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microb - viruses > Hepatitis Viruses > Flashcards

Hepatitis Viruses Flashcards

1
Q

Features of hepatitis viruses

A
  • Cause inflammation of the liver
  • Common symptoms: feeling unwell, jaundice
  • Other viruses that can cause hepatitis but rare in the region: Yellow fever virus, EBV, CMV, Rubella, Haantan virus
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2
Q

Examples of hepatitis viruses

A

Blood borne

  1. Hepatitis B - DNA hepadnavirus
  2. Hepatitis C - RNA flavivirus
  3. Hepatitis D - RNA satellite virus

Waterborne

  1. Hepatitis A - RNA picornavirus
  2. Hepatitis E - RNA calicivirus
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3
Q

Structure of Hep B virus

A
  • Enveloped (with surface Ag HBsAg), with core (HBcAg) and core associated (HBeAg) proteins stimulating anti-HBs, anti-HBc, anti-HBe
  • HBcAg cannot be detected in infected person’s blood
  • HBcAg is found in infected liver, in blood it is coated with HBsAg (Dane particle)
  • HBsAg is made in excess - exists alone (not infectious) or part of Dane particle
  • ds DNA of unequal length
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4
Q

Transmission of Hep B

A
  1. Infected blood & blood products - needlestick contamination, surgical & dental procedures, drug addicts sharing needles, barbers, acupuncture, tattooing, sharing razors
  2. Carrier mothers to infants - transplacental 10%, perinatal 80%, post natal 10%
  3. Sexual
  4. Others - contact sports, wounds
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5
Q

Symptoms of Hep B

A
  1. Acute Hep B infection
    - mostly subclinical 90%
    - initially non-specific, later jaundice, long incubation period - 3-4m
    - most recover, develop anti-HBs
    - some become carriers (source of infection), 15-30% develop chronic hepatitis, cirrhosis, liver cancer; 1% lose HBsAg and recover
  2. Chronic/persistent Hepatitis
    - typically reactivation
    - cirrhosis, liver cancer
    - no CTLs against HBsAg/HBcAg, no anti-HBs
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6
Q

Complications of Hep B

A
  • Carriers, chronic hepatitis, cirrhosis, liver cancer

- Polyarteritis nodosa, glomerulonephritis

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7
Q

Diagnosis of Hep B (3)

A
  1. Antigen Detection (HBsAg, HBeAg, HBcAg - only in liver)
  2. Serology (Anti-HBc: IgM - IgG; Anti-HBs; Anti-HBe)
  3. PCR - HBV DNA

(A) Acute Hep B infection
- HBsAg - detectable first, in blood before onset of symptoms - IgM anti-HBc - IgG anti-HBc - anti-HBs
- HBeAg is a marker for infectiousness & viremia
(B) Chronic Hepatitis
- HBsAg persist +/- HBeAg, patient becomes a carrier
- carrier of HBsAg - detectable in the blood 6m apart
(C) HBeAg & HBV DNA (PCR) - markers for presence of core particles (HBcAg)
(D) Pre-core mutants are infectious with undetectable HBeAg - HBV DNA is the only marker

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8
Q

Treatment of Hep B

A
  1. Vaccines
    - 1G: plasma based, HBsAg purified from carriers
    - 2G: yeast based recombinant HBsAg ‘a’ epitope
    - 1G & 2G: safe & effective, cannot be frozen - loses antigenicity, store at 2-8C, 5-10% non responders
    - 3G: contains pre S1, pre S2 & HBsAg peptides, may be effective against vaccine escape mutants & non responders - more effective in stimulating T cells
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9
Q

Prevention of Hep B

A
  1. Vaccines - pre infection, post infection, infants
  2. Avoid infected material from entering body - screening of blood/products, single use needles & syringes, precaution in handling potential infective materials, autoclave
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10
Q

Structure of Hep C virus

A
  • ssRNA
  • enveloped
  • variations: 6 major genotypes with numerous subtypes
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11
Q

Transmission of Hep C

A
  1. Blood & blood products, drug abusers - screening

2. Mother to child & sexual - possible but rare due to little circulating virus

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12
Q

Incubation period of Hep C

A

6-12 weeks

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13
Q

Symptoms of Hep C

A
  • milder than Hep B

- progress to chronicity is the main feature with fluctuating liver enzymes, may first present as chronic hepatitis

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14
Q

Complications of Hep C

A
  • chronic hepatitis, cirrhosis, liver cancer
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15
Q

Diagnosis of Hep C (3)

A
  1. HCV-RNA by RT-PCR
  2. Serology: anti-HCV, confirmation by recombinant immunoblot assay (RIBA) or synthetic peptide strips (Inno-Lia)
  3. IgM anti-HCV not used - low sensitivity
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16
Q

Treatment of Hep C

A
  • similar to Hep B
  • no vaccine
  • Recent new drugs eg Sovaldi
17
Q

Structure of Hep D

A
  • ssRNA

- defective, needs HBsAg coat to infect cells (HBV serves as a helper virus)

18
Q

Features of Hep D

A
  1. 2 types of infection (A) Superinfection - infects HBsAg carrier (B) Co-infection - infects at the same time as HBV
  2. Asia - mainly genotypes 1&2, milder disease
  3. Genotype 3 - outbreaks in S America & E Europe, severe
  4. Rare in SG, few mild cases, Hep B vaccination automatically protects
19
Q

Transmission of Hep A

A
  • Faecal-oral

- eating raw/partially cooked cockles & oysters, river mouth filter feeders, sexual oral-anal

20
Q

Incubation period of Hep A

A
  • 4-6 weeks

- appears in stool before clinical symptoms

21
Q

Symptoms of Hep A

A
  • mostly subclinical

- usually milder disease than Hep B

22
Q

Complications of Hep A

A
  • Liver necrosis & failure

- no sequelae, lifelong protection upon recovery (no chronic infection)

23
Q

Diagnosis of Hep A

A

Serology: IgM anti-HAV

24
Q

Treatment of Hep A

A
  1. Vaccine
    - killed virus grown in tissue culture
    - very effective with single dose 2w before travelling, traveller’s vaccine
    - stops outbreaks of 50-60% if population is vaccinated
25
Q

Prevention of Hep A

A
  • avoid eating contaminated food/drinks, boil for 5 min
  • chlorine eg swimming pools
  • passive immunization with Ig before travelling to high risk countries
26
Q

Transmission of Hep E

A
  • Faecal-oral
  • Water borne
  • Zoonotic in pigs

Incubation period slightly longer than Hep A (which is 4-6w)

27
Q

Symptoms of Hep E

A
  • Symptomatic in older people

- Severe disease in pregnant women, 25% fatal, fetal mortality high

28
Q

Diagnosis of Hep E (2)

A
  1. IgM anti-HEV

2. HEV-RNA RT-PCR

29
Q

Treatment of Hep E

A
  • vaccines on trial

- protective antibodies do not last

microb - viruses (10 decks)

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