Viruses of the hematopoietic system Flashcards

1
Q

parvovirus B19 stats:

A

linear ssDNA(-)

non-enveloped

icosahedral capsid symetry

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2
Q

Tropism of parvovirus B19:

A

human erythroid progenitor cells

blood group P antigen (people deficient in P antigen are immune)

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3
Q

Transmission of parvovirus B19?

A

respiratory droplets

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4
Q

Role of viral protein NS1?

A

induction of erythroid apoptosis

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5
Q

typical clinical presentation of parvovirus B19?

A

fifth disease

“slapped cheek”–>lacy macular rash on extremeties

arthralgias

Tx: supportive of sx, no vac or antiviral available
-give immunocompromised pts IV-Ig

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6
Q

Colorado tick fever virus stats:

A

Linear dsRNA

non-enveloped

icosahedral symetry

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7
Q

Tropism of Colorado tick fever virus:

A

Erythrocytes

Animal vectors:

  • Rocky mountain wood tick
  • small mammals

spring/summer

Rockies/west coast

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8
Q

CTFV method of replication:

A

uses negative strand of its genome for transcription and as a template for replication of the positive strand

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9
Q

Typical clinical presentation of CTFV…

A

fever/chills, body aches, lethargy malaise

dx: PCR of blood or CSF–detection of viral RNA/IgM

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10
Q

Tx of CTFV?

A

supportive care

**may be more complicated in form of meningitis or encephalitis

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11
Q

Epstein Barr Virus stats:

A

dsDNA (gamma-1 herpes virus)

enveloped

icosahedral capsid symmetry

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12
Q

tropism of EBV?

A

Lytic cycle in epithelial tissue

Latent infx in B-cells

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13
Q

Malignancies associated with EBV:

A
  • Burkitt’s lymphoma
  • anaplastic nasopharyngeal carcinoma
  • Hodgkin’s disease
  • Lymphomatoid granulomatosis
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14
Q

How does EBV establish infx?

A
  • contact with CD21 on surface of B-cells
    • directly in tonsillar region
    • indirectly through contact with epithelial cells
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15
Q

What is LMP1?

A

EBV oncogene homolog of CD40-TNF subtype

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16
Q

What is LMP2?

A

EBV oncogene homolog of BCL2–>antiapoptotic–>B-cell proliferation

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17
Q

What is EBNA-3C?

A

EBV oncogene:

essential for EBV’s ability to cause B-cell transformation

induces epigenetic silencing of pro-apoptotic protein BIM

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18
Q

Presentation of infectious mononucleosis:

Dx?

A

Fever 10-14 days

sore throat

3-5 days severe swollen glands (usually posterior cervical lymph nodes)

Dx: monospot test detects IgM produces by B cells

-Downey cells in blood smear

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19
Q

EBV x-linked lymphoproliferative disease presents as?

A

Recessive disorder in young boys, can present as severe infectious mononucleosis and be fatal

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20
Q

Important molecule in mediating X-linked proliferative disease?

A

SAP proteins

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21
Q

Cytomegalovirus stats:

A

dsDNA

enveloped

icosahedral nucleocapsid

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22
Q

Tropism of cytomegalovirus:

A

Systemic infx: epithelial cells, smooth muscle cells, macrophages, neurons

Latent infx: CD34 myeloid progenitor cells

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23
Q

How does cytomegalovirus establish infx?

A

attaches to host cell via glycoprotein B [gB] and a gH-gL dimer

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24
Q

How does cytomegalovirus evade host immune system?

A

MHC-1 is destabilized in infected host cells so viral antigens are not presented to cytotoxic T-cells

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25
A typical clinical presentation of CMV infectious mononucleosis is . . .
Infants: microcephaly, seizures, deafness, jaundice, and purpura. The purpuric lesions resemble a “blueberry muffin” and are due to thrombocytopenia. Hepatosplenomegaly is very common. Adults: heterophil-negative mononucleosis: -fever, lethargy, and the presence of abnormal lymphocytes -Systemic CMV infections, especially pneumonitis, esophagitis, and hepatitis, occur in a high proportion of immunosuppressed individuals.
26
CMV Dx?
enzyme linked immunoassay for pp65 within leukocytes and... "OWL'S EYE" in blood smear
27
Tx for CMV: Complicated and uncomplicated
uncomplicated: supportive care severe systemic can be treated with Ganciclovir
28
Why is acyclovir ineffective in CMV?
CMV has no thymidine kinase
29
HHV 6&7 stats:
dsDNA enveloped icosahedral
30
HHV 6&7 tropism:
CFU-GEMM (hematopoietic stem cells), monocytes, peripheral blood mononuclear (neutrophil, macrophage, eosinophil, basophil, T & B cells), epithelial cells
31
Difference between HHV 6 & 7?
HHV-7 has narrower tissue tropism
32
Clinical presentation of HHV 6/7?
exanthem subitum (also called sixth disease or Roseola infantum)--occurs mostly in infancy or early childhood -faint pink or rose colored, non-puritic rash following approx 72 hrs after a high fever
33
Tx for HHV 6/7:
Ganciclovir, foscarnet, cidofovir
34
Kaposi sarcoma virus stats:
(HHV-8) dsDNA enveloped icosahedral related malignancies: Kaposi sarcoma People affected: immuncompromised pts
35
Kaposi sarcoma virus (HHV-8) tropisms:
B-cells
36
Kaposi sarcoma virus (KSV) (HHV-8) protein that messes with apoptosis?
vFLIP--> replaces FLIP which is pro-apoptotic meaning vFLIP is anti-apoptotic and therefore oncogenic
37
Treatment for KSV target_______.
lytic pase
38
Tx options for KSV? how do they work?
Ganciclovir--chain terminator Cidofir--inhibits viral DNA polymerase Foscarnet--inhibits binding site on viral DNA polymerase (dose not affect human DNA polymerase)
39
Human T-cell Lyphotrophic Virus (HTLV-1 and HTLV-2) stats:
ssRNA w/reverse transcriptase enveloped icosahedral
40
HTLV tropism:
T-cells
41
How are HTLV-1 and HTLV-2 different?
1-causes T-cell leukemia and myelopathy/troapical spastic paraperris 2-is non pathogenic, more common in caribbean, eastern SA, west africe, and south japan
42
How does HTLV enter host cells?
binds host cell gp46 --> fusion with cell's plasma membrane **must integrate into host cell's DNA to become pro virus gene expression: - Tax-transcription - Rex-translation of viral mRNA
43
HTLV causes leukemia by ...
Tax upregulates NFkB, IFN-I, IFN-B, TBK1 and IKKE downregulates p53
44
Typical clinical presentation of Acute T-cell Lymphoma:
- malaise - night sweats - fever - cachexia - adenopathy
45
What is HAM/TSP? How does it present?
HTLV-1 Associated Myelopathy aka Tropical Spastic Paraparesis -infected T cells trafficked into spinal cord and cause astrocytosis and inflammation of gray and whit matter leading to progressive demyelination Presenting sx: - gait disturbance - stiffness/weakness in legs - back aches - "weak" bladder - constipation
46
Human Immunodeficiency Virus (HIV-1, HIV-2) stats?
Lentivirus (subgroup of retrovirus group VI) ssRNA (+) w/reverse transcriptase enveloped capsid symmetry: icosahedral
47
HIV tropism:
CD4+ T-cells primarily (also Macs and Dendrites) - CD4 - CCR5 - CXCR4
48
What is the difference between HIV 1 and 2?
2 has lower transmissibility and less potential to progress to AIDS. 1 is world wide, 2 is more confined to West Africa
49
Number of CD4+ T-cells to be considered AIDS?
50
Do patients die of HIV or AIDS?
No, the die of inability to respond to another disease
51
thymidine analog (nucleoside reverse transcriptase inhibitor), blocks RT at active site.
zidovudine (Retrovir)
52
non-nucleoside reverse transcriptase inhibitor (NNRTI), binds RT far from active site
efavirenz
53
Entry inhibitor, inhibits catalytic activity of HIV integrase
raltegrovir
54
HIV protease inhibitor
ritonavir
55
Chemokine receptor 5 antagonist. HIV entry inhibitor.
maroviroc
56
Ebola virus stats:
non-segmented negative strand RNA -group V enveloped **Helical capsid
57
Ebola virus tropism:
Can infect many cells. Blood cells: monocytes, macrophages, dendrites
58
Clinical presentation of Ebola:
very general - fever, myalgia, and general malaise and sometimes accompanied by chills - often confused with malaria or dengue in tropical climates. -initial period is followed by flu-like symptoms, gastro-intestinal symptoms and in severe cases maculo-papulary rash, petichae, conjunctival hemorrhage, epistaxis, melena, hematemesis, shock and encephalopathy
59
Supportive care for Ebola patients:
aggressive replacement of fluids and electrolytes - oral rehydration solution when possible, intravenous infusion when necessary - Oxygen and vasopressors should be used if available and necessary to maintain adequate bodily function
60
Cause of death from Ebola?
End stage disease w/ severe organ dysfunction, encephalitis, anuria, seizures