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» OCW Home » Microbiology » Student Notes 
Lecture 20 - Hepatitis
Author: Amelia Virostko
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1. Identification

  1. Hepatitis A: positive-stranded non-enveloped RNA virus
  2. Hepatitis B: partially double-stranded DNA virus with outer lipoprotein envelope with 3 important proteins - surface, core, and envelope antigens
  3. Hepatitis C: positive-stranded enveloped RNA virus
  4. Hepatitis D: partially paired single-stranded RNA virus that requires hepatitis B as its helper virus
  5. Hepatitis E: similar to hepatitis A
  6. Hepatitis G: similar to hepatitis C

2. Hepatitis A

2.1. Encounter

  1. Spread via the fecal/oral route
  2. Host encounters virus by ingestion of contaminated food, water, or contact with infected individuals
  3. Endemic in parts of the world with poor sanitation

2.2. Spread/Multiplicaction

  1. Absorbed into the bloodstream from the intestine, and reaches the liver via portal circulation
  2. Rapidly multiplies shedding viral particles into bile and circulation

2.3. Damage

  1. Immune response causes acute hepatitis
  2. Disease is more severe in adults than children

2.4. Key Virulence Factors

  1. Viral antigens that stimulate an immune response

2.5. Outcome

  1. Usually resolves over 2-3 months following infection
  2. Protective IgM and IgG antibodies form which confer lifetime immunity
  3. No carrier state

2.6. Diagnosis

  1. Anti-HAV antibodies are diagnostic of infection

2.7. Treatment

  1. No treatment exists for active infection
  2. Effective vaccine exists for people traveling to areas where HAV is endemic

3. Hepatitis B

3.1. Encounter

  1. Virus is spread through blood, semen, and vaginal secretions
  2. Transmission through IV drug use, sexual contact, blood transfusions, or vertically

3.2. Spread/Multiplication

  1. Virus travels to the liver, attaches to receptors on the cell surface, and enters the cell
  2. Genome is transported to the nucleus

3.3. Damage

  1. Incubation period of virus is 6-24 weeks
  2. Damage to liver occurs due to host immune response destroying infected cells
  3. 90% of the time, the course of disease is 1-3 months, as immune system kills infected cells faster than the virus can spread
  4. 5-10% of the time, the patient progresses to chronic infection that is never fully cleared
  5. 1% of the time, patients experience acute liver failure from fulminant hepatitis

3.4. Key Virulence Factors

  1. HBV can hide surface antigen from the immune system, thereby maintaining chronic infection

3.5. Diagnosis

  1. 1 month after infection, HBsAg, HBeAg, and viral DNA can be detected
  2. IgG antibodies to viral antigens can be detected after 3 months
  3. HBsAb are protective and confer immunity
  4. HBsAg for 6 months indicates chronic HBV infection

3.6. Treatment

  1. Vaccine that contains a recombinant HBsAg protein
  2. 30% respond to interferon-alpha
  3. Lamivudine and adefovir can treat chronic infections
  4. Resistance can develop over time

3.7. Outcome

  1. Most cases result in acute infections that resolve over time
  2. Chronic infections place patients at increased risk of hepatocellular carcinoma and cirrhosis

4. Hepatitis C

4.1. Encounter

  1. Spread through blood, semen, and vaginal secretions
  2. Transmission through IV drug use, sexual contact, blood transfusions, and vertically

4.2. Spread/Multiplication

  1. Virus travels to liver, attaches to cell surface receptors, and enters the cell
  2. RNA is translated as single polypeptide capable of cleaving itself into smaller functional proteins

4.3. Damage

  1. Shorter incubation period than HBV but longer than HAV
  2. Damage to liver believed to occur due to host immune response to infected hepatocytes

4.4. Key Virulence Factors

  1. Envelope helps virus evade the immune system

4.5. Diagnosis

  1. Anti-HCV antibodies can be used to diagnose HCV
  2. PCR to detect viral RNA

4.6. Treatment

  1. No successful treatment
  2. 25% respond to interferon-alpha

4.7. Outcome

  1. Can be cleared or progress to chronic infection (80%)
  2. Increased risk of cirrhosis and hepatocellular carcinoma

5. Hepatitis D

  1. Able to reproduce by creating an outer envelope using HBV envelope proteins
  2. Infection tends to increase risk of fulminant hepatitis as compared to infection with HBV alone
  3. Vaccination against HBV protects against HDV as well

6. Hepatitis E

  1. Causes disease similar to HAV, with similar fecal/oral transmission
  2. Higher mortality, particularly in pregnant women

7. Hepatitis G

  1. Related to HCV
  2. HIV patients co-infected with HGV progress to AIDS more slowly
    1. Possibly due to down-regulation of HIV co-receptor CCR5
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