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VIRAL HEPATITIS - by viruses having special affinity for liver; other viruses like Epstein Barr virus, cyto megalo virus (newborn/immuno suppressed) and yellow fever virus Q


Hepatitis A

Hepatitis B

Hepatitis C

Hepatitis D

Hepatitis E







Type of virus Viral family

ssRNA Hepatovirus; related to picornavirus

partially dsDNA Hepadnavirus

ssRNA Flaviridae

Circular defective ssRNA Subviral particle in Deltaviridae family

ssRNA Calicivirus







Route of transmission

Fecal-oral (contaminated food or water)

Parenteral, sexual contact, perinatal

Parenteral; intranasal cocaine use is a risk factor









Mean incubation period

2-4 weeks

1-4 months

7-8 weeks

Same as HBV

4-5 weeks







Frequency of chronic liver disease




5% (coinfection); ≤70% for superinfection









Detection of serum IgM antibodies

Detection of HBsAg or antibody to HBcAg

PCR for HCV RNA; 3rd-generation ELISA for antibody detection

Detection of IgM and IgG antibodies; HDV RNA serum; HDAg in liver

PCR for HEV RNA; detection of serum IgM and IgG antibodies


Hepatitis A virus Infections hepatitis –

  1. Benign, self-limited disease
  2. IP: 2-6 weeks
  3. Chronic hepatitis - None
  4. Carrier state – None Q
  5. Fulminant hepatitis - Rarely
  6. Fatality: 0.1%
  7. World wide, bad hygiene
  8. Accounts for 25 % of clinically evident cases of acute hepatitis world wide
  9. Un enveloped, SS RNA virus (Picorna virus)  Hepatovirusi. Icosahedral capsid: 27mm in diameter
  10. Spread: Feco - oral Route.Q In developed countries raw or steamed shellfish may spread the infection Present in stools: 2-3 weeks before and 1 week after onset of jaundice Q

  1. Transient Viremia Transmission (rare blood bore)­
  1. Serodiagnosis - IgM antibody appears in blood with onset of symptoms - marker of acute infection.
  1. IgG antibody - life long immunity

HEPATITIS B VIRUS (Serum Hepatitis) Q

  1. Acute hepatitis
  2. Non-progressive chronic hepatitis
  3. Progressive chronic hepatitis cirrhosis
  4. Fulminant hepatitis
  5. Carrier state
  6. Back drop for HDV infection
  7. HCC 

IP 30-180 days (1-6 months)

a. HBV remains in blood: last stage of IP Active disease (Acute and chronic)

b. Present in all physiologic and pathologic body fluids, except in stools (unlike HAV)

: -
  1. Blood products, needle sticks etc. (30%)
  2. Sexual transmission
  3. Vertical → Carrier state
b. Virus
  1. Hepadnaviridae family
  2. Spherical, double layered 'Dane particle' 42 mm in size
  3. DS DNA


  1. HBc Ag: Nucleo capsid core protein Q
  2. HBe Ag: Both precore and core region
  3. HBs Ag: Envelope glycoproteins Synthesized and secreted by infected hepatocytes Q
  4. DNA polymerase that exhibits reverse transcriptase activity
  5. Transcriptional transactivation of viral genes and host gene promoters'
  6. Role in HCC

Phase of Infections

1. Proliferative phase:  

  1. HBV DNA in episomal form
  2. Formation of complete virion with associated antigens
  3. MHC class I CD8+ T cells activation Infected hepatocyte destruction

2. Integrative phase:

  1. Viral DNA incorporated 'into host DNA. Occurs in hepatocytes not destroyed by immune response. Q
  2. With cessation of viral replication within hepatocytes and appearance of antibodies, infectivity ends and liver damage subsides Q 

Serological Diagnosis –

1. HBs Ag

  1. Appears before onset of symptomsQ
  2. Peaks during overt disease
  3. To undetected levels in 3-6 months

HBe Ag, HBV DNA, DNA polymerase appearQ

-  After HBs Ag

- Signify active viral replicationQ

2. IgM Anti HBc

  1. Appear shortly before onset of symptoms
  2. Concurrent with onset of S. aminotransferases
  3. Marker of window periodQ.
  4. IgM IgG

3. Anti HBe

-  Shortly appear after disappearance of HBe Ag (i.e. acute infection has peaked and disease is on its wane)   .


4. IgG Anti HBS -

  1. Doesn't rise till acute disease is over
  2. Not detectable for few weeks to several months after disappearance of HBs Ag (window period)
  3. Persists for life, conferring protection.
Carrier State
HBs Ag ³ 6 months Q (doesn't necessarily indicate replication)
Chronic replication
  • Persistence of circulating HBs Ag. HBeAg, HBV DNA usually with ant HBc and occasionally with anti Hbs Q
  • Progressive liver damage can occur.

  1. MOI: Inoculation and Blood transfusion
    1. Sexual and vertical transmission →  Infrequent causes: (risk of perinatal transmission is much lower will hepatitis C-6% births to infected mother than with' hepatitis B - 20-60% of births to infected mothers)
    2. Most important Cause of transfusion associated hepatitis
    3. Acute HCV infection is generally undetected clinically
    4. In contrast HBV, Chronic disease occurs in majority of infected individuals and cirrhosis develops in 20% patients
    5. Leading. infectious cause of chronic Liver disease world wide
  2. Virus: Flaviviridae
    1. IgE anti HCV
      1. SS RNA
      2. Unstable => Types and sub types
    2. Difficulty in vaccine development.
      1. ↑ IgG. Anti -+ No effective immunity
      2. Cirrhosis - in 5-10 years
    3. Serology Q
      1. IP: 2-26 weeks
      2. HCV RNA: present in blood for 1-3 weeks (with ↑ S. transaminase)
      3. Acute illness: Asymptomatic / mild
      4. IgM Anti HCV → IgG Anti HCV
      5. Chronic infection: Episodic elevations in S. transaminase with intervening (n) period HCV RNA persists in blood.
  1. Delta agent
  2. Replication defective
  3. Infection when encapsulated by HBs Ag
  4. Acute Co- infection
  5. Simultaneous exposure
  6. HBV- must establish first
  7. Fulminant Hepatitis: 3-4%
  8. Chronic Hepatitis: Rare
  9. Super infection: In chronic carriers of HBV followed by, HDV infection
  10. Disease after 30-50 d    
  11. Acute disease → Recovery: 10% - 15%
  12. Fulminant hepatitis → 7% - 10%
  13. Chronic HBV/HDV hepatitis → 80%
  14. HDV: 35 mm SSRNA
  1. HDV RNA + in blood and liver just before and in early days of acute symptomatic disease
  2. IgM Anti HDV - most reliable marker (late and short lived)
  1. Enterically transmitted Q
  2. Sporadic infection
  3. Young - middle age adults (Rare in children)
  4. Accounts for over 50% of cases of acute hepatitis in India.
  5. Pregnancy → high mortality (20%) Q
  6. Self limited (not associated with chronic disease) 
IP: 2-8 weeks: not associated with persistent viremia & chronic liver disease
Virus: SSRNA. Caliciviridae unenveloped

Serology: HEV RNA & Virions + in stool & liver - before onset of clinical illness
  1. S. transaminases
  2. IgM anti HEV  IgG (in 2-4 wks)
- Flaviviridae

MOI: parenteral - Contaminated blood/blood products

Possibly sexual.
  1. Prevalence of HGV RNA in blood donors 1-4% Q
  2. In up to 75% of infections, HGV cleaned from plasma, in remainder, infection becomes chronic  Q
  3. Site of HGV replication is mononuclear cells
  4. No rise in S. amino transferases. Non- pathogenic
  5. Co-infects patients with/HIV dual infection protective against HIV disease
Clinicopathologic Syndromes
  1. Asymptomatic infections with recovery:
    - ↑ S. transaminase / presence of antiviral antibodies
  2. Acute viral Hepatitis: 4 phases
    1. Phase:
      a. IP (incubation period) Q
      b. II   - Symptomatic preicteric phase Q
      c. Non - specific, constitutional symptoms 10% have serum sickness like picture
      d. Symptomatic icteric phase Q - Usual in adults with acute HAV (not children)
      Absent in about half cases of HBV and in majority of cases of HCV.   
      Jaundice is predominantly conjugated hyperbilirubinemia
    2. Convalescence Q
      Peak infectivity: Last days of IP & early days of acute infection
  3. Chronic Viral Hepatitis:
    1. Symptomatic, Biochemical or serologic evidence of continuing or relapsing disease for >6 months with histologic documentation of inflammation / necrosis.
    2. Etiology most important indicator of likelihood to progress to cirrhosis
    1. Chronic hepatitis constitutes a “Carrier State" Q
      1. Healthy carrier - Harbor the virus without adverse clinical/ histological
      2. Carriers with chronic liver disease but free of symptoms/ disability
      3. Carriers with symptoms of chronic disease
    2. Early infection (Particularly vertical) →  90-95%
    3. Adult infection  → 1-10%
  5. Old classification
    1. Chronic Persistent Hepatitis (CPH)
    2. Chronic Active Hepatitis (CAH)
    3. Chronic Lobular Hepatitis (CLH)
    4. CPH: In. in PT, no piecemeal necrosis
    5. CAH: Piecemeal necrosis
    6. CLH: Within Lobules
  6. Newer Classification: (i) Etiology (ii) Grading (iii) Staging
  7. Morphology
    HBV infection
    Ground glass hepatocytes →  HBsAg spheres & tubules in cytoplasms.
    Sanded nuclei → HBc Ag in nucleus.
  8. Acute hepatitis
    1. Ballooning degeneration (Swelling) Q
    2. Cholestasis
    3. Cell death - Cytolysis Apoptosis - councilman bodies
    4. Bridging necrosis
    5. Hepatocyte swelling and regeneration, loss of radial array Q
    6. Kupffer cell hyperplasia and hypertrophy Q
    7. Portal tracts inflammatory infiltrate
    8. Interface hepatitis, spillage of inflammatory cells from portal tracts into adjacent parenchyma with necrosis
  9. Chronic hepatitis:
    1. Mild to severe
    2. Continued interface hepatitis and bridging necrosis
    3. Bridging fibrosis
    4. Periportal fibrosis, Portal fibrosis
    5. Eventually cirrhosis (post necrotic cirrhosis)
  10. HCV infection: Special features Q
    1. Bile duct damage
    2. Steatosis - Macrovesicular type
    3. Portal lymphoid aggregates

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