Hepatitis A virus Hepatitis B virus
Family PicornaViruses Hepadnaviruses
Genome ssRNA dsDNA
Structure Non-enveloped Enveloped dsDNA virus.
One serotype (gives lifelong immunity) Virion named → Dane particle → spherical with 42 nm Diameter.
Human are the only reservoir Contains 3 antigens →
1. HBsAg (surface antigen) → released into bloodstream → may be 22 nm
spherical or 200 nm tubular (contains no DNA so it is not infectious).
2. HBcAg (core antigen) → confined to liver cells.
3. HBeAg (envelope antigen) → secreted from infected cells into the blood.
Transmission Feco-Oral → ingestion of contaminated food or HBV is present in all body fluids of infected patients.
water. 1. Blood transfusion / injection
Rarely by blood (due to short duration and low level 2. Sexual transmission
of viremia). 3. Perinatal transmission (majority of cases)
Viral load is very high → the possibility or transmission is highest among hepatitis
viruses.
Pathogenesis Virus replicated in the GIT → spread via the blood to Virus reach blood → Liver → inflammation and necrosis.
the liver → replicates in hepatocytes → excreted in The main cause of hepatic damage is immune-mediated by T cytotoxic cells (HBV
bile → excreted in urine and feces. itself doesn’t cause damage).
Humoral immunity leads to formation of HBsAb → bind to HBsAg → immune
complexes → extra-hepatic manifestations (10-20% of patients) due to deposition
complexes in skin, joints and glomeruli.
IP 2-6 weeks 6 weeks – 6 months
Clinical Most infections are asymptomatic. Many infections are asymptomatic.
features Symptoms → fever – anorexia – nausea – vomiting – Symptoms → nausea – vomiting – abdominal pain – enlarged tender liver – anorex
dark urine – tender liver. – malaise – jaundice.
Self-limited usually. Extra-hepatic manifestations → skin rash – urticaria – polyarthralgia –
Infection is followed by life-long immunity (IgG) Glomerulonephritis.
Does not progress to chronic hepatitis. Clinical outcomes →
a. Full recovery → within 4-6 months (most cases).
Due to effective immune response.
Complications b. Fulminant hepatitis → occurs in 1-2% of patients → due to massive lysis of
hepatocytes by immunity of HBV or co-infection with another hepatitis virus.
c. Chronic infection → occurs in 5-10 % of patients → due to limited immune
response → may be → chronic hepatitis (ends with cirrhosis and hepatocellula
Family PicornaViruses Hepadnaviruses
Genome ssRNA dsDNA
Structure Non-enveloped Enveloped dsDNA virus.
One serotype (gives lifelong immunity) Virion named → Dane particle → spherical with 42 nm Diameter.
Human are the only reservoir Contains 3 antigens →
1. HBsAg (surface antigen) → released into bloodstream → may be 22 nm
spherical or 200 nm tubular (contains no DNA so it is not infectious).
2. HBcAg (core antigen) → confined to liver cells.
3. HBeAg (envelope antigen) → secreted from infected cells into the blood.
Transmission Feco-Oral → ingestion of contaminated food or HBV is present in all body fluids of infected patients.
water. 1. Blood transfusion / injection
Rarely by blood (due to short duration and low level 2. Sexual transmission
of viremia). 3. Perinatal transmission (majority of cases)
Viral load is very high → the possibility or transmission is highest among hepatitis
viruses.
Pathogenesis Virus replicated in the GIT → spread via the blood to Virus reach blood → Liver → inflammation and necrosis.
the liver → replicates in hepatocytes → excreted in The main cause of hepatic damage is immune-mediated by T cytotoxic cells (HBV
bile → excreted in urine and feces. itself doesn’t cause damage).
Humoral immunity leads to formation of HBsAb → bind to HBsAg → immune
complexes → extra-hepatic manifestations (10-20% of patients) due to deposition
complexes in skin, joints and glomeruli.
IP 2-6 weeks 6 weeks – 6 months
Clinical Most infections are asymptomatic. Many infections are asymptomatic.
features Symptoms → fever – anorexia – nausea – vomiting – Symptoms → nausea – vomiting – abdominal pain – enlarged tender liver – anorex
dark urine – tender liver. – malaise – jaundice.
Self-limited usually. Extra-hepatic manifestations → skin rash – urticaria – polyarthralgia –
Infection is followed by life-long immunity (IgG) Glomerulonephritis.
Does not progress to chronic hepatitis. Clinical outcomes →
a. Full recovery → within 4-6 months (most cases).
Due to effective immune response.
Complications b. Fulminant hepatitis → occurs in 1-2% of patients → due to massive lysis of
hepatocytes by immunity of HBV or co-infection with another hepatitis virus.
c. Chronic infection → occurs in 5-10 % of patients → due to limited immune
response → may be → chronic hepatitis (ends with cirrhosis and hepatocellula
