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Medical Virology L1-10 > HBV > Flashcards

HBV Flashcards

1
Q

What family of virus is HBV?

A

Hepadna

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2
Q

How is HBV transmitted and what is the disease pattern and latency period?

A

Parenteral; sexual, acute and chronic with latency of 3-6 months

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3
Q

What are the three particles related to HepB?

A

L-HBs, M-HBs, S-HBs

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4
Q

What type of genome does HepB have and what is associated with it/ how does it replicate

A

A small DNA genome (smallest of any virus) uses a reverse transcriptase to replicate its own genome. It has both positive and negative sense DNA strands with the positive being slightly larger than the negative

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5
Q

Size and enveloping of HBV

A

42nm and enveloped virus

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6
Q

Describe HBV incomplete double strand

A

Partial double stranding with a cohesive overlap that spans the 5’ regions of each strand

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7
Q

What is the HBcAg protein in HBV

A

Secreted and a good marker.

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8
Q

What is the polymerase attached to in HBV and how?

A

Covalently to the negative strand

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9
Q

What do PreS1 and PreS2 make up in HBV?

A

Make up the Pres and S polyprotein that contains the virus receptor for the infection of hepatocytes

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10
Q

What type of polymerase is the HBV pol?

A

A RT DNA dependent DNA polymerase with an RNaseH

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11
Q

HBxAg does what in HBV?

A

A small regulatory protein that stimulates gene expression and replication and protection of virally infected cells from immune cells

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12
Q

What cells does HBV replicate in?

A

Hepatocytes

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13
Q

Describe HBV replication

A

Virus fuses with cell membrane and Uncoated the DNA is removed and cccDNA (Covalently closed circular DNA - a mini chromosome indistinguishable from the host chromosome) enters the nucleus the positive sense pregenome is produced with shorted transcripts that are then translated by host ribosomes. PreS and S ℅ translationally fed into the ER whilst other proteins (P protein and capsid are translated in the nucleus for form virus particles which then combine with the components in the ER and are released

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14
Q

What is secreted into the blood in HBV infection?

A

Non infectious surface antigen particles and filaments

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15
Q

What is he most common route of HBV transmission and it’s incidence?

A

Perinatal 10% in Caucasian mothers and 50% in Asian mothers

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16
Q

Perinatal transmission of HBV does not occur in the placenta it occurs in the…

A

Labour and delivery

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17
Q

Percutaneous

A

Infection through the skin (needle stick or blood transfusion

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18
Q

Parenteral

A

Introduction into the body other than by the mouth or gut eg during sex

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19
Q

Perinatal

A

Infection during birth

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20
Q

Concentration of HBV in bodily fluids

A

High- blood, serum, wound exudates
Moderate - semen, vaginal fluid, saliva
Low/not detectable - urine, faeces, sweat, tears, breastmilk

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21
Q

What are the main differences in transmission between HBV and HCV?

A

HCV is not sexual or perinatal so often

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22
Q

How many of the worlds population has been infected with HBV in their lifetime?

A

1/3

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23
Q

How many people chronically infected worldwide and how many is that compared to HCV?

A

350 million twice as many than HCV

24
Q

What do 25% of carriers of HBV develop?

A

Liver disease, chronic hep, cirrhosis and primary HCC?

25
Q

What is the antigen for chronic HBV infection and how does carrier rates vary?

A

HBsAg, carrier rates vary from 0.1 to 20% depending on where in the world you are

26
Q

What is the incidence of HBsAg related to?

A

Incidence of HBV and age of primary infection

27
Q

When do most people get HBV?

A

When adult and they clear the infection

28
Q

Global patterns of chronic HBV

A

High - 45% of population have lifetime risk of infection >60%, early childhood infections are common
Intermediate - 43% of global population, lifetime risk of infection 20-60%, infections in all age groups
Low -12% of global population, lifetime risk of infection

29
Q

Clinical HBV features in adults

A 
Aniceteric (not assoc with jaundice) or no disease = 60-70%
Icteric disease (liver complications jaundice etc)= 20-35%
Complete recovery =90% 
Persistent chronic disease = 2-10% 
Mortality rate = 0.2-0.5%
30
Q

Think about and describe the acute HBV and chronic HBV infection graphs

A

Look and check

31
Q

How many liver cancers are HBV positive and how many cases of liver cancers are caused by HBV per year?

A

50% and 340,000 cases

32
Q

Cases of liver cancer due to HCV for year and percentage of HCV positive cancers

A

195,000 cases and 25%

33
Q

Where are HBV specific lymphocytes detected in chronic disease?

A

In liver lesions and they are not enough to clear the virus, similarly with NK and NKT cells and macrophagesx

34
Q

What happens to IFN in HBV?

A

It is deficiently produced, IFN replacement in humans only reduces viral titres and disease progression in a small number of number of HBV patients

35
Q

Viral factors associated with risk of HCC in HBV carriers

A

Viral factors - persistently high viremia, HBeAg positivity, HBV genotype, HBV variants: mutations in the basal core promoter and in the preS region causing truncation a of the protein at the c- terminus. During regeneration after hepatic damage, HBx and preS/S genes increasingly integrate into host DNA = increased ic levels of HBx. this affects pathways such as rad and PI3K and IGFR1 and VEGF etc. (HCV persistence does not include integration and maintains itself in the er associated episode)

36
Q

Host factors assoc with increased risk of HCC in HBV

A

Male gender (1.5-2 fold more), age, liver cirrhosis, age at primary infection, polymorphism a in genes encoding cytokines and detoxification enzymes, diabetes and obesity

37
Q

Environmental factors assoc with increased of HCC in HBV carriers

A

Dietary exposure to aflatoxin B1 (in grains), alcohol consumption, nutritional factors (dietary iron overload, starvation)

38
Q

Breakdown of HCC development in humans

A 
Long process
Chronic hepatitis (HBsAg) - liver damage - transformed liver cells - selection acting on transformed cells - outgrowth of clinal focus - malignant conversion - HCC
39
Q

What miRNA is affected by HBx?

A

MiR181 and miR 148a

40
Q

Where does HBV DNA exist?

A

As an episode in the form of a mini chromosome in cell nuclei

41
Q

What do HBV and HCV show in terms of co infection?

A

Reciprocal interference is one has markers in blood and other doesn’t and vice versa

42
Q

What does expression of HBV proteins stimulate in the host?

A

The immune response and triggers liver inflammation, some viral proteins as well as insertion of the viral DNA into liver cell genome (inducing genetic alterations) and directly interferes with cell proliferation and viability.

43
Q

What are the mechanisms of HBV induced liver damage?

A

HBV is not cytopathic.
Hypothesis: intrahepatic antigen specific cellular immune responses initiate the process, damage is largely due to cellular and molecular effector systems - lacking deets

44
Q

Non HBV HCC is associated with liver damage, describe

A

Cirrhosis not associated with persistent HBV infection is the major risk factor for HBV in the west. Cirrhosis can be associated with alcohol abuse and or persistent infection with other viruses particularly hepC

45
Q

What are the four potential virus-specific mechanism of virus action in addition to immune/chronic inflammatory damage

A

1 virus integration resulting in insertional mutagenesis (IM doesn’t happen by chance/randomly)
2 effects of x gene produce (whether integrated or expressed
3 effects of genotype (not yet defined)
4 emergence of variants (mutant or otherwise) of the core promoter and pre-s region

46
Q

Role of HBV X protein in the development of HCC (9)

A

1 viral replication
2 interference with transcription machinery
3 pro/anti apoptosis
4 genetic stability interference
5 activation/inhibition signal transduction cascades
6 transformation/ tumour promoter
7 modulation of gene expression
8 modulation of proteolytic activity
9 HBx is involved in many IC signalling pathways that are closely correlated to cell prolif and cell apoptosis

47
Q

How many HBV genotype are there, what are they based on and how are they distributed?

A

8 based on the S protein gene

(A-H) and are geographically distributed C>B<a>E </a>

48
Q

What are the possible explanations for the relationship between different genotypes and disease Phenotypes

A

Differences in host immune response - especially B and T cell response to HBsAg, HBcAg and HBcpreAg
Differences in the levels of viral replication
Inactivation of pro-oncogenic viral protein function
Activation of regulatory pathways, especially HBsAg and HBcAg
Modified antigenic characteristics and evasion if immune surveillance
Lack of HBeAg production, down regulation of cell cycle inhibitors, increased persistence
Antiviral resistant variants

49
Q

Mutations in what genes lead to predisposition for HCC?

A

PreS1 and PreS2 both deletion mutants

50
Q

What are the treatments of HBV

A

Antiviral treatments
Vaccination
Behavioural measures

So far no drugs are able to remove the cccDNA which is capable of initiation of infection so once infected always infected (if not cleared)

51
Q

What is lamivudine and adefovir dipivoxil

A

Lamivudine is the L-enantiomer of the deoxycytidine anologur 2’3’ - deoxy-3’ thiacytidine.
Adefovir dipivoxil (hepsera) is a prodrug of adefovir which is also a nucleotide analogue.
They both target the HBV polymerase complex and causes chain termination

52
Q

What HBV vaccines exist?

A

Plasma derived HBV vaccine consists of biochemically and bio physically inactivated HBV surface antigen (HBsAg) particles obtained from healthy chronic HBsAg carriers
Recombinant HBV is derived from HBsAg in yeast cells these vaccines have the advantage of reduction of plasma transferred virus (AIDS) complications
HBV vaccine induces protective anti-HBsAg in most individuals receiving the recommended three dose regimen
Antibody titre of >10mU/mL against HBsAg are recognised conferring protection against HBV

53
Q

Why might a cure be possible for HCV but not HBV?

A

Because HCV exists in the episode but in HBV, proteins made from integrated virus templates may still trigger and promote CLD even if episomal DNA (incl cccDNA) is cleared

54
Q

Early vaccines are:

A

Subvirion vaccines obtained from asymptomatic healthy carriers of HBV. HBsAg (22nm particle s ag) was harvester from the plasma of HBV carriers
1 formulin treated 2 heat inactivated 3 alum absorbed
Purification and inactivation steps removed from HBV and other infectious agents (I know agents that may not be inactivated)
Excellent safety record, no HIV seroconversion has ever been observed, no apparent side effects and no deaths. 30 million doses so far

55
Q

Recombinant yeast vaccines:

A

Expansion of S gene in yeast leads to self-assembling 22nm particles purified from large batches of yeast cells
1 formulin treated and mixed with alum and thimerosal
Product is identical to HBV product but not properly glycosylated
Yeast product carries epitope a which induce virus neutralising antibodies. Long term efficacy yet to be firmly established but is likely to be identical to the early subunit vaccine

56
Q

What has the vaccine done?

A

Decrease infection rates and cancer rates

57
Q

In HIV positive men sex men, how effective is the vaccine?

A

Only 33.3-56.3% response rate in HIV + men where’s 86.5-84.4% response in HIV - men

Medical Virology L1-10 (2 decks)

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