Hepatatis virus Flashcards

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1
Q

Hepatatis viruses - types

A

HAV, HBV, HCV, HDV, HEV

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2
Q

Hepatatis viruses - RNA OR DNA?

A

all rna except HBV

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3
Q

Hepatatis viruses - transmission

A

HAV –> fecal-oral (shellfish, travellers, day care)
HBV –> parenteral, sexual, perinatal
HCV –> primarily blood (IVDU, post-transfusion)
HDV –> Parental, sexual, perinatal
HEV –> fecal-oral (espcecially waterborne, undercooked seafood)

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4
Q

Hepatatis viruses - carrier?

A

all except HAV and HEV

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5
Q

Hepatatis viruses - risk for hepatocellular Carcinoma

A

all except HAV and HEV

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6
Q

Hepatatis viruses - incubation

A
HAV --> short (weeks)
HBV --> long (months)
HCV --> long
HDV --> if superinfection (after HBV),  short.
If coinfection with HBV, long
HEV --> short
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7
Q

Hepatatis viruses - characteristics and family

A

HAV –> RNA-icosahedral-nonenveloped-SS+nonsegmented-Picornavirus
HBV –> DNA-icosahedral-enveloped-DS circular-Hepadnaviridaeg
HCV –> RNA-icosahedral-enveloped-SS+nonsegmented-Flavivirus
HDV –> RNA-NOT EXACTLY icosahedral nucleocapsid-enveloped-SS(-)circular
HEV –> RNA-icosahedral-nonenveloped-SS+nonsegmented-calcivirus (hepevirus)

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8
Q

HDV functional special characteristics

A

HDV is a “defective” virus that requires the presence of HBV to replicate

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9
Q

HDV superinfection (after HBV) vs coinfection (with HBV) according to prognosis

A

superinfection is more severe

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10
Q

HAV - how many serotypes / MC season

A

only 1.. MC season –> autumn

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11
Q

Symptoms and labs for all hepatitis virus (not biopsy)

A
  1. fever
  2. jaundice
  3. INCREASED ALT and AST
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12
Q

beside HAVb, Councilman bodies can also be seen in

A

yellow fever

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13
Q

HEV - liver biopsy

A

patchy necrosis

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14
Q

HAV - liver biospy

A
  1. hepatocyte swelling
  2. monocyte infiltration
  3. Councilman bodies
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15
Q

Fecal-oral hepatitis virus - mechanism

A

HAV, HEV

Naked virus do not rely on an envelope, so they are not destroyed by the gut

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16
Q

nonenveloped hepatitis virus

A

HAV

HEV

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17
Q

HBV - cycle of live

A

the DNA polymerase has both DNA- and RNA-dependent activities. Upon entry into the nucleus, the polymerrase functions to complete the partial dsDNA. The host RNA polymerase transcribes mRNA from viral DNA to make viral proteins. The DNA polymerase then reverse transcribes viral RNA to DNA, which is genome of the progeny virus

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18
Q

HCV - liver biopsy

A

Lymphoid aggregates with focal areas of macrovesicular steatosis

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19
Q

HBV - liver biopsy

A
  • granular eosiniphilic “ground glass appearance”

- cytotoxic T cells

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20
Q

HDV - liver biopsy

A
  • granular eosiniphilic “ground glass appearance”
  • cytotoxic T cells
    (SIMILAR TO HBV)
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21
Q

breastfeeding - HBV vs HCV according to transmission?

A

neither

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22
Q

Hepatitis serologic markers (all)

A
  1. anti-HAV (IgM)
  2. anti-HAV (IgG)
  3. HBsAg
  4. anti-HBs
  5. HBcAg
  6. anti-HBc
  7. HBeAg
  8. anti-HBe
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23
Q

HCV diagnosis

A

anti-HCV

direct dirextion of HCV RNA (gold standard)

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24
Q

anti-HAV (IgM) - marker?

A

IgM antibody to HAV –> best test to detect acute Hepatitis A

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25
Q

anti-HAV (IgG) - marker?

A

IgG antibody indicates prior HAV infection and/or prior vaccination
protects against reinfection

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26
Q

HBsAg - marker / indicates

A

antigen found on surface of HBV

indicates hepatitis B infection (acute or chronic)

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27
Q

anti-HBs - marker / indicates

A

antibody to HBsAg

indicates immunity to hepatitis B

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28
Q

HBcAg

A

antigen associated with core of HBV

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29
Q

anti-HBc - marker

A

antibody to HBcAg (HBV)
IgM = acute/recent infection (+ in window)
IgG = prior exposure or chronic infection

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30
Q

anti-HBc - window

A

IgM anti-HBc may be the sole positive marker of infection during window period

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31
Q

HBeAg - marker

A

a differnet antigenic determinant in the HBV core

indicates active viral replication and therefore high transmissibility (acute HBV or chronic high infectivity)

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32
Q

anti-HBe - marker

A

antibody to HBeAg

indicates low transmissibility (positive in window, recovery, chronic HBV infection with low infectivity)

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33
Q

HBV structure

A
DNA-icosahedral-enveloped-DS circular (PARTIALLY)
diameter 42mm
DNA polymerase 
Core antigens: HBcAg, HBeAG
Coat proteins: HBsAG
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34
Q

HBV: DNA polymerase abilities

A

has both DNA- and RNA-dependent activities

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35
Q

HBV serologic markers

A
HBsAG
anti-HBs
HBeAg
Anti-HBe
anti-HBc
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36
Q

HBV - states

A
Acute HBV
window
Chronic HBV (high infectivity)
Chronic HBV (low inectivity)
Revocery
Immunized
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37
Q

HBV - markes during acute infection

A

HBsAG
HBeAg
anti-HBc - IgM

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38
Q

HBV - markes during window

A

anti-HBc - IgM

Anti-HBe

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39
Q

HBV - markes during Chronic infection with high infectivity

A

HBsAG
HBeAg
anti-HBc - IgG

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40
Q

HBV - markes during Chronic infection with low infectivity

A

HBsAG
Anti-HBe
anti-HBc - IgG

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41
Q

HBV - markes during recovery

A

anti-HBs
Anti-HBe
anti-HBc - IgG

42
Q

HBV - markes during immunized

A

anti-HBs

43
Q

HBV infection - serology during incubation period

A

HBsAg

44
Q

HBV infection - anti-HBc is getting + at (time)

A

the beginning of the acute state (2 months)

45
Q

HBV infection - HBsAg is getting + at (time)

A

the incubation period (1 month)

46
Q

viral hepatitis vs alchoholic hepatitis according to labs

A

viral: ALT>AST
alcoholic: AST>ALT

47
Q

Hepatatis viruses - vaccines and types

A
HAV --> yes (killed)
HBV --> yes (subunit)
HCV -->  no
HDV --> no
HEV --> no
48
Q

viral subunit vaccines - types

A

HBV (HBsAG)

HPV (types 6, 11, 16, 18)

49
Q

HBV - window period - when

A

5,5-6 months

50
Q

HBV - anti-HBs if recovery - when

A

after windorw period (6 months)

51
Q

HBV - acute disease - when

A

2.25-5.25 mounths

52
Q

HIV - characteristics

A

RNA virus - icosahedral nucleocapsid - enveloped - SS+ diploid - Retrovirus -

53
Q

Retrovirus - viruses?

A
  1. HIV
  2. HTLV - 1
  3. HTLV - 2
54
Q

HIV - structural genes - how many and which

A
  1. env (gp120 and gp41)
  2. gag (p24 and p17)
  3. pol
55
Q

HIV - structural genes - env is formed from

A

cleavage of gp160 to form envelop glycoproteins (gp120 and gp41)

56
Q

HIV - structural genes - function

A
  1. env (gp120 and gp41)
    gp120 –> attachment to host CD4+ T cells (docking protein)
    GP41 –> fusion and entry
  2. gag (p24 and p17)
    p24 –> capsid protein
    p17 –> matrix protein
  3. pol –> reverse transcriptase, aspartate protease, integrase
57
Q

HIV - gp120 and gp41 - according to location

A

both on lipid membrane
gp120 outer (non-transmembrane)
gp41 transmembrane

58
Q

HIV - gp120 and gp41 -aquired through

A

budding from host cell plasma membrane

59
Q

HIV - proteins from outer to inner

A

out - gp120 - gp41 - Matrix protein (p17) - capsid protein p24 - reverse transcriptase - inne

60
Q

HIV1 vs HIV2

A

HIV1 –> worldwide and more severe and more transmissible

HIV2 –> primarily in West Africa, less severe, less transmissible

61
Q

HIV - reverse transciptase - function

A

synthesize dsDNA from genomic RNA

62
Q

HIV - synthesis of dsDNA - next?

A

dsDNA integrats into host genome

63
Q

virus to enter the host cells –> ….

A

binds CD4 as well as coreceptor, either CCR5 on macrophages (early infection) or CXCR4 on T cells (late infection)

64
Q

HIV - mutations on host coreceptors:??

A

homozygous CCR5 mutation = immunity

Heterozygous CCR5 mutation = slower course

65
Q

HIV diagnosis - protocol

A

Presumptive diagnosis made with ELISA –> positive results are then confirmed with Western blot assay

66
Q

HIV diagnosis - characteristics of ELISA

A

sensitive, high false positive, low threshold, RULE OUT test

67
Q

HIV diagnosis - characteristics of Western Blot assay

A

specific, low false-positive, rate and high threshold, rule in test

68
Q

HIV diagnosis - rule in and rule out test

A

rule in –> Western Blot assay

rule out –> ELISA

69
Q

HIV - ELISA/Western blot test look for

A

antibodies to viral proteins

70
Q

HIV - ELISA/Western blot test - disadvantages

A
  1. falsely negative in the fist 1-2 months of HIV infection

2. falsely positive in babies born to infected mothers (anti-gp120 crosses placenta)

71
Q

how to diagnose HIV in infants younger than 18 months (no antibodies production) born to seropositive mothers

A

p24 antigen test
PCR
viral culture (not common)

72
Q

AIDS diagnosis?

A
  1. less than two hundred CD4+ cells/mm3
  2. HIV+ with AIDS-defining conditions
  3. CD4 percentage less than 14%
73
Q

normal CD4 COUNT

A

500-1500 cells/mm3

74
Q

HIV transmission

A
  1. sexual contact
  2. infected blood,
  3. cross placenta
  4. birth
  5. breast milk
75
Q

HIV infection - first signs (and when)

A

acute HIV syndrome (not always) - flu like

2 weeks-2.5 months

76
Q

HIV infection - stages (and when)

A

four stages (4fs)

  1. flu like (acute) –> 2 weeks-2.5 months
  2. Feeling fine (latent) –> 2.5 months-8 years
  3. Falling count
  4. Final crisis
77
Q

constitutional symptoms of HIV (AND WHEN)

A

fever, night sweats, diarrhoea, weight loss.

8-11 years

78
Q

HIV infection - death - when (if untreated)

A

11 years

79
Q

HIV infection - opportunistic infection - when (if untreated)

A

9-11 years

80
Q

mechanism of virus during the acute phase of infection

A

wide dissemination of virus

seding of lymphoid organs

81
Q

mechanism of virus during the latent phase of infection

A

virus replicates in lymph nodes

82
Q

Common diseases of HIV positive adults - mechanism

A

As CD4+ decreases:

  1. risks of reactivation of past infections (e.g. TB, HSV, shingles)
  2. dissemination of bacterial infections and fungual infections (e.g. coccidioidomycoses)
  3. increased risk for non-Hodgkin lymphomas
83
Q

HIV - disease (and pathogen) IF CD4 lower than 500

A
  1. oral thrush - Candida ablicans
  2. Oral hairy leukoplakia (EBV)
  3. Kaposi sarcoma (HHV-8)
  4. Chronic Watery diarrhea (Cryptosporidium spp)
  5. SCC, commonly of anus (men who have sex with men, or cervix (HPV)
  6. Bartonella henselae
84
Q

Candida related oral thrush - findings

A

Scrapaple white plaque

pseuohyphae on microscopy

85
Q

Oral hairy leukoplakia - findings

A

Unscrapable white plaque on lateral tongue

86
Q

Chronic Watery diarrhea (Cryptosporidium spp) - findings

A

acid-fast oocyts in stool

87
Q

HIV - disease (and pathogen) IF CD4 lower than 200

A
  1. dementia (HIV)
  2. Progressive multifocal leukoencephalopathy (JC)
  3. Pneumocystic pneumonia (Pneumocystis jirovecii)
88
Q

Brain abscesses (Toxoplasma gondi) - findings

A

Multiple ring-enhancing lesions on MRI

89
Q

Progressive multifocal leukoencephalopathy (JC) findings

A

Non-enhancing areas of demyelination on MRI

90
Q

Pneumocystic pneumonia (Pneumocystis jirovecii) - findings

A

Ground-glass opacities on CXR

91
Q

HIV - disease (and pathogen) IF CD4 lower than 100

A
  1. Hemoptysis, pleuritic pain (Aspergilus)
  2. Meningitis (Cryptococcus neoformans)
  3. esophagitis (Candida)
  4. Retinitis, esophagitis, colitis, pneumonitis, encephalitis (CMV)
  5. B-cell lymphoma (non-Hodgkin, CNS) (EBV)
  6. Fever, weight loss, fatique, cough, dyspnea, nausea, vomiting, diarrhea (Histoplasma)
  7. Nonspecific systemic infection (fever, nigh sweats, weight loss) or focal lymphadenitis (M. avium-intracellulare)
  8. Brain abscesses (Toxoplasma gondi)
92
Q

HIV - Hemoptysis, pleuritic pain (Aspergilus) - findings

A

Caviation or infiltrates on chest imaging

93
Q

HIV - esophagitis (Candida) - findings

A

white plaques on endoscopy

yeast and pseudohyphae on biopsy

94
Q

HIV - Retinitis, esophagitis, colitis, pneumonitis, encephalitis (CMV) - findings

A

linear ulcer on endoscopy
cotton-wool spots on fundoscopy
Biopsy: cells with intranuclear (owl eye) inclusion bodies

95
Q

HIV - EBV - CNS lymphoma - findings

A

ring enhancing, may be solid solitary

96
Q

HIV - IMAGING - toxoplasma vs CNS lymphoma

A

both ring enhancing
Toxoplasma –> multiple
CNS lymphoma –> solitary

97
Q

HIV - Fever, weight loss, fatique, cough, dyspnea, nausea, vomiting, diarrhea (Histoplasma) - findings

A

oval yeast cells with macrophages

98
Q

HDV - antigen / protection against

A

HBsAg

HBV vaccine

99
Q

HIV - viral load test determine

A

the amount of viral RNA in the plasma

100
Q

HIV - viral load test determinations - clinical importance

A

High viral load associated with poor prognosis

monitor effect of drug therapy