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1Principles of Biomedicine - MD1 > 109 - Viral Hepatitis 1 and 2 > Flashcards

109 - Viral Hepatitis 1 and 2 Flashcards

1
Q

Cause of jaundice

A

Hyperbilireubinaemia

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2
Q

Type of cancer that hepatitis can lead to

A

Hepatocellular carcinoma

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3
Q

Effect of hepatitis viruses on host cells

A

Cytopathic (cause pathology), but not cytolytic (don’t lyse host cells)

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4
Q

Different prognosis of hepatitis disease based on age of transmission

A

Younger exposure leads to less severe acute disease, greater likelihood of chronic diseaseOlder exposure leads to more severe acute disease, lesser likelihood of chronic disease

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5
Q

Is there any cross-protection between hepatitis viruses?

A

No

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6
Q

Enteric hepatitis viruses

A

Hep A and E

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7
Q

Chronic hepatitis viruses

A

Hep B, D and C

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8
Q

How are hep B, C and D transmitted?

A

Percutaneously, permucosally

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9
Q

How to diagnose acute hepatitis 1 2

A

1) Serological tests (EG: ELISA) 2) Nucleic acid tests (EG: PCR). This is less effective than ELISA.

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10
Q

ELISA tests for acute hepatitis1)2)3)

A

1) Over 90% sensitive, over 99% specific
2) IgM antibodies detectable at between 1-2 weeks after exposure.
3) Rising IgG titres indicates an acute infection

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11
Q

Hepatitis A viral family

A

Picornaviridae

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12
Q

Hep A virion characteristics1)2)3)

A

1) Non-enveloped, (+)ssRNA virus
2) 30nm particle, resistent to stomach acid
3) 7.5nt genome, coding for a single polyprotein

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13
Q

Serotypes of hep A

A

Single serotype worldwide. All viral strains elicit the same antibody response.

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14
Q

Hep A and hep E life cycles1)2)3)4)

A

1) Ingested from contaminated food or water
2) Replication in intestinal epithelia
3) Enters blood, replicates in the liver
4) Excreted via the bile canaliculi into faeces

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15
Q

Fulminant infection

A

Extremely-rapid onset

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16
Q

A spike in what coincides with hepatitis symptoms?

A

Liver enzyme ALT (alanine aminotransferase, coincides with damaged liver)

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17
Q

Hep A incubation period

A

Average 30 days.15-50 day range

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18
Q

Hep A symptoms by age group1)2)3)

A

1) Under 6 years, 10% show symptoms 2) Between 6-14 years, 40-50% 3) Over 14 years, 70-80%

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19
Q

Hep A symptoms

A

Jaundice, vomiting, pale faeces, dark urine

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20
Q

Hep A complications

A

Fulminant hepatitis (rarely), cholestatic hepatitis

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21
Q

Chronic sequelae of hep A and E

A

None

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22
Q

Typical serological course of hep A infection

A
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23
Q

Length of hep A symptoms

A

2-3 weeks

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24
Q

Hep A prevention and treatment1)2)3)4)

A

1) Sanitation
2) Pre-exposure (for travellers) or post-exposure (within 14 days of exposure) immunoglobulin
3) Supportive rehydration and nutrition
4) Vaccine

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25
Q

Hep A vaccine1)2)3)4)5)6)

A

1) Virus grown in a diploid cell culture
2) Inactivated whole virus with formalin
3) Alum adjuvant
4) 2-3 doses
5) Over 95% effective after 1 dose, ~100% after 2
6) Expensive to produce (because of diploid cells, testing for viral inactivation)

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26
Q

Hep E viral family

A

Hepeviridae.Formerly caliciviridae

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27
Q

Hep E virion characteristics1)2)3)4)

A

1) Non-enveloped, (+)ssRNA virus.
2) Icosahedral.
3) 7.7kb genome
4) Slightly more fragile virion than hep A

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28
Q

Differences between hep A and hep E distribution

A

Both affect Africa, central America, but hep E has a greater burden on Asia

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29
Q

Hep E epidemiology1)2)3)

A

1) Outbreaks associated with faecally-contaminated drinking water.
2) Minimal human-human transmission
3) Closely-related to a virus infecting pigs. Could be a zoonosis.

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30
Q

Hep E incubation period

A

Average 40 days.

2-10 week range

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31
Q

Hep E case fatality rate

A

~1-3% normally.

15-25% in pregnant women

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32
Q

Hep E typical serological course

A
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33
Q

Hepatitis viruses that can be sexually-transmitted

A

All, though hep B is the most likely to be transmitted

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34
Q

Hepatitis viruses that can be transmitted through intravenous drug use

A

Hep B and C

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35
Q

Proportion of Australian intravenous drug users who have hep C

A

50-60%

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36
Q

Hep B virion structure

A

Enveloped, with hep B surface antigen in envelopeViral DNA within a core (leading to double-walled structure in an electron micrograph)HBsAg can form VLPs

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37
Q

Hep B genome1)2)3)4)

A

1) 3kb relaxed circle of dsDNA
2) Viral polymerase on 5’ end of (-) strand
3) 2 12bp short direct repeats
4) 18nt ssRNA cap on 5’ end of (+) strand

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38
Q

HBeAg

A

A variant of the core protein, which has the pre-C region included

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39
Q

HBcAg

A

Hep B core protein (missing pre-C region, which would turn it into HBeAg

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40
Q

Life cycle of hep B, C, D1)2)3)4)

A

1) Contact via blood, sexual fluids
2) Virus penetrates intestinal epithelia (does not replicate here like hep A and E do)
3) Enters blood, travels to liver.
4) Replication in hepatocytes

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41
Q

Concentrations of hep B virus in body fluids1)2)3)

A

1) High - Blood, serum, wound exudates 2) Moderate - Semen, vaginal fluid, saliva 3) Low - Urine, faeces, sweat, tears, breast milk

42
Q

Role of hep B pre-core

A

Essential for production of replication-competent viruses

43
Q

Perinatial hep B transmission

A

Pregnant women who are HBeAg positive have a much higher risk of transmitting virus to child. Perinatal is the main source of transmission in high-prevalence areas

44
Q

Hep B incubation period

A

Average 60-90 days 45-180 day range

45
Q

Hep B different proportions of clinical jaundice based on age

A

Under 5 years, under 10% develop symptomsOver 5 years, 30-50%

46
Q

Hep B case fatality rate

A

0.5-1%

47
Q

Hep B chronic infection rate

A

Exposure when under 5 years - 30-90% chronic illness Exposure when over 5 years - 2-10%

48
Q

Hep B mortality from chronic liver disease

A

15-25%

49
Q

Two types of cirrhosis

A

Compensated and decompensated. Decompensated leads to death

50
Q

Acute hep B typical serological course

A
51
Q

Chronic hep B typical serological response

A
52
Q

Hep B sequelae1)2)

A

1) Immune-mediated liver damage, leading to cirrhosis, maybe primary hepatocellular carcinoma
2) Most-common cause of liver cancer

53
Q

Number of carriers of hep B worldwide

A

500 million

54
Q

Complication of end-stage liver disease

A

Abdominal ascites

55
Q

Proportion of hep B patients that develop hepatocellular carcinoma

A

2-10%

56
Q

Cause of hepatocellular carcinoma

A

Random integration of hep B genome. Repeated destruction and regeneration of hepatocytes can lead to accumulation of chromosomal damage

57
Q

General biomarker for hep B infection

A

HBsAg

58
Q

Biomarker for recovery from hep B, or vaccination

A

anti-HBsAg Ig

59
Q

Marker of acute hep B infection

A

Anti-HBsAg IgM

60
Q

Marker of chronic or past hep B infection

A

Anti-HBsAg IgG

61
Q

Marker of current hep B viral replication

A

HBeAg, hep B DNA

62
Q

Biomarker that indicates that hep B is no longer replicating

A

Anti-HBeAg Ig

63
Q

Hep B vaccine 1)2)3)

A

1) Subviral particles purified from yeast
2) Alum adjuvant
3) 2-3 doses

64
Q

Hep D viral family

A

Deltaviridae

65
Q

Hep D characteristics 1) 2) 3)

A

1) 70% complementary ssRNA genome
2) Only encodes a delta protein, which surrounds genome,
3) Requires hep B infection

66
Q

Different ways to be infected with both hep B and D1)2)

A

1) Coinfection - Exposure to hep B and D at the same time. Severe acute disease, low risk of chronic infection. 2) Superinfection - Exposure to hep D when already infected with hep C. Usually develop chronic hep D infection. High risk of severe, chronic liver disease

67
Q

Proportion of global population infected with hep C

A

3%

68
Q

Proportion of hep C infections that occur through injecting drug use

A

80%

69
Q

Proportion of hep C patients that develop chronic infection

A

70%

70
Q

Hepatitis virus that can be initially asymptomatic

A

Hep C

71
Q

Can hep C be cleared?

A

Yes. 30% clear the virus

72
Q

Leading indicator for liver transplantation

A

Hep C infection

73
Q

Hepatitis virus without a vaccine

A

Hep C

74
Q

Hep C viral family

A

Flaviviridae

75
Q

Mutation rate of hep C

A

Greater than that of HIV

76
Q

Immunity against hep C

A

Very poor. Carriers can be superinfected with more than one strain of hep C

77
Q

Is hep C culturable?

A

Not until recently. One strain can now be cultured in cells

78
Q

Hep C virion characteristics1)2)3)4)5)

A

1) Double lipid membrane
2) E1E2 glycoprotein envelope dimer
3) Capsid
4) +ssRNA genome
5) Cholesterol droplet within envelope

79
Q

Organisation of HCV genome1)2)3)4)

A

1) 9.4kb genome
2) 5’ UTR IRES
3) 5’ end of genome has structural proteins. 3’ end has nonstructural proteins
4) Encodes a polyprotein

80
Q

HCV RDRP

A

NS5B

81
Q

Receptors used by HCV

A

CD81, SR-BI, , Claudin-1, OCLDN, LDL-R.Complex series of receptors

82
Q

Hep C incubation period

A

Average 6-7 weeks2-26 week range

83
Q

Proportion of HCV patients that develop jaundice

A

30-40%

84
Q

Proportion of HCV patients that develop chronic hepatitis

A

70%

85
Q

Proportion of hep C patients that are chronic carriers

A

70-90%

86
Q

Hepatitis virus that is hard to resolve using transmission electron microscopy

A

Hep C

87
Q

Hep E common symptoms in adults

A

100% get jaundice.

100% get malaise

88
Q

Hep C host cells

A

Kupfer cells, hepatocytes.

89
Q

When is hep E secreted in faeces?

A

2 weeks before, 1 week after symptoms

90
Q

Enteric hepatitis which can’t be treated with IV antibodies

A

Hep E

91
Q

Big source of hep B genome mutations

A

Reverse transcription of genome

92
Q

Strategies used by hep B to wnsure persistence

1

2

3

A

1) HBeAg - solible and secreted protein, both a tolerogen (perinatal transmission) and might regulate host immune system
2) HBsAg - Divers anti-HBs antibodies
3) HBV cccDNA - Major transcriptional template that persists in host cells. REsistant to nucleoside analogue therapy

93
Q

Good hep B biomarker for active replication of escape mutants

A

Hep B DNA

94
Q

HBV current antiviral drugs

1

2

A

1) Pegylated IFNa (for HBeAg + carriers)
2) Nucleoside/nucleotide analogues (low rate of viral clearance. Relapse almost inevitable)

95
Q

Response rate of HBV infections to pegylated IFN

A

30-40%

96
Q

Examples of anti-HBV nucleoside/nucleotide analogues, and basic function

1

2

3

4

A

1) 3TC (Lamivudine), Entecavir
2) Adefovir, Tenofovir (nucleoside analogues)
3) Target polymerase functions (RT)
4) Relapse almost inevitable after treatment stops

97
Q
A
98
Q

Enzymes involved in HCV genome replication

A

NSP5B, NS3

99
Q

Clinical features of HCV

1

2

3

A

1) 30-40% develop clinical illness (jaundice)
2) 70-90% become chronic carriers
3) Cirrhosis, liver failiure, hepatocellular carcinoma

100
Q

HCV antivirals

1

2

3

4

5

A

1) Ribavirin + pegylated IFNa (not always effective, can have serious side-effects)
2) Protease inhibitors (very effective when prescribed as a cotherapy with pegylated IFNa, ribavirin)
3) NS5B polymerase inhibitors
4) Cyclophilin B inhibitors (essential host cofactor)
5) NS5A inhibitors (IFN resistence gene)

101
Q

Determinent of whether pegyylated IFNa therapy will be effective for HCV infection

A

IL28B gene genetic variation predicts response.

102
Q

FDA-approved single-tablet anti-HCV drugs

1

2

A

1) Ledipsavir (NS5A inhibitor)
2) Sofosbuvir (NS5B inhibitor)

1Principles of Biomedicine - MD1 (157 decks)

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