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Virology > Hepatitis > Flashcards

Hepatitis Flashcards

1
Q

HAV class

A

Picornaviridae

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2
Q

HBV class

A

Hepadnaviridae

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3
Q

HCV class

A

Flaviviridae

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4
Q

Hep D class

A

Satellite, coinfect with B

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5
Q

Hep F class

A

???

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6
Q

Hep G class

A

Flaviviridae

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7
Q

HAV genome and structure

A

ss+RNA

Icosahedral capsid of 4 polypeptides (VP1-4)

Non-enveloped

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8
Q

HAV genome distinguishing feature:

A

VPg (protein) on 5’ end

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9
Q

HAV inactivated by (5 things)

A

Chlorine

Formalin

Peracetic acid

Beta-propiolactone

UV

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10
Q

Replication of HAV (6 steps)

A

Receptor binding

Uncoating (+RNA)

Translation/Proteolytic processing

Replication

Assembly

Maturation and release

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11
Q

HAV produces _____ infection

A

acute

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12
Q

HAV incubation period length

A

2-6 weeks

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13
Q

2 phases of HAV infection

A

1. Prodrome (flu-like, immune mediated hepatic damage)

2. Icteric (billirubinemia, jaundice, abdominal pain)

  • symptoms wax/wane
  • complete recovery in 99% cases
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14
Q

Immunogically, acute HAV infection results in

A

lifelong immunity

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15
Q

icterus is an increase in

A

unconjugated bilirubin

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16
Q

What happens to conjugated bilirubin?

A

Water soluble, renal excretion

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17
Q

HAV replication occurs in __________ (in body)

A

Oropharynx or GI tract

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18
Q

HAV is shed in the _______

A

bile and feces

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19
Q

Does HAV cause viremia?

A

Yes

Brief

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20
Q

HAV can be detected…

A

in the stool before symptoms occur

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21
Q

Three serological peaks during HAV infection

A

ALT at 2 months

IgM anti-HAV at 3 months (recent infection)

Total anti-HAV (immunity

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22
Q

HAV transmission routes (3 categories)

A

Close personal contact

Contaminated food

Blood exposure (rare)

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23
Q

Seroprevalence of HAV antibodies

A

40-70% of adults

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24
Q

Serological distinction between acute and past HAV infection

A

IgM = Acute

IgG = Past

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25
Q

IgM and IgG are detected by

A

ELISA

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26
Q

Is RT PCR useful in detection of HAV?

A

It may detect earlier than serology, but it is rarely performed

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27
Q

HAV vaccines

A

HAVRIX

VAQTA

TWINRX

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28
Q

Who is TwinRx not recommended for? What’s the dosing schedule?

A

All patients under 18 years of age.

3 doses @ 0, 1, 6 months

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29
Q

HBV genome and structure

A

Genome: Circular dsDNA

Capsid: Icosahedral

Enveloped

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30
Q

HBV capsid proteins

A
  1. Core Protein
    (HBcAG)
  2. Soluble core protein

(HBeAG)

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31
Q

What is HBeAG?

A

Indicator of active HBV replication phase

(it is a variant of the core protein that was modified within the cell)

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32
Q

HBV envelope proteins

A

Surface antige (HBsAG)

3 forms:

  1. S = large
  2. S2 = medium
  3. S1 - small
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33
Q

Unique feature of the DNA virus HBV

A

Encodes a RT enzyme

replicates through RNA intermediate

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34
Q

The first weird step of HBV replication cycle

Second and third steps?

A
  1. After uncoating, partially double stranded DNA genome is completed by host enzymes – becomes CCCDNA (Covalently Closed Circular DNA)
  2. Four mRNAs are made (one giant one)
  3. Goes to cytoplasm where the mRNAs assemble around the big one, and NEGATIVE DNA is made by Reverse Transcriptase
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35
Q

What happens after DNA is synthesized in HBV replication?

A

RNA Degrades, and the POSITIVE counterpart to the negative DNA is synthesized.

The envelope forms before this completes

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36
Q

HBV released from cell via ______ after assembly

A

Exocytosis

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37
Q

HBV causes what kinds of infections?

A

Acute or chronic

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38
Q

Acute HBV incubation time

A

1-6 months

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39
Q

Most HBV acute patients are ________

A

asymptomatic

40
Q

Some Acute HBV patients progress to

41
Q

Few patients progress to _________ during acute HBV infection

A

Fulminant Hepatitis

risks = GI bleed, coma, encephalopathy, ascites, coagulopathy)

42
Q

Survival from acute HBV results in _____________

A

lifelong immunity

(patients will never develop chronic infection)

43
Q

Fulminant Hepatitis requires…

A

Delta agent

44
Q

Chronic HBV patients may…

A

transmit infection throughout life

45
Q

Chronic HBV is definied as

A

longer than 6 months

46
Q

Infants with perinatal HBV infection will…

A

almost always develop CHRONIC hep B infection

47
Q

Chronic HBV = increased risk of

A

cirrhosis, liver cancer, liver failure

48
Q

HBV infects the liver but does not…

A

cause direct cytopathology

49
Q

_____ is the leading cause of liver transplantation in the US

A

Chronic HBV

50
Q

Titer cuves for acute HBV

A

1st peak = HBsAG

2nd peak = IgM ant-iHBc (Also TOTAL anti-HBc increases here)

Last = anti-HBs

51
Q

Chronic HBV, _____ and ______last much longer in serum titer

A

HBeAG

HBsAG

52
Q

______ doesn’t have a titer peak in chronic HBV

53
Q

HBV transmission

A

Blood, sex, contact

Transplacental (or perinatal)

54
Q

Areas of highest HBV incidence

A

Subsaharan Afriaca, SE Asia

55
Q

HBV treatment

A

Acute HBV = (None)

Chronic HBV = Reverse Transcriptase Inhibitors

  1. Lamivudine
  2. Adefovir + alpha-Interferon
56
Q

HBV control (3)

A
  1. Blood donation screening
  2. Universal precautions
  3. Passive or Active Vax
57
Q

HBV vaccine based on ____. This is recommended for whom? Dosing Schedule?

A

HBsAG

recommended for young and high risk

3 injections (TwinRX = HAV + HBV together)

58
Q

HCV genus, genome, and structure

A

Hepacivirus

ss+RNA (looks like Flavivirus)

59
Q

HVC is classified into _______ genotypes. Which are the most common?

A

6 genotypes

Types 1-3 are most common

60
Q

HVC Clades nucleotides differ by 25%, but difference is not correlated to…

A

differences in clinical disease

61
Q

HCV displays classic _____ replication

A

+RNA

(everything happens in the cytoplasm)

62
Q

Acute HCV is _______ in most patients

A

asymptomatic

63
Q

“Persistent HCV” definition

A

detectable HCV RNA for more than 6 months from the time of presumed infection

64
Q

Jaundice rate in HCV patients

65
Q

__________ is responsible for HCV hepatic damage

A

CMI leading to inflammation of the liver

66
Q

Hepatocellular pathogenesis of HCV (three things)

A
  1. Miscroscopically spotted parenchymal cell degeneration
  2. Necrosis of hepatocytes
  3. MQ accumulate near the degenerating hepatocytes
67
Q

Acute HCV infection shows __________multiplication

A

high, fast

68
Q

Sx of acute HCV coincide with increase in

69
Q

_______ appears in serum after about 8 weeks post-HCV exposure

A

Anti-HCV (EIA-III)

70
Q

Highest source for HCV infection

A

IV drug use

71
Q

Sources (3) with least prevalence for HCV infection

A

nosocomial

iatrogenic

*perinatal*

72
Q

Vertical transmission to fetus occurs in __ % of HCV cases

73
Q

% risk for HCV transmission from breastfeeding

74
Q

Sexual transmission of HCV is _____ than HIV and HBV

75
Q

HCV transmission between partners may be associated with ….

A

shared use of Razors and toothbrushes

76
Q

Needlestick transmission rate for HCV is _____ than HIV

A

HIGHER

1.8% versus 0.35%

77
Q

HCV treatments (3)

A
  1. Interferon + Ribavirin
  2. Pegylated Interferon alpha + Ribavirin
    (3. Bocepravir + Telaprivir (protease inhibitors))
78
Q

HDV needs _____ for infection

A

HBsAG

envelope protein from other virus

79
Q

HDV genus, genome and structure

A
  • Deltavirus
  • ss (-) RNA, Circular
  • Enveloped
80
Q

HDV RNA encodes _________ that complexes with _______

A

Delta agent

complexes with RNA

81
Q

Chronic infection with HDV occurs in ___% of cases

82
Q

Two types of HDV infections:

A
  1. Co-infection (fulminant in 1%)
  2. Super-infection (fulminant in 5%)
83
Q

________ HDV infection is far more likely to develop into a chronic infection

A

Superinfection - 80-90% of patients

84
Q

What is a HDV superinfection?

A

Infection with HDV in a patient that is already positive for HBsAG

85
Q

Superinfection HDV causes rapid…

A

cirrhosis and hepatocellular carcinoma

86
Q

HDV treatment

A

alpha interferon + lamivudine

87
Q

HEV genome and structure

A

ss+RNA

icosahedral

nonenveloped

88
Q

Number of HEV genotypes? Which cause human diseases?

A

Four

Only #1 causes human disease

89
Q

Phases of HEV infection

A

Prodromal and icteric

90
Q

HEV infection is _________

A

self-limited

91
Q

HEV…E stands for

A

Enteric + Epidemic

92
Q

HEV spread via…

A

fecal oral route

93
Q

Epidemics of HEV reporded where…

A

fecal contamination of drinking water is common

94
Q

Most important prevention measure for HEV is

A

Sanitation

95
Q

HEV chronic infection length

A

HEV doesn’t cause chronic infection

Virology (13 decks)

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