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*B33VPI - Biology & Physiology > Viral Hepatitis and Vaccinology > Flashcards

Viral Hepatitis and Vaccinology Flashcards

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1
Q

What is hepatitis?

A

Inflammation of the liver (varying causes)

Causes:

  • Trauma
  • Alcohol abuse
  • Drug-induced toxicity
  • Viral infection (main cause)
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2
Q

What is liver cirrhosis?

A
  • Advanced consequence of chronic liver disease (years)
  • Characterised by fibrosis; liver tissue replacement by collagenous scars with no function, and regenerative nodules; attempts to repair damaged tissue
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3
Q

Why do the ‘regenerative nodules’ seen in liver cirrhosis not work?

A
  • They are not hepatocytes any more
  • They are fibroblasts, producing collagen
  • Results in scarring (collagenous scars w/no function)
  • Collagen has no function; hepatocytes have been replaced w/collagen
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4
Q

What is a common complication of cirrhosis? How can cirrhosis be treated?

A
  • Ascites; fluid retention in the abdominal cavity ‘big belly’
  • Cirrhosis is irreversible; liver transplant is the only therapeutic option
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5
Q

What causes viral hepatitis? List.

A
  • Hepatitis A (HepA; HAV; naked; IV)
  • Hepatitis B (HepB; HBV; enveloped; VII)
  • Hepatitis C (HepC; HCV; enveloped; IV)
  • Hepatitis D (HepD; HDV; enveloped; V)
  • Hepatitis E (HepE; HEV; naked; IV)
  • Can also be caused by other viruses e.g. Adenovirus, SARS, Ebola, Influenza etc.; but these mainly cause other symptoms (uncommon to result in hepatitis)
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6
Q

How do the differences in HepA - E impact on the type of infection they cause?

A
  • Naked hepatitis viruses (Hep A, E) tend to cause acute infections
  • Enveloped hepatitis viruses (Hep B, C, D) tend to cause persistent and chronic infections; have developed ways of evading immunity
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7
Q

How do the differences in HepA - E influence routes of transmission?

A

Naked (Hep A, E):

  • Non-enveloped
  • Oral-faecal transmission e.g. unwashed food
  • Resistant to dryness, acids etc, can survive outside the body
  • Cause acute hepatitis

Enveloped:

  • Blood and other bodily fluids (contaminated blood transfusion, needle-stick injury, unprotected sexual intercourse)
  • Envelope = sensitive to dryness and will not survive outside the body; transfer via bodily fluids
  • Cause chronic disease
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8
Q

What is the characteristic symptom of hepatitis?

A

Jaundice (jaune; French for yellow) AKA icterus:

  • Yellowing of the skin and eyes
  • Due to increased levels of bilirubin (a haemoglobin breakdown product) in the blood
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9
Q

Describe how bilirubin is rid of in the healthy liver, and the precursors which contribute to jaundice.

A
  • Heme is broken down in the liver to Biliverdin (non-soluble) via Heme oxygenase first
  • Non-soluble biliverdin then reduced to bilirubin (via biliverdin reductase); but still not soluble
  • These insoluble compounds build-up in the body w/poo liver function as the liver can’t keep up with degradation of RBCs

> > > In healthy liver, biliverdin is then conjugated with glucuronic acid to form the water-soluble product, bilirubin diglucuronide, which is then excreted.

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10
Q

Describe what other symptoms can arise from hepatitis infection aside from jaundice.

A

Jaundice in 70-80% of people 14+ y/o (but only 10% in children).

Other symptoms:

  • Fatigue
  • Abdominal pain
  • Loss of appetite
  • N&V
  • Dark urine (more characteristic, above more non-specific)
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11
Q

What are the other causes of jaundice aside from hepatitis?

A
  • Gilbert syndrome (mild hereditary hyperbilirubinemia)

- And other shit

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12
Q

What is the difference/purpose between pre-exposure immunisation and post-exposure immunisation?

A

Pre-exposure:
- To protect HCP against needlestick injury etc. (have antibodies)

Post-exposure:
- Vaccination given ASAP after being pricked

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13
Q

Describe the Hepatitis A virus; severity of infection, immunity, transmission etc.

A
  • Self-limiting; HAV does not lead to chronic/persistent hepatitis (immune response sufficient)
  • CAN result in fulminant (lightning/v. quick) hepatitis and death in small proportion; not reversible thus ICU/transplant required
  • HAV induces lifelong protection against reinfection
  • Transmission: mainly oral-faecal
  • Occurs worldwide; risk of infection inversely proportion to levels of sanitation and personal hygiene
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14
Q

Describe the structure of the Hepatitis A virus.

A

Capsid:

  • Densely packed icosahedral (20 faces) arrangement
  • Consists of 60 promoters, each consisting of 3 polypeptides; VP1, VP2 and VP3 (Viral Protein 1…)
  • VP4 not incorporated into outer capsid (inner capsid?)
  • Non-enveloped
  • Spherical (pseudo icosahedral)
  • 30 nm positive ss(+)RNA virus; Group IV (4)
  • Genus; hepatovirus, of the picornavirus family
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15
Q

Describe the Hepatitis B virus; severity of infection, complications, transmission etc.

A
  • In most cases; HBV only stays in the body for 1 - 3 months (Acute Hep B)
  • 1 in 20 cases; virus stays for 6 months+; usually w/o causing any noticeable symptoms (Chronic Hep B)
    »> 20-25% of Chronic Hep B have progressive liver disease (degeneration), leading to cirrhosis
    »»> Around 10% of Chronic Hep B w/cirrhosis etc. will develop liver cancer (0.1% of everyone developing Hep B)

Transmission:
• Sexual transmission (STI)
• Blood-to-blood contact; needle-sharing etc, needle-stick injuries
• Perinatal transmission from mother to child

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16
Q

Describe the structure of the Hepatitis B virus.

A
  • Enveloped (stolen from host cell)
  • Spherical
  • Diameter; 42mn (smallish)
  • Icosahedric capsid (within envelope)
  • dsDNA, Baltimore VII (mix of dsDNA and sDNA w/RNA primer; exception to I - VI)

> > > Reverse transcriptase activity; HBV one of few non-retroviral viruses which use reverse transcription as part of its replication process
HBsAg (HepB Surface Antigens); 3 sub-units (Large S, Middle S, Small S) of different lengths on envelope
HBcAg (HepB Capsid Antigen)

17
Q

Describe the Hepatitis C virus; epidemiology, symptoms, immunity, transmission etc.

A

Epidemiology:

  • 170 million infected w/Hep C worldwide (loads more than HIV)
  • 216,000 in UK have chronic hepatitis C
  • 87% are current/past drug users (needle sharing)

Symptoms:

  • No noticeable symptoms in most cases until liver has already become significantly damaged
  • HCV infection progresses to chronic liver disease in 70-75% of cases; 3x more than HepB, resulting in liver failure, cancer

Immunity:
- There is no vaccine of HCV

Transmission:
- HCV concentrated in blood; transmitted through blood-to-blood contact (e.g. needle-sharing by IVDUs)
- Via saliva, semen or vaginal fluid (latter mostly in HepB)
to a much lesser extent

18
Q

Describe the structure of HCV.

A
  • Enveloped, spherical
  • Icosahedral capsid
  • 50nm diameter
  • Mature virions contain two virus-encoded membrane proteins (E1, E2; form dimer), as well as capsid protein (within envelope)
  • Baltimore IV; ssRNA(+)
  • Genus: Hepacivirus, of the Flaviviridae family
19
Q

Why is the genotype of HCV important?

A
  • Dictates type of therapy to be used
  • At least 11 genotypes (strains)
  • Genotypes 1, 2 and 3 most widespread in Europe and North America
  • Genotype 4 in AFrica
20
Q

How is Hepatitis C infection treated?

A
  • Combination therapy of Ribavirin (oral guanosine nucleoside analogue) and PEGylated IFN-α (cytokine peptide)
  • Treatment duration; 6-12 months, BUT only 20-40% cure rate
21
Q

What cautions are there with Ribavirin (+ PEGylated IFN-α) therapy of HCV? What influences outcome?

A
  • Teratogenic; not to be given to pregnant women
  • HCV Genotype affects treatment success; 2 or 3 and three times more likely to respond to therapy than Genotype 1 (dickhead ting)
    »> Different strategies for different genotypes
22
Q

What newer therapies have been devised for HCV treatment?

A

HCV protease inhibitors:

  • Boceprevir and Telaprevir (UK)
  • For HepC Genotype 1 in combination w/ribavirin (OG)

HCV Polymerase inhibitors:

  • Sofosbuvir (Sovaldi)
  • HepC Genotypes 2 & 3 as combination therapy with ribavirin (OG)
  • HepC Genotypes 1 & 4 as triple therapy with ribavirin and PEGylated IFN-α (BUT; long + expensive treatment, w/low success)
23
Q

Describe the Hepatitis D virus. Why is it peculiar?

A
  • Defective, ‘satellite’ virus; cannot exist on its own
  • Requires co-infection w/HBV; provides the antigens needed for cell host cell attachment and infection
  • HDV does not have surface antigens required for infection
  • But once inside cell, HDV can replicate independently
  • Uses HBV surface antigens (HBsAg) as its own virion coat
24
Q

Describe the structure of HDV, and how its boiz w/HBV.

A
  • Enveloped
  • Spherical
  • 22nm diameter (small)
  • Membrane proteins (M-glycoprotein, S-glycoprotein, L-glycoprotein) originate from HBV helper virus
  • Delta antigen (HDAg) stabilises RNA genome within viral envelope; HDV has NO capsid, just the envelope
25
Q

What is the significance of HDV infection (co-infection w/HBV)?

A
  • Virus-like (no capsid) delta agent associated w/most severe forms of acute and chronic hepatitis in many HBsAg-positive patients
  • Disease = Type D/Delta hepatitis
  • Chronic hepatitis D may also lead to development of hepatocellular carcinoma (liver cancer)
    »> WORST hepatitis.
26
Q

What is passive immunisation? Adv vs. disadv?

A
  • Injection of pathogen-specific pooled human Igs (antibodies)
  • Used when no time for active immunisation, or in post-exposure prophylaxis; offers immediate protection e.g. rabies
  • But, does not confer long-term protection (no immunity, foreign antibodies are degraded)
27
Q

What are the different types of active immunisation availible?

A
  • Live attenuated vaccines (#1)
  • Inactivated vaccines (#2)
  • Subunit vaccines (#3)
28
Q

What do live attenuated vaccines entail?

A

Best active immunisation:
- Viruses grown in cultures and repeatedly passaged through rounds of culture (less pathogenic after each round)
- Low virulence viruses selected; these attenuated strains then reproduced in large quantities for vaccination
- Full immune response; without causing full illness (mild symptoms possible)
- Immune memory of pathogen generated
»> AVOID in immunosuppressed (CAN/HIV)

29
Q

What are inactivated vaccines?

A
  • Viruses cultured as per Live Attenuated Vaccines, but then inactivated w/formaldehyde ‘killed’
  • # 2 Active Vaccination
  • Fewer S/Es (symptoms) than LAVs
    »> But immune response is less vigorous
30
Q

What are subunit vaccines?

A

3 Active Vaccines:

  • Surface antigens produced by recombinant DNA technologies (e.g. yeast)
  • Recombinant protein given as single protein alone, or up to 20 different proteins together w/adjuvant (e.g. aluminum hydroxide, strengthens immune response)
  • Safe approach; pathogen is not present, and pose nor risk to immunocompromised patients either (unlike LAVs)
    »> BUT, evoked immune response may be weaker, hence less protection
    E.g. Influenza vaccines, HBV vaccines.
31
Q

What does vaccination against Hep A entail?

A
  • There is one HAV serotype, but at least 7 different genotypes
  • Antibodies against just one genotype protects against all other genotypes!!!!
  • No specific treatment
  • Vaccination; inactivated whole viruses propagated in MRC-5 human lung fibroblast cell line
32
Q

What are the three types of vaccine that protect against HAV infection?

A
  • Monovalent vaccine; protection against HepA
  • Combined HepA and HepB vaccine (useful for HCPs)
  • Combined HepA and typhoid fever vaccine (typhoid fever serious bacterial infection; useful for travellers)
33
Q

What does HepB vaccination consist of?

A
  • Subunit vaccine consisting of HBsAg (surface antigen) absorbed onto aluminium hydroxide adjuvant, prepared from yeast cells via recombinant DNA technology
  • Combined vaccine containing purified inactivated HAV and purified recombinant HBsAg also availible
  • Usually 3 doses, with a potential 4th booster after checking Ab level
  • HepB vaccine highly effective at preventing infection if given shortly after exposure; needle-stick injuries
  • 10-15% adults fail to respond to 3 doses of vaccine, or respond poorly (>40 y/o)

E.g.:
• Monovalent: Hep B
• Combined: HepA + Hep B

*B33VPI - Biology & Physiology (8 decks)

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