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Hepatitis Flashcards

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1
Q

What is Hepatitis B?

A

Small DNA virus
Infects hepatocytes

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2
Q

What can hepatitis B cause?

A

Acute infection
Chronic infection
Predisposes to hepatocellular carcinoma
Extrahepatic disease

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3
Q

Describe hepatitis B in the UK

A

96% of new chronic hepatitis B in UK found in migrants
Intermediate prevalence in large urban centres in low endemic countries

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4
Q

How is hepatitis B spread?

A

Parentally via blood and bodily fluids
Not spread by saliva, insect bites or casual contact
Sexual contact, drug use, blood transfusion, haemodialysis

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5
Q

How are chronic hepatitis B infections transmitted?

A

Mostly vertical (mother to baby) or early horizontal (among individuals of the same generation) globally

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6
Q

How much blood is sufficient for transmission of hepatitis B?

A

0.00004ml - highly infectious

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7
Q

Is hepatitis B more or less infectious than HIV?

A

50-100x more infectious than HIV

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8
Q

What are risk factors of hepatitis B?

A

Age at acquisition determines outcome - 95% or neonates develop chronic infection, 95% of immunocompetent adults spontaneously clear HBV (sAG loss)
Chronicity higher in immunosuppressed (more chronic)

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9
Q

When does vertical transmission occur?

A

Usually at delivery
Depends on viral load and Hepatitis B e-antigen (HBeAg) status of mother - transmission occurs in 90% of HBeAg+ where HBV > 10^7 IU/ml)

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10
Q

Describe hepatitis B structure

A

Small surface proteins
Icosahedral core
Polymerase
DNA
Large surface proteins
Medium surface proteins

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11
Q

Describe the genome of HBV

A

Partially double stranded
Inner strand shorter than outer strand
Enters hepatocytes
In nucleus, inner strand completed by cellular polymerases
Forms covalently closed circular DNA (cccDNA)

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12
Q

How is cccDNA formed?

A

Mutistep process converting relaxed circular DNA of HBV to cccDNA

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13
Q

What happens once cccDNA formed?

A

Incorporated to host genome as an episome
Template for HBV replication
Remains in infected cells for the life of the cell
Implications for reactivation of HBV even after long-term quiescence

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14
Q

What does a HBsAg serology test for?

A

Ongoing HBV infection

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15
Q

What is an anti-HB serology?

A

Tests immunity - natural or vaccine

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16
Q

What is an anti-HBc (IgG) serology for?

A

Current or resolved HBV infection

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17
Q

What is an anti-HBc (IgM) serology for?

A

Acute HBV infection or flare of chronic HBV

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18
Q

What is a HBeAg serology for?

A

Active viral replication (tolaragen - helps evade host immunity)

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19
Q

What is an anti-HBe serology for?

A

May indicate immune control but active replication may occur

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20
Q

What is a HBV DNA serology for?

A

Direct measure of viral particles

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21
Q

Describe the immunopathology of hepatitis B

A

Injury to HSC, fibrocytes, Kpuffer cells and portal fibroblasts cause oxidative stress, TLR4 signalling/innate immunity and NFkB/JNK signalling
Inflammation due to chemokine and cytokine prod
Injury to hepatocytes and cholangiocytes leads to epithelial mesenchymal transition (EMT) and hepatocellular EMT
Fibrogenesis and cancer

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22
Q

What are the stages of infection of HBV?

A

Immune tolerant - high HBV DNA, low ALT (alanine transaminase)
Immune clearance (HBeAg+ chronic hepatitis) - decreased HBV DNA, high ALT
Inactive carrier phase - low HBV and ALT
Reactivation (HBeAg- chronic hepatitis) - low HBV and ALT

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23
Q

Describe post-exposure prophylaxis for HBV

A

For unvaccinated individuals - Hepatitis B immunoglobulin (HBIG) within 48hrs and HBV vaccination
For vaccinated individuals - Anti-HBs titres assessed, if < 10 IU/ml treat as unvaccinated, if > 10 IU/ml no action required

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24
Q

How is prophylaxis done for infants of HBsAg+ mothers?

A

HBIG at birth
HBV vaccination schedule
Not 100% effective

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25
Describe prophylaxis in pregnancy
Antivirals in third trimester Infant vaccine only if mother has unkown HBsAg and father HBsAg+ve Test infants at 9-12 months
26
Describe prophylaxis in pregnancy
Antivirals in third trimester Infant vaccine only if mother has unkown HBsAg and father HBsAg+ve Test infants at 9-12 months
27
Describe HBV therapy
Direct-acting antivirals - nucleoside/nucleotide analogues Immune stimulation - interferon Important indications for treatment Reactivation Extrahepatic manifestations
28
What do nucleotide/nucleoside analogues do?
Inhibit reverse transcriptase activity of HBV polymerase NAs incorporated to virions, leading to chain termination and non-functional viral DNA Well tolerated oral treatment
29
What does interferon do?
Activates antiviral genes in infected cells and adaptive immune systems PEG-IFN once weekly No resistance Poor tolerability - flu-like symptoms, BM suppression, depression, can trigger latent autoimmunity, avoid in cirrhotics with synthetic failure
30
What happens in reactivation of HBV?
Sudden reappearance/increase HBV replication in patient with prior evidence of resolved or inactive infection
31
Describe a typical clinical scenario in which the risk of reactivation if very high
HBsAg +ve and receiving anti-CD20 (e.g. rituximab) and/or stem cell transplantation
32
Describe a typical clinical scenario in which the risk of reactivation is high
HBsAg +ve and will receive high dose steroids (>20mg/d for >4 weeks) or anti-cytokine agents (e.g. Campath)
33
Describe a typical clinical scenario in which the risk of reactivation is moderate
HBsAg +ve and chemotherapy without steroids or anti-TNFa treatment or anti-rejection therapy for solid organ transplants
34
Describe a typical clinical scenario in which the risk of reactivation is low
HBsAg +ve methotrexate/azathioprine HBsAg -ve high dose steroids or anti-cytokine agents
35
Describe a typical clinical scenario in which the risk of reactivation is very low
HBsAg -ve chemotherapy without steroids or anti-TNFa treatment or anti-rejection therapy for solid organ transplants or methotrexate/azathioprine
36
Describe reactivation
Occurs in HBsAg +ve usually Can occur for HBsAg -ve HBsAb +ve Always check HBsAg/HBcAb/HBV DNA for any immunomodulation Especially rituximab and steroids
37
How is reactivation managed?
Stop cytotxics/immunosuppressants Tenofovir/entacavir +/- liver transplantation
38
Describe the incidence of hepatocellular carcinoma
0.3-0.6% incidence in non-cirrhotics 2.2-3.7% incidence in compensated cirrhotics
39
What is hepatocellular carcinoma?
Most common type of primary liver cancer Occurs most often in people with chronic liver diseases e.g. cirrhosis caused by HBV
40
What can cause HBV to be carcinogenic?
BCP mutations Genotype C Male Older age Heavy EtOH Family Hx HCC Metabolic syndrome
41
Describe future therapy options for HBV
Entry inhibitors (e.g. Bulevirtide) Core protein binders RNA interference (e.g. siRNA) Inhibitors of HBsAg release HBsAg neutralisation Inhibitors of cccDNA TLR agonists (immune modulation) Immune checkpoint inhibitors Engineered T cells Therapeutic vaccines Multi-targeted immunotherapy
42
Describe delta virus
Small enveloped RNA virus Requires co-infection with HBV (uses HBsAg as its own envelope) Systematically screen patients with HBVsAg +ve for HDV Check HDV RNA in anti-HDV Ab Co-infection or superinfection Synergistic fibrosis
43
Describe treatment of HDV
Traditional = 48 weeks of PEG-IFNa Poor efficacy and tolerability Combination IFN and nucleoside/nucleotide not effective Novel therapies - bulevirtide (HDV entry inhibitor) - approved by EMA, awaiting NICE, lonafarnib in evaluation, other drugs (silencing RNA), combinations
44
Describe the structure and genome of HCV
E1 and E2 surface envelope glycoproteins Core forms nucleocapsid Non-structural proteins
45
How is HCV diagnosed?
History - risk factors HCV Ab EIA - if negative then immunocompetent and no chronic HCV, if positive then patient has had contact with the virus Positive HCV Ab means HCV RNA present Presence of Abs 2 weeks after exposure but can be longer HCV RNA present early as 1 week Babies tested after 18months Check genotype
46
How is HCV treated?
Traditionally PEG-IFN and ribavarin but this had poor tolerability and cannot be used in advanced cirrhosis/fibrosis so searching for new drugs
47
What do direct-acting antivirals (DAAs) target?
Viral replication
48
What are combinations of DAAs based on?
HCV genotype Presence of cirrhosis Treatment history Severity of cirrhosis Blood counts Renal impairment
49
How do DAAs work?
Inhibit specific non-structural proteins that are vital for HCV replication
50
What DAAs target translation of the virus?
NS3/4A protease inhibitors: - Telaprevir - Boceprevir - Simeprevir - Faldaprevir - Paritaprevir - Ritonavir
51
What DAAs target the replication stage of the virus?
NS5B polymerase inhibitors: - Sofosbuvir - Dasabuvir
52
What other type of DAA is there?
NS5A inhibitors (MOA not known): - Daclatasvir - Ledipasvir - Ombitasvir
53
How do resistance mutations occur?
Due to high replication rate of virus, leading to novel strains and quasi-species of HCV Mutations in NS3, NS5A and NS5B genes Resistance testing may be of less value given the multitude of retreatment options
54
What is extrahepatic disease?
Disease located or occurring outside the liver as a result of HCV
55
Give examples of extrahepatic disease
Cardiovascular disease Chronic kidney disease Insulin resistance and T2D B cell lymphoma Cryoglobulinaemic vasculitis - immune complex-mediated inflammation of blood vessels
56
What are the challenges of HCV treatment?
Resistance mutations Cost of DAA regimens and retreatment esp in LMICs Screening and access to treatment in vulnerable groups
57
What type of virus is hepatitis A?
Single stranded RNA
58
How is hepatitis A transmitted?
Faeco-oral route
59
Describe effects of hepatitis A
Acute self-limiting episode of hepatitis Asymptomatic/symptomatic Can survive in dried faeces for 4 weeks Self-limiting jaundice/cholestasis > 10wks Acute hepatic failure possible (1%)
60
How long does it take to recover from hepatitis A?
Full recovery in almost by 6 months Relapsing over 2-3 months
61
What kind of virus is hepatitis E?
Small RNA virus
62
How is hepatitis E transmitted?
Faeco-oral transmission via water or pork products
63
Where is hepatitis E found?
North Africa and Middle East
64
What are the effects of hepatitis E?
Self-limited acute hepatitis or chronic hepatitis in immunocompromised Anorexia, nausea, abdominal pain and transaminitis +/- diarrhoea, arthralgia, rash 60% prolonged cholestasis for months Fulminant hepatic failure (FHF) possible - liver begins to fail very quickly
65
When does FHF occur more frequently?
In pregnant women 15-25% mortality and worse fetal outcomes
66
What is used to treat hepatitis E?
Ribavarin may be used to treat in certain circumstances

Medical Microbiology (23 decks)

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