Q

Kaposi Sarcoma virus vFLIP

A

homolog of a normal cellular protein that regulates apoptosis, FLIP. (FLIP inhibits formation of active caspase-8, always on so no apoptosis?_

130
Q

KSV’s vBcl-2

A

homolog of a normal cellular protein that regulates apoptosis, Bcl-2 (Bcl-2 inhibits apoptosis, so always on –> no apoptosis)

131
Q

KSV’s vGPCR

A

homolog of a normal cellular protein that regulates cell fate, GPCR (always growing).

132
Q

KSV’s vCyclin

A

homolog of normal cell protein that regulates apoptosis (Cyclin D1 = constitutively active –> always going through cell cycle)

133
Q

Treatments for KSV target the

A

lytic phase - prevent reinfection only

134
Q

Ganciclovir is the antiviral for

A

beta herpes virsues

135
Q

Cidofir mechanism

A

viral DNA polymerase inhibitor

136
Q

Cidofir effectiveness

A

Cidofovir is an antiviral drug that acts against many types of herpesvirus, and may be an effective treatment for Kaposi’s sarcoma. Use it to treat CMV retinitis in AIDS PTs

137
Q

Foscarnet mechanism

A

viral DNA polymerase inhibitor

138
Q

How does HHV-7 differ from HHV-6?

A 
HHV-6 can integrate into the 
genome
HHV-6 infects peripheral blood mononuclear cells (PBMCs) and cells in the liver, salivary glands, endothelial cells, and central nervous system.
HHV-7 is more found in the saliva 
than HHV-6
HHV-7 can be found in breast milk
while HHV-6 cannot
HHV-7 occurs later in life
139
Q

exanthem subitum

A

roseola or sixth disease

Fever then a rash

140
Q

tx in uncomplicated exanthem subitum

A

Antipyretic, no antiviral

141
Q

What can occur in adults infected with HHV6 and HHV7?

A

May be asymptomatic.

If IC, may see mono, encephalitis, disseminated disease, pneumonitis, syncytial giant-cell hepatitis

142
Q

typical presentation CMV infectious mononucleosis

A

Prolonged high fevers, sometimes w/ chills, fatigue, and malaise. Myalgia, headache, and splenomegaly are common but exudative pharyngitis and cervical lymphadenopathy are rare. Can develop rubelliform rash after exposure to ampicillin. Rare cases can get Guillain-Barré
Heterophile ab NEGATIVE.

143
Q

What is measured in diagnosing CMV infection by enzyme linked immunoassays?

A

p65 in peripheral blood leukocytes

144
Q

What type of cell in a blood smear indicates CMV infection

A

Owl’s eye cells

145
Q

Other conditions associated with CMV

A

Can cause congenital deafness, jaundice, thrombocytopenic purpura, hepatosplenomegaly, microcephaly, and mental retardation. For immunocompromised- hepatitis, penumonitis, esophagitis

146
Q

Why isn’t acyclovir effective for CMV infections?

A

Requires the first phosphorylation (no thymidine kinase)

IHO Week 6 (EH) (9 decks)

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