micro Flashcards

1
Q

what are the flaviviridae? how are they transmitted? how do they spread through body?

A

Dengue and Yellow fever
insects (mosquitoes)
replicate at epithelial cells around bite then spread to macrophages/spleen/lymph nodes
-secondary viremia can cause hemorrhagic fever/shock

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2
Q

vaccination for what virus is complicated by antibody responses? explain. what’s the potential solution

A

Dengue

  • previous infection with one serotype exarcerbates subsequent infection b/c antibodies help virus get into and infect immune cells
  • tetravalent vaccine with envelope proteins from all 4 serotypes
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3
Q

what are characteristic two signs and two symptoms of classic Dengue?

A

signs: thrombocytopenia and mottled rash
symptoms: bone pain and metallic taste in mouth

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4
Q

what heralds Dengue hemorrhagic fever? what are the signs and what is the pathology?

A

drop in platelet count

  • increased vascular permeability leading to shock
  • restlessness, hypothermia and change in mental status
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5
Q

what virus has three transmission cycles? what are they? what are the reservoir and transmission vector?

A

Yellow fever

  • jungle, intermediate (savannah) and urban
  • primates and mosquitoes
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6
Q

what are the three characteristic signs of hemorrhagic Yellow fever and their cause?

A

stomach hemorrhage: black vomit

liver damage: jaundice and high serum transaminases

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7
Q

what kind of virus is Rift Valley virus and where is it found? how is it primarily transmitted? what is the reservoir? how is it prevented? how do humans get it? what are the symptoms?

A
  • bunyaviridae, Africa
  • mosquitoes
  • livestock
    • vaccinate livestock
  • contact with blood of infected animal
  • flu-like, rarely progresses to hemorrhagic hepatitis
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8
Q

what kind of virus is Crimean-Congo Hemorrhagic Fever Virus and where is it found? what transmits it? what does it affect and what are the signs/symptoms?

A
  • bunyaviridae, Middle East and Africa
  • tick
  • liver and vascular endothelium
  • bone pain and bleeding from multiple orifices
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9
Q

what kind of virus is Hemorrhagic fever with Renal Syndrome and where is it found? what is it transmitted by? what does it target and what is the result?

A
  • bunyaviridae, Europe and Asia
  • rodents: aerosolized urine, droppings, saliva, or dust from nests
  • liver and vascular endothelium
  • renal failure, hemorrhage, fever
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10
Q

what type of viruses are ambisense RNA genome? what are the viruses? what kind of illness do they cause and how do they cause hemorrhage?

A

arenaviridae

  • Lass Fever Virus and South American Hemorrhagic Fever Viruses
  • usually mild
  • multisystem disease
  • hemorrhage due to thrombocytopenia and lymphopenia
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11
Q

what type of virus is Ebola? how does it cause disease? how does it cause hemorrhaging? what are signs/symptoms? how does it kill?

A

filoviridae

  • infects macrophages/monocytes eliciting cytokine storm
  • pancytopenia leads to loss of coagulation and vascular abnormalities
  • rapid onset of symptoms, flu-like symptoms, maculopapular rash
  • succumb to hypovolemic/hemorrhagic shock and systemic organ failure
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12
Q

how do you confirm that the illness is Ebola?

A

RT-PCR 72 hours after symptoms begin

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13
Q

what is the evidence that Ebola elicits a neutralizing antibody response?

A
  1. successful treatment of ill patients with convalescent serum of survivors
  2. ZMapp-drug with monoclonal antibodies that neutralize the virus has shown success
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14
Q

what drug is indicated for HSV, VZV and EBV? for CMV retinitis? for CMV in transplant?

A
  • acyclovir
  • ganciclovir, foscarnet, cidofovir
  • valganciclovir
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15
Q

what virus can cause retardation and deafness due to neonatal infection?

A

CMV

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16
Q

how is CMV spread? where does it replicate initially and where does it spread to? what is the characteristic sign of CMV?

A
  • bodily secretions
  • epithelial cells then spreads to lymphoid tissue
  • large, puffed up cells
17
Q

what is associated with transplant infection and what does it cause? what’s the time table?

A

CMV: pneumonitis 1-4 months after transplant

18
Q

what does CMV do in AIDS patients?

A

retinitis, colitis, and pneumonitis

19
Q

what is used to diagnose CMV, beside PCR?

A

shell vial assay for IE proteins

20
Q

how is EBV spread? what does it replicate in then spread to? where is it latent?

A
  • saliva
  • oropharyngeal epithelium, to lymphocytes, spleen, liver
  • latent in throat epithelium and B cells
21
Q

what do the following results mean?
anti-VCA+, anti-EBNA-
anti-VCA+, anti-EBNA+

A
  • primary EBV infection

- recovered from EBV infection

22
Q

what is the monospot test?

A

tests for EBV mononucleosis

  • heterophile antibodies
  • agglutinate sheep RBC if positive for them
23
Q

what acute issue can EBV cause in AIDS patients and how is it treated?

A

oral leukoplakia

  • productive infection of tongue epithelium
  • acyclovir
24
Q

what can EBV cause in transplants? how?

A

PTLD-transforms B cells in transplant

25
Q

what neoplasm (beside Burkitt’s) is EBV associated with? what else is associated with that neoplasm?

A

nasopharyngeal carcinoma

-high salt diet in South China

26
Q

what three diseases can HHV-8 cause?

A

KS: tumor of lining of lymphatic system so lymph channels fill with blood
primary effusion lymphoma: non-Hodgkin’s
Castleman’s disease: lymph node tumors

27
Q

what is the core capsid protein of HIV? what two things is it important in?

A

p24

  • used in diagnosis/virus quantification via ELISA
  • if cleavage prevented by protease inhibitors, virion is noninfectious
28
Q

describe the lytic cycle of HIV after integration?

A

1) transcribe full length RNA copy of provirus (integrated in host genome)
2) tat (transactivator of transcription) binds TAR and increases transcription
3) rev mediates transition to late gene expression (structural protein production)
- binds RRE (rev response element), facilitates transport of unspliced mRNAs out of nucleus
- unspliced mRNAs encode structural proteins
4) gag, gag-pol and env proteins now synthesized, create virion

29
Q

what are elite controllers? how might they achieve that?

A

long term non-progressors, viral load <50/mL

  • HLA-B57 allele
  • missense mutation in CCR5
30
Q

what are long term survivors? how might they achieve that?

A

survive >10 years

-may be infected with HIV strain with nef-deletion