This document summarizes and compares key aspects of 5 types of viral hepatitis: HAV, HBV, HCV, HDV, and HEV. It outlines their signatures, RNA/DNA type, virulence, carrier state potential, spread method, transmission period, incubation period, epidemiology, available vaccines, clinical features, diagnostic antibodies, and diagnosis methods. The viruses cause acute or chronic hepatitis and some can lead to liver cancer. They differ in factors like persistence in the body after infection and presence of vaccines.
This document summarizes and compares key aspects of 5 types of viral hepatitis: HAV, HBV, HCV, HDV, and HEV. It outlines their signatures, RNA/DNA type, virulence, carrier state potential, spread method, transmission period, incubation period, epidemiology, available vaccines, clinical features, diagnostic antibodies, and diagnosis methods. The viruses cause acute or chronic hepatitis and some can lead to liver cancer. They differ in factors like persistence in the body after infection and presence of vaccines.
Copyright:
Attribution Non-Commercial (BY-NC)
Available Formats
Download as DOCX, PDF, TXT or read online from Scribd
This document summarizes and compares key aspects of 5 types of viral hepatitis: HAV, HBV, HCV, HDV, and HEV. It outlines their signatures, RNA/DNA type, virulence, carrier state potential, spread method, transmission period, incubation period, epidemiology, available vaccines, clinical features, diagnostic antibodies, and diagnosis methods. The viruses cause acute or chronic hepatitis and some can lead to liver cancer. They differ in factors like persistence in the body after infection and presence of vaccines.
Copyright:
Attribution Non-Commercial (BY-NC)
Available Formats
Download as DOCX, PDF, TXT or read online from Scribd
Signature Acute; dirty food Gives HCC; HK and S China Gives HCC; no vaccine Friend of HBV Acute; dirty food RNA/DN ssRNA Part ssDNA Linear ssRNA Circular defective ssRNA ssRNA A Virulence Direct cytopathic HBV infects liver cells T cell attacks - Can transform mild chronic - effect/T-cell HBV & own liver cells hepatitis hep B into severe chronic mediated injury hep B & cirrhosis (?) Carrier No Yes Yes Yes Low risk/None state? Acute, self- (95% full recovery) Wide spectrum of outcomes, Requires HBs-Agaemic to Full recovery limiting disease May develop chronic hepatitis +/- similar to Hep B be effective expected (99% full cirrhosis, +/- HCC (100x RR) 50% progress to chronic hepatitis & Co-infection: Simultaneous May cause recovery), rarely *Infection in infants (~95% chronicity; cirrhosis +/- HCC introduction of HBV & HDV severe disease fatal associated with poor cell-mediated Causes: Superinfection: HDV into esp. pregnant immune response to HBV?) 1. Acute/chronic hepatitis HBsAg+ve host women Broad definition: Presence of HBV 2. Carrier state regardless of symptoms 3. End-stage liver Narrow definition: replication of HBV 4. HCC w/o symptoms Spread Faecal-oral route Parenteral route Faecal-oral Ingestion of 1. Transfusion of blood and blood products route contaminated 2. Contamination of needles water and foods 3. Medical and dental procedures e.g. not well 4. Intimate contact esp. sexual cooked shellfish 5. HBV: Vertical transmission during perinatal period (X pregnancy, V at the time of birth!) [Food to subject/subject to subject] Transmis Shed in stool 2-3 - - - Caused sion weeks before massive and 1 week after outbreaks onset of jaundice water-borne hepatitis Incubatio Short Long Long Long Short n period 15-40 days (1 1-4 months 7-8 weeks 1-4 months 4-5 weeks month) HK % - 1/10 = carrier <1% - - 4/10 = recovered (exclude vaccinated) Epidemol Occurs Extremely common in HK and S China N Africa - - ogy throughout the 400 million HBV subjects; 75% Chinese Case: Egypt 1960-70s, world Incidence varies greatly in different schistosomiasis vaccination; use Endemic in parts of the world same needle HCV countries with 1. Urban > rural substandard 2. Male > female hygiene and 3. Certain groups regardless of sanitation location 4. Poor SES [HBsAg in 5-20% of apparently healthy persons in SE Asia and tropical Africa; 0.1-0.6% in W Europe and USA] Vaccine Yes Yes No No; use HBV vaccine Yes, safe? Clinical - Acute Hep B tend to be more severe Mild clinically Acute HBV/HDV infection - features than Hep A/C may be indistinguishable Subclinical infection frequent esp. in from hep B, but associated infants and children with relatively high rate of fulminant hepatitis Antibody Anti-HAV - Anti-HCV not protective - - appears during Appears several weeks later than attack and HCV RNA persists Diagnosis Serum IgM HBsAg/Ab to HBcAg 1. +ve anti-HCV Ab; PCR for HCV IgM & IgG PCR for HEV RNA HDV RNA serum RNA 2. Raised AST, ALT HDAg in liver Serum IgM & 3. Biopsy IgG a. Portal tract inflammatory infiltrates rich in lymphocytes b. Interface hepatitis c. Macrovesicular steatosis (fatty change) Macro = nucleus distorted Micro = nucleus X distorted