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a path 3 > MICRO: Viral hepatitis > Flashcards

MICRO: Viral hepatitis Flashcards

1
Q

Summarise the hepatitis viruses stating whether each is a DNA/RNA virus and the route of transmission.

A
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2
Q

What is the route of transmission of HAV? Where is it more common?

A

Faeco-oral and blood-borne spread e.g. MSM and IVDU

More common where there is poor access to clean water

Schools and MSM

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3
Q

What is the incubation period of HAV? What is the presentation?

A

Incubation: 2-6 weeks (15-50 days)

Presentation: often subclinical in children and symptomatic in 70% of adults (symptoms: fever, malaise, anorexia/nausea, abdominal discomfort, diarrhoea, jaundice)

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4
Q

Is HAV notifiable? What professions is this most important for?

A

Notifiable disease - mainly for occupational risks e.g.sewage workers, plumbers, chefs

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5
Q

Describe the course of HAV infection.

A

Incubation for 2-6 weeks followed by a transaminitis (high ALT).

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6
Q

What test is diagnostic for HAV? What if you had the vaccine?

A

Diagnostic for acute infection: Anti-HAV IgM reactive NB: unlikley if bilirubin <30umol/L

If you have had the vaccine you will also have IgG i.e.

  • High IgM non-reactive; and
  • High IgG WITHOUT the high ALT
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7
Q

Who are vaccines for Hepatitis A offerred to?

A

Pre-exposure immunisation among population at risk

Post-exposure prophylaxis

  • Within 14 days of exposure to index case: HAV vaccine +/- HNIG (for 60 years and above, chronic liver diseases inc CHB/CHC, immunocompromised contact)
  • Over 14 days: HAV vaccine +/- HNIG (for chronic liver diseases inc CHB/CHC, immunocompromised contact)
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8
Q

What are the presenting features of HAV? Which populations become symptomatic?

A

Strong correlation with age: <10% symptomatic among children <6 years old versus 70% in adults

Typical symptoms: fever, malaise, anorexia/nausea, abdominal discomfort, diarrhoea, jaundice, extra-hepatic diseases

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9
Q

What period is HAV infectious?

A

2 weeks before onset of first symptoms and until 1week after the onset of jaundice

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10
Q

What is the diagnosis suggested by HAV IbM positive and HAV IgG negative?

A
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11
Q

How many genotypes of HBV are there?

A

10 genotypes (A-J) with distinctive geographic distribution

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12
Q

What features are seen on this EM image of HBV?

A

Dane particle = a spherical particle found in the serum in hepatitis B that is the virion of the causative double-stranded DNA virus.

Tubules and spheres = forms of the SAg of the virus (detected using Australian antigen test)

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13
Q

What type of virus is HBV? How does it replicate?

A

The family Hepadnaviridae

Double-strained DNA with reverse transcriptase

Produces enveloped virions

DNA virus BUT still uses reverse transcriptase to replicate so some HIV drugs are effective against it

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14
Q

Is HBeAg important in HBV? Where is it found in the virus particle?

A

Most people with HBV are HBeAg positive BUT some patients do NOT have HBeAg

It is found in the pre-core part of the core reading frame

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15
Q

What governs the risk of vertical transmission in pregnancy with HBV?

A

HBeAg is the most important risk predictor for vertical transmission

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16
Q

Summarise the molecular organisation of HBV. Why is there potential for mutation?

A

It has FOUR overlapping reading frames –> potential for mutation in polymerase gene to change surface antigen -> undetected by routine tests for SAgs

The role of the X antigen is unknown

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17
Q

Give 3 routes of transmission of HBV.

A
  • Sexual
  • Vertical
  • Blood products

(bloodborne horizontal and vertical)

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18
Q

What are the clinical features of HBV?

A

Acute OR chronic infection (NB: chronic =lasting 6 months or more) associated with ALT rise

Presentation:

  • Neonates & children: mostly asymptomatic or anicteric; 90% HBV-infected neonates develop CHB, and 30% among children age <5 years
  • Adult: 30-50% icteric hepatitis; 10% become CHB

~0.05% risk of fulminant hepatitis; related to co-infection with HCV/HDV

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19
Q

What is the incubation period of HBV? Describe the course of the infection.

A

Incubation period is 2-6 months

NB:

  • Anti-HBc IgM positive = recent infection
  • Sag positive = you cannot tell if it is acute or chronic
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20
Q

What do these different markers in serology indicate in HBV?

  • HBsAg
  • HBsAb
  • HBcAb
  • HBeAg
A
  • HBsAg: infection
  • HBsAb: immunity through either immunisation or past infection
  • HBcAb: exposure (IgM: acute infection)
  • HbeAg: replication activity
  • HBeAB
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21
Q

Is HBc IgM positivity diagnostic of acute HBV?

A

No, you cannot tell if it means acute or chronic infection unlike in HAV where it is diagnostic for acute infection.

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22
Q

Define chronic hepatitis B and name 2 complications.

A

Definition: persistence of HBsAg for 6 months or more after acute HBV infection

Complications

  • Cirrhosis (8-20% untreated in 5 years)
  • Hepatocellular carcinoma: (annual risk of 2-5% in cirrhosis)
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23
Q

What are the stages of chronic HBV?

A

New terminology: HBeAg positive or negative

Old terminology:

  • Immune tolerant
  • Immune reactive
  • Inactive HBV carrier state
  • HBeAg negative chronic HBV
  • HBsAg negative phase
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24
Q

How does baseline HBV-DNA level correspond to severity of disease?

A

REVEAL study showed that with increasing baseline serum HBV DNA level:

  • incidence of cirrhosis increases
  • incidence of HCC increases

Therefore this is an indicator for the need to treat.

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25
Q

What is the management of HBV infection? Which medications should not be given to those who may later require a transplant?

A

Chronic HBV Treatment

  • Interferon Alpha (used in a subset of patients who look like they are clearing the virus by themselves). Do not use in patients who may require a liver transplant.
  • Lamivudine
  • Tenofovir
  • Entecavir
  • Emtricitabine

Liver Transplantation – requires various other treatments (e.g. immunosuppression, nucleoside analogues, hepatitis B Ig)

Liver Failure

  • Antivirals are very effective in treating the viral hepatitis - usually takes ~9 months in liver failure
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26
Q

Who is HBV vaccination offered to?

A

Pre-exposure prophylaxis

  • Routine childhood immunisation in the UK since 2017
  • High risk population

Post-exposure prophylaxis

  • Neonate born to mother living with hepatitis B
  • Sexual partner: HBV vaccine +/- HBIG (within one week from the contact)
  • Needle stick injury
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27
Q

Should vaccination +/- HBIg be offered to the neonate in these cases?

A
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28
Q

Should HBV prophylaxis be given in these cases?

  • Vaccinated
  • Partially vaccinated
  • Fully vaccinated with primary course
  • Known non-responder to HBV vaccines
A
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29
Q

Are hepatitis B boosters required? What antibody is used for protection?

A

Little need for boosters - likely to get a boost when you are exposed.

Protection conferred by anti-HBsAg

30
Q
A

Previous vaccination

31
Q
A

Acute infection

32
Q
A

10%

33
Q
A

HCC

34
Q

What class of virus is hepatitis C? What type of virus is it?

A
  • Family: Flaviviridae
  • Genus: Hepacivirus

Single-stranded, positive sense RNA genome

35
Q

How is HCV transmitted? What is the incubation period?What % develop chronic infection?

A
  • Blood-borne
  • Incubation 2-6 weeks

Chronicity:

  • 70% become chronic hepatitis C (females 60% but 80% males)
  • 30% spontaneous clearance
36
Q

Describe the molecular characteristics of HCV.

A
  • Single stranded RNA virus
  • Consists of components for the Core (C), Envelope (E) and Non-Structural (NS) components
  • Most antivirals are protease inhibitors and inhibitors of non-structural components

Protease inhibitors can target NS5A and NS5B etc

37
Q

What is the incubation period of HCV? Are antibodies diagnostic of acute infection? What is the course of HCV?

A

Incubation period: 6-8 weeks (week 0 lecture) // 2-6 weeks (later lecture)

Course: transaminitis then deveopment of antibodies

Diagnosis of acute infection: HCV RNA

38
Q

What test is diagnostic of acute HCV infection? Why?

A

NB: cannot check anti-HCV during acute hepatitis – check the viral load (HCV RNA) instead because anti-HCV antibodies only develpo after the transaminitis/acute infection

39
Q

What is the prognosis in HCV on treatment?

A

Early treatment with interferon has a HIGH success rate (54% in combination therapy)

Monotherapy with interferon: by 24 weeks you would treat 6% of patients etc

40
Q

What is the main drug used in HCV treatment?

A
  1. Peginterferon alfa-2b by once weekly depot injection
  2. AND ribavarin

= >90% cure rate

NB: this lasts longer in the plasma than normal interferon.

41
Q

What is SVR12 and its use?

A

Sustained viral response at 12 weeks - 3 months after stopping treatment if the virus is gone = cured.

Used for direct acting antiviral (DAA) monitoring

42
Q

What are the genotypes of HCV? What is their significance for treatment?

A

There are 6 genotypes of HCV (1, 2 and 3 are most common). Genotype 1 is the hardest to treat

  • Genotype 1= longer duration and higher doses (of PEG-INF a2a)
  • Genotype non-1 = shorter duration and lower doses
43
Q

List 3 targets of new HCV drugs (direct acting antivirals).

A
  • NS3/4serineprotease=‘-revir’
  • NS5aRNA (unknown action) =‘-asvir’
  • NS5bRNA dependentRNA polymerase=‘-buvir’

2 regimens:

  • Pan-genotypic regimen
  • Single-tablet regimen
44
Q

What do NS3/4 serine protease DAAs end in ? What genotype do they work against?

A

Genotype 1

‘-revir’ - e.g.

  • telaprevir
  • boceprevir
  • simeprevir
  • asunaprevir
  • paritaprevir (ABT-450/r)
  • grazoprevir (MK5172)
  • vaniprevir
  • faldaprevir
  • deleoprevir
45
Q

What genotype do NS5a RNA DAAs work against? What do they end in?

A
  • Genotype 1 and non-genotype 1
  • -‘asvir’ e.g.
    • ledipasvir
    • daclatasvir
    • ombitasvir (ABT- 267)
    • elbasvir (MK-8742)
46
Q

What are the disadvantages of DAAs against NS3/4 protease?

A
  • Low barrier to resistance
  • Interactions+
47
Q

What are the disadvantages of NS5a RNA DAAs?

A
  • Low barrier to resistance
48
Q

What genotype do NS5b RNA dependent RNA polymerase DAAs work against? What do their names end in?

A

Sofosbuvir: genotype 1 and non-genotype 1

Others: genotype 1 only e.g.

  • dasabuvir (ABT-333)
  • beclabuvir (BMS- 791325)
  • ABT-072
  • deleobuvir

‘-buvir’

49
Q

What are the disadvantages of NS5b RNA dependent polymerase DAAs?

A

Sofosbuvir = good because HIGH barrier to resistance

But others have a low barrier to resistance.

50
Q

Which DAAs target all stages of the HCV lifecycle?

A

NS5A DAAs (-asvir)

51
Q

What prevention strategies are present for HCV?

A
  • Notifiable disease in UK
  • Active HCV screening
  • Risk reduction (e.g. safe handling and disposal of sharps, protected sex)

NB:

  • Nil vaccine available
  • Nil post-prophylaxis available
52
Q

What is the size of hepatitis D relative to other viruses? What type of virus is it?

A

Single-stranded, defective, circular RNA genome virus that relies on HBV for replication

Smallest virus known to infect man

53
Q

What is the route of infection of HDV? What is the incubation period?

A

Blood-borne transmission

Incubation period: 3-6 weeks

54
Q

What are the two patterns of infection with HBV? Compare and contrast the course of each.

A
  1. HBV-HDV coinfection
  • Getting both B and D at the same time
    • Similar to classic acute HBV - causes elevated ALT and IgM anti-HDV at the same time as symptoms; mostly self limited
  • Gives acute HBV (<5% progress to chronic)
  1. HBV-HDV superinfectioin
  • When you already have B and you get D.
  • 80% risk of chronic infection
  • Increased risk of cirrhosis and HCC than chronic hep B alone
55
Q

How is HDV diagnosed?

A

Anti-HDV serology; other HDV investigations rarely used

56
Q

How do you treat HDV? How do you prevent it?

A

Treatment : PEG-interferon alpha licensed for HDV superinfection in CHB

Prevention : pre-exposure HBV immunisation

57
Q
A
58
Q

What type of virus is HEV?

A
  • Single-stranded, positive sense RNA genome
  • Quasi-enveloped HEV
59
Q

What family does hepatitis E belong to? Which ones infect humans?

A

Hepeviridae family (genus – hepevirus) genus Orthohepevirus;

Species A strains (8 genotypes) infect humans BUT the same strain A (different genotypes) also infect animals:

  • G1 & G2: obligate human pathogens
  • G3 & G4: zoonotic; pigs & wild boar are natural hosts
60
Q

UK is an endemic country of which HEV genotype?

A

Genotype 3

61
Q

Which population is most at risk from complications of hepatitis E? What are the complications?

A

High mortality in pregnant women - unexplained. MAinly with genotype 1.

Complications include:

  • fulminant hepatic failure
  • obstetric complications (e.g. eclampsia and haemorrhage);
  • 25% maternal mortality & high perinatal infant mortality
62
Q

Which patient groups are at risk of chronic hepatitis E?

A

Immunocompromised patients - may develop chronic hepatitis E (G3 & G4)

63
Q

What are the other complications associated with HEV?

A
  • CNS disease
    • Bell’s palsy
    • Guillain Barre
    • other neuropathy
  • Chronic infection
64
Q

What are the genotypes of HEV and which ones cause epidemics?

A
  • Genotype 1 and 2 – human, epidemic (water etc)
  • Genotype 3 and 4 – swine and other

(humans accidental host = zoonosis)

65
Q

What is the route of transmission of HEV? What are some examples of sources of HEV?

A

Faeco-oral spread = generally HEV is uncommon + little person to person spread.

Case reports of HEV from:

  • Shellfish consumption
  • blood transfusion
  • Sausages
  • pig liver consumption
66
Q

How is HEV diagnosed?

A
  • Immunocompetent: HEV serology
  • Immunocompromised: HEV PCR
67
Q

What is the treatment of HEV?

A
  • Supportive
  • Ribavirin only used in chronic Hepatitis E as most infections are self limited
68
Q

What is the incubation period of HEV?

A

3-8 weeks (later lecture: 15-60 days)

69
Q

Describe the course of infection in HEV.

A
  • The acute infection is accompanied by a rise in anti-HEV IgM
  • HEV RNA detectable in serum and stool in incubation period
  • Rarely high levels of HEV RNA can persist - this generally responds well to antiviral therapy (with ribavirin)
70
Q

Where can HEV RNA persist once the virus is cleared serologically?

A

Stools - perists for longer whereas HEV RNA disappears from serum with recovery

71
Q

What about hepatitis F and G?

A

F - probably does not exist

G - reclassified as a pegivirus which is more of a Simian virus

72
Q

What type of prevention strategies are used in HEV?

A
  • Nnotifiable disease
  • HEV patient should avoid prepping food during the first 2 weeks
  • Immunocompromised and chronic liver disease patients should avoid consumption of undercooked meat (pork, wild boar and venison) and shellfish
  • HEV vaccination: only licensed in China

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