In this capsule between your hands, we have done hard and precise work to summarise systemic virology and mycology (for undergraduate medical students) in table forms, one of the best ways to create a visual memory helping you to recall, without damaging the scientific core. We hope you all guys fi...
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
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