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IHO Week 1 > Viruses > Flashcards

Viruses Flashcards

1
Q

What is the genomic organization of parvovirus B19?

A
  • neg ssDNA
  • linear
  • small (5000) nucleotides
  • non enveloped
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2
Q

What is the capsid symmetry of parvovirus B19?

A

Icosahedral

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3
Q

What is the only virus we must know whose capsid symmetry is not icosahedral?

A

Ebola virus - helical

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4
Q

What does parvovirus B19 target?

A
  • The erythroid progenitor cell specifically the P antigen.
  • only humans
  • immune if no P antigen
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5
Q

How does parvovirus B19 gain access to the body?

A

Respiratory route

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6
Q

What does the NS1 viral protein do in parvovirus B19?

A

It induces erythroid apoptosis

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7
Q

What is the typical clinical presentation of fifth disease?

A
  • Erythrema infectiosum: macular rash and arthralgia
  • slapped cheek appearance
  • no vaccine or antiviral
  • transient aplastic crisis if there is a blood problem
  • chronic anemia
  • fetal loss
  • give IV-IgG in immunocompromized Pxs
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8
Q

How is parvovirus B19 diagnosed?

A
  • clinical presentation
  • IgG (7th day and on)
  • PCR
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9
Q

What is the genomic organization of Colorado tick fever virus?

A
  • DsRNA
  • linear
  • no envelope
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10
Q

What two viruses we need to know are non enveloped?

A
  • parvovirus B19

- Colorado tick fever virus

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11
Q

What does the Colorado tick fever virus target?

A
  • erythroid progenitor cells
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12
Q

What does the Colorado tick fever virus use to replicate?

A

The negative strand of its RNA

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13
Q

What is the clinical presentation of Colorado tick fever virus?

A
  • fever (biphasic)
  • chills,
  • body ache
  • lethargy/malaise
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14
Q

How is Colorado tick fever virus diagnosed?

A
  • IgM
  • ## reverse transcriptase PCR from blood or CSF
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15
Q

What is the treatment for Colorado tick fever virus?

A

Supportive care

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16
Q

What are some complications with Colorado tick fever virus?

A
  • meningitis and encephalitis

- get blood culture and CT

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17
Q

What is the genomic organization of the EB virus?

A
  • dsDNA
  • gamma-1 herpes virus
  • enveloped
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18
Q

What is the infection of the EB virus?

A
  • lytic in epithelial cells

- latent on B-cells

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19
Q

What malignancies occur in EB?

A
  • Burkitt’s and Hogkin’s lymphoma
  • anaplastic nasopharyngeal carcinoma
  • lymphoma food granulomatosis
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20
Q

How does the EB virus access B cells?

A
  • in the tonsillar regions by CD21 on Bcells

- contact with epithelial cells

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21
Q

What is the EB virus oncogene and what is it’s homologous?

A
  • LMP1 a homologous of CD40 TNF subtype

- activates an epidermal growth factor

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22
Q

What is LMP2 and what virus is it associated with?

A
  • homologous of BCL-2

- activates B-cell proliferation/Antiapoptotic

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23
Q

What is the essential oncogene for EBV for Bcell transformation and what does it do?

A
  • EBAN3C
  • effects G1–>S checkpoint
  • down regulates p53 and possibly a apoptotic protein
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24
Q

What is the classical presentation of EBV?

A
  • Classic triad of infectious mononucleosis
  • ## fever (10-14days mild), sore throat (3-5days severe), swollen lymph nodes (cervical)
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25
Q

How do you diagnosis EBV?

A
  • VCA-IgM first until 4-6 weeks
  • VCA-IgG forever
  • mono spot test, IgM antibodies by bcells
  • Downey cells - atypical lymphocytes, dark deformed nucleus and dark rimmed cytoplasm
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26
Q

What is X-linked lymphoproliferative disease?

A
  • EBV
  • develop fatal lymphoproliferative disease after EBV infection
  • most die from IM
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27
Q

What is the molecular basis for X-linked lymphoproliferative disease in EBV?

A
  • SAP proteins
  • mutations in XIAP
  • ITK, MagT1, CD27
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28
Q

What is the genomic organization of CMV?

A

DsDNA

Enveloped

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29
Q

What is the tropism for CMV infection?

A
  • systemic: epithelial, endothelial, smooth muscle, macrophages, neurons
  • latent: p antigen CD34 myeloid progenitor cells
30
Q

How does CMV gain entry into the body and cells?

A
  • sex, transfusion, saliva, urine, transplant

- 2 membrane glycoproteins (gB and gH-gL dimer)

31
Q

How does CMV evade the immune system?

A
  • disrupts MHC-1 viral protein complex

- makes miRNA that stop production of MCH-1

32
Q

What is the clinical presentation for CMV and what does it cause?

A
  • CMV infectious mononucleosis
  • microcephaly, seizures, deafness, jaundice
  • purpuric lesions resembling a blueberry muffin
  • mental retardation
  • hepatoslenomegaly
  • heterophil mononucleosis (fever, lethargy, abnormal lymphocytes)
33
Q

How do you diagnosis CMV?

A
  • owl’s eyes on a blood smear
  • ELISA for pp65 within leukocytes
  • pp65 is part of the necleocapsid
34
Q

What is the treatment for CMV?

A
  • supportive if not bad

- for severe systemic congenital CMV use ganciclovir

35
Q

What is the genomic organization of human herpes virus 6 and 7?

A
  • DsDNA
  • betaherpesvirinae
  • roseolovirus
  • lipid envelope
36
Q

What virus is called roseola?

A

HHV 6 & 7

37
Q

What is the tropism for HHV 6 & 7?

A
  • CFU-GEMM (hematopoietic stem cell) and all derivatives

- epithelial cells

38
Q

How do HHV 6 and 7 differ?

A

6:
7: more narrow tropism, Helper T cells, and epithelial cells in salivary glands and cells of the lung and skin

39
Q

What is the clinical presentation of HHV 6 & 7?

A
  • roseola or sixth disease
  • exanthem subitum
  • infancy or early childhood
  • not itchy, morbilliform rash on trunk after a high fever resolves
40
Q

How is HHV 6/7 treated?

A

Perhaps ganciclovir and foscarnet

41
Q

What does HHV 6/7 cause in adults and immunocompromized people?

A

Adults: mononucleosis
Immcom: encephalitis (ganciclovir, foscarnet, Cidofovir) against HHV 6

42
Q

What is the genomic organization of Kaposi Sarcoma virus (HHV 8)?

A

DsDN

43
Q

What does HHV 8 cause?

A

Kaposi Sarcoma in immunocompromized Pxs

44
Q

What is the tropism of Kaposi sarcoma virus?

A

B cells

45
Q

What are the four proteins that HHV 8 (Kaposi sarcoma virus) has?

A
  • vFLIP: regulates apoptosis
  • vBcl-2: regulates apoptosis (both stop apoptosis)
  • vGPCR: regulates cell fate (growth and migration)
  • vCyclin: regulates cell division and apoptosis(?)
46
Q

What is the treatment for HHV 8?

A

Latent phase targeting for re infection

  • ganciclovir: chain termination
  • Cidofir: inhib viral DNA pol
  • foscarnet: pyro phosphate mimic on vDNA pol
47
Q

What is the genomic organization of Human T-cell Lymphotrophic virus (HTLV1 & 2)?

A
  • positive ssRNA
  • reverse transcriptase
  • enveloped
48
Q

What is the tropism for HTLV?

A

T-cells

49
Q

What is HTLV2 associated with?

A

No pathogenesis, more common in warm places

50
Q

How does HTLV enter and activate?

A
  • bind gp46 through fusion
  • integrates into host DNA
  • tax induced transcription
  • Rex induced translation
51
Q

What gene does Tax up and downregulate?

A

NF kappa beta (bind also to CREB, CREM) UP

DLG and IKB (degrade) DOWN

52
Q

How does altering gene transcription contribute to transformation?

A
  • activate cellular promoters and cell signaling cascades (Jak/Stat, PI3kinase, JNK)
  • upregulate gene expression (protein)
53
Q

What two things does HTLV cause?

A
  • acute T-cell lymphoma (leukemia)

- HTLV-1 associated myeolopathy (HAM)/ tropical spastic paraparesis (TSP)

54
Q

What is the presentation of ATL?

A
  • malaise
  • night sweats
  • fever
  • cachexia
  • adenopathy
55
Q

What is the clinical presentation of HAM/TSP?

A
  • tcells trafficked into areas of spinal cord leading to astrocytosis and inflammation –> demyelination
  • gait disturbance
  • stiffness and weakness in legs
  • back aches
  • weak bladder
  • constipation
56
Q

What is the genomic organization of HIV?

A
  • positive ssRNA with RT
  • retrovirus of lentivirus
  • envelope
57
Q

What two viruses that we need to know are retroviruses?

A

HTLV and HIV

58
Q

What is the tropism of HIV?

A
  • CD4+ T helper cells primarily
  • macrophages
  • DCs
59
Q

What are the key target molecules of HIV?

A
  • CD4
  • CCR5
  • CXCR4
60
Q

How does HIV-2 differ from 1?

A
  • lower transmissibility and less potential to progress to AIDS
  • more in west Africa
61
Q

What are the t helper cell amounts by disease?

A
  • normal: 1200-1500 per cubic mm
  • immunocompromized: below 500
  • AIDS: below 200
62
Q

What is the role of t helper cells?

A
  • mediate inflammation
  • recruit B cells and proliferation
  • decide when to stop the immune response
63
Q

How is HIV diagnosed?

A

ELISA comfirmed by a western blot

64
Q

What is the genomic organization of Ebola Hemmorrhagic Virus?

A
  • neg ssRNA group V
  • enveloped
  • helical capsid
65
Q

What viruses are dsRNA?

A
  • Colorado fever tick disease
66
Q

What viruses are dsDNA?

A
  • EBV
  • CMV
  • HHV 6 & 7
  • HHV 8
67
Q

What is the tropism of Ebola virus?

A
  • monocytes (macrophages and DCs)
68
Q

What is the clinical presentation of Ebola?

A
  • fever, myalgia, malaise,
  • maybe chills,
  • confused with malaria or dengue
  • flu like symptoms and bleeding
69
Q

How is death from Ebola?

A
  • severe organ dysfunction
  • encephalitis
  • Anuria
  • seizures
70
Q

What is parvovirus 19 infection called?

A

Fifths disease

IHO Week 1 (2 decks)

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