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IHO Week 1 > Hemaptopoietic VIruses > Flashcards

Hemaptopoietic VIruses Flashcards

1
Q

What is the general mechanism of most current antiviral drugs?

A

they inhibit viral genome replication by mimicing the shape of a nucleotide (or nucleoside) and plugging up the enzymes that replicate the viral genome.

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2
Q

What nucleoside does acyclovir mimic?

A

guanosine

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3
Q

What must happen to acyclovir for it to be active?

A

it has to be phosphorylated by viral thymidine kinase

after that, host kinases will continue the process until it can be incorporated

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4
Q

Why does acyclovir only work on cells that are actively proliferating?

A

Because expression of thymidine kinase only occurs when the cells enter S phase

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5
Q

What does viral pathogenesis involve in the acute phase? In the long term?

A

acute: cell death and inflammation

long term: malignancies and immune suppression (with opportunistic infections)

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6
Q

How can viruses cause cancer (in general terms)?

A

they express viral oncogenes that mimic and interact with the host cell’s normal replication machinery and promote uncontrolled cellular proliferation

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7
Q

What are the three stages viral oncogenes can act at?

A
  1. the G1-S phase checkpoint
  2. The regulation of cell death by apoptosis
  3. the immunological synapse
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8
Q

Activation of what molecule is the first step in progression to S phase?

A

Cyclin D/CDK4

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9
Q

What signalling pathway controls the cell’s normal apoptotic machinery?

A

In the mitohcondrial membrane, when Bid makes a complex with Bax, it forms a pore that allows cytochrome C release to the cytoplasm where it activates caspases and causes apoptotic cell death

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10
Q

Which complex opposes the Bid/Bax complex and inhibits cytochrome C release (antiapoptotic)?

A

Bcl2/Bid

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11
Q

What is the genomic organization of parvovirus

A

linear ssDNA (group 2)

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12
Q

Does parvovirus have an envelope?

A

no

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13
Q

What is the capsid symmetry of parvovirus

A

icosahedral

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14
Q

What is the tropism for parvovirus?

A

erythroid progenitor cells

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15
Q

How does parvovirus establish infection in the host cell?

A
  1. recognizes a p antgien (globoside) on progenitor cells
  2. binds to it
  3. internalized through coated pits
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16
Q

How does parvovirus replicate

A

enters nucleus and forms a hairpin structure which is a self primer for DNA replication

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17
Q

The relationship between the viral protein NS1 and pathogenesis is….

A

NS1 is a cytotoxic molecule and causes hemolysis of the RBC

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18
Q

A typical clinical presentation of erythema infectiosum is…

A

fifth’s disease: fever, slapped cheek and lacy rash on extremities

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19
Q

What is the treatment for parvovirus?

A

There is no effective antiviral, so supportive

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20
Q

Transient aplastic crisis can occur when…

A

If a person already has a baseline blood disorder and they get parvovirus - they pretty much get a total lack of RBCs

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21
Q

Other conditions caused by parvovirus are…

A

hydrops faetalis: birth defect causing eye disformity

or chronic anemia in immunosuppressed patients

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22
Q

How is parvovivur diagnosed? aka…what do you do assays for?

A

immunofluoescence antibody assay - there are three things you can test for: b19 DNA (the earliest detection) or b19 IgM (the usually test - but remains detectable for 3 months after infection), or PCR (detected for years after infection)

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23
Q

Colorado tick fever: genomic organization

A

segmented dsDNA

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24
Q

Colorado tick fever: enveloped?

A

naked

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25
Q

Colorado tick fever: capsid symmetry

A

icosahedral

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26
Q

colorado tick fever: tropism?

A

erythroblasts

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27
Q

Animal vector for colorado tick fever?

A

rocky mountain wood tick

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28
Q

Geography and season for colorado tick fever?

A

high altitudes

march - november (summer basically)

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29
Q

What is the clinical presentation of colorado tick fever?

A

biphasic fever, myalgia, light sensitivity, rash is uncommon, also uncommon is hemorrhagic disease, meningioencephalitis

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30
Q

What is the substrate of the Dicer/RISC complex for colorado tick fever

A

dsRNA is cleaved by dicer and then RISC is the thing that binds the complementary ssRNA, which will go to the complementary mRNA to break it down and halt translation

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31
Q

How does CTFV protect its genome from DICER/RISC

A

RNA replication occurs in cytoplasmatic viral factories - protects it from the complex

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32
Q

CTFV uses the ___ stand of its genome for transcription and as a template for replication of the ___strand.

A

+RNA of the -RNA strand

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33
Q

CTFV diagnosis?

A

immunofluorescent antibody test for CTFV IgMs

plus CBC with leukocytopenia and thrombocytopenia

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34
Q

CTFV treatment?

A

supportive - no effective antiviral

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35
Q

Associated conditions for CTFV?

A

Rocky mountain fever - very similar clinical presentation (but it’s bacterial)

36
Q

CMV genomic organization

A

linear ssDNA

37
Q

CMV envelope?

A

yes

38
Q

CMV capsid symmetric?

A

icosahedral

39
Q

CMV tropism? systemic? latent?

A

epithelial cells as systemic infection (lytic)

Latent in lineage-commited myeloid cells

40
Q

How does CMV get into the host cell and replicate?

A

viral gycoproteins bind receptor on host cell and enter by endocytosis

41
Q

How does CMV evade host immune response?

A

uses nuclear viral factories and the virus buds out through golgi bodies - so it’s never in contact with cytoplasm

42
Q

A typical presentation of CMS infections mononucleosis…

A

same presentation as mono: fever, sore throat, lymphadenopathy, lymphocytosis

43
Q

What’s the diagnosis for CMS

A

enzyme linked immuno assay - for protein pp65 found in neutrophils that are infected plus the present of owl eye’s cells in blood smear

44
Q

What are the associated conditionsf or CMV?

A

microcephaly with fetal infections

CMV retinitis

hepatosplenomegaly and jaundice and meningioencephalitis

45
Q

What’s the treatment for uncomplicated CMV infection?

A

supportive

46
Q

WHat’s the treatment for severe systemic CMV infections?

A

ganciclovir

47
Q

Why is acyclovir not effective against CMV?

A

CMV doesn’t have thymidine kinase

48
Q

Human Herpes VIrus - genomic organization?

A

linear dsDNA

49
Q

HHV envelope?

A

yes

50
Q

HHV capsid symmetry?

A

icosahedral

51
Q

HHV tropism?

A

CD4 T cells

52
Q

How do HHV 6 and HHV7 differ?

A

6 - T cells, B cells, and NK -d detected in low levels of saliva
7 - mostly just T lymphocytes, high detection in saliva

53
Q

WHat does HHV 6 use to enter host cell?

A

CD46

54
Q

How does HHV 7 enter the cell?

A

binds to CD4

55
Q

Most cases of exanthem subitum (roseola) occur in children of what age?

A

under 2

56
Q

What are the symptoms of exanthem subitum?

A

nonpuritic morbiliform rash, usually on the trunk - always develops after a high fever (this is the happy rash kid)

57
Q

Treatment for HHV6 or 7?

A

supportive - acet and ibu for fever

58
Q

WHat happens in adults?

A

IT’s more of a mono-like illness.

59
Q

What can the reactivated infection cause/

A

encephalitis

60
Q

In immunocompromised patients, what can happen?

A

enephalitis, plus all the other normal symptoms

61
Q

Treatment for severe HHV if encephaitis?

A

ganciclovir, foscarnet, and cytoforvir

62
Q

Genomic orgnization of kaposi?

A

circular dsDNA

63
Q

Kaposi envelopes? capsid?

A

yes - icosahedral

64
Q

What are the malignancies associated with KSV?

A

Kaposi sarcoma

Primary effusion lymphoma

Multicentric Castleman’s disease

65
Q

Who are affected by KSV?

A

People with immune compromise; especially HIV

subsaharan africa, 50% of people are infected

66
Q

KSV tropism?

A

B cells

67
Q

What is vFLIP a homologue of? What does it do?

A

FLICE (which normally regulate apoptosis by inhibiting it)….so it inhibits apoptosis ,thus causing cancer

68
Q

What is KSV’s vBcl-2 a homolog of? What does it do?

A

Bcl-2 of the host cell (duh)

so it also inhibits apoptosis

69
Q

KSV vGPCR is a homolog of what?

A

IL6 - which will increase B cell proliferation

70
Q

KSV’s vCyclin is a homolog of what? what does it do?

A

host cyclin

so it will go thorugh the G1-S checkpoint and continue proliferating

71
Q

What’s the treatment for KSV?

A

Ganciclovir, Cidofir and Foscarnet (just like HHV)

72
Q

What is ganciclovir?

A

synthetic analog of 2’ deoxy guanosine that acts as a chain terminator in virally infected cell

73
Q

What is cidofir?

A

a monophosphate nucleotide analog - acts as a competitive inhibitor of DNA polymerase to terminate chain

74
Q

What is foscarnet?

A

binds to pyrophosphate analog that binding site of DNA polymerases - don’t affect human DNA polymerase at the levels given

75
Q

What is the genomic organization of human T cell lymphotrophic virus

A

ssRNA+

76
Q

Is HTLV enveloped? capsid?

A

yes - icosahedral

77
Q

What is the tropism for HTLV? How are HTLV1 and 2 different in this regard?

A

T cells: HTLV1 does CD4 and HTLV2 does CD8

78
Q

In what population is HTLV2 most common?

A

american indians and injection drug users

79
Q

How does HTLV enter the host cell?

A

It binds to GLUT-1 on the T cells

80
Q

How does HTLV become a provirus?

A

After it enters the host cells, the capsid uncoats and the virally encoded reverse transcriptase creates a DNA copy that is then integrated into the host genome under the influence of viral integrase

81
Q

What does the transcription factor Tax doe for HTLV?

A

It upregulates expression of IL-2 and the IL-2 receptor, which induces proliferation of T cells (also protooncogenes c-fas, c-erg and then GM-CSF)

82
Q

What cancer is associated with HTLV?

A

acute T-cell lymphoma (ATL)

83
Q

What is the typical presentation of ATL?

A

lymphadenopathy, hypercalcemia, lytic bone lesions and cutaneous skin involvement: ranges from papules, nodules, plaques, pathces, and diffuse erythroderma

84
Q

What is HTLV Associated Myelopathy (HAM)

A

It’s a chronic progressive demyelinating disease caused by auto-reactivity

85
Q

What is the typical presentation of HAM?

A

4th decade of life…sublte onset of progressively stiff gait, gradually progressing to weakness, spasticity, back pain, urinary incontinence, apresthesias, hyperreflexia, clonus, babinski, etc.

IHO Week 1 (11 decks)

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