HEPATITIS B VIRUS – HBV (Micro made easy pp 182)

General: HBV = Big and Bad. It is a big virus (42NM) and has an enveloped capsid and is a DNA virus. It is part of the hepatoviridae family, and is transmitted parenterally + body fluids. Fig 24-6 provides illustrations. This is the virion structure. Blood films will also contain filamentous structures and this is known as hepatitis B surface antigen (HBsAg). Having anti-HBsAg means patient is immune to HBV. The left over part is called hepatitis B core antigen (HBcAg). Having anti-HBcAg is not protective from HBV. During active disease, a soluble component of core antigen is released ≫ HBeAg. Detecting this in serum means the patient has active disease + highly infectious. If a pregnant mother has this marker, then 90% of the time – she will transmit the infection to the baby too! The virus is found in all body fluids (in order of concentrations): blood, serum, wound exudates, semen, saliva, vaginal fluid, urine, sweat, breast milk, faeces.

Epidemiology/At risk individuals: Transmission is by parenteral route. At risk groups are: health care workers, IVDU, HBV infected pregnant women, blood transfusion / organ transplant patients etc etc.

Clinical features: Incubation period is 60-90 days (45-180 day range), the younger the patient the less chance of developing jaundice. Normal course is: Flue like symptoms ≫ liver function tests abnormal ≫ jaundice ≫ acute hepatitis. HBV is a bad virus because it can lead to further complications: fulminant hepatitis (severe case of acute hepatitis), chronic hepatitis – 3 types – a) asymptomatic carrier: never develop antibodies against HBsAg, no symptoms, b) chronic persistent hepatitis, c) chronic active hepatitis: same as acute hepatitis but goes for 6-12 months. Cell mediated immunity is involved, with deposition of immune complexes ≫ arthritis/rashes etc. Complication: HBV can lead to primary hepatocellular carcinoma. The DNA of virus becomes embedded in hepatocyte DNA and trigger malignant growth. HBV infection can lead to liver cirrhosis.

Serology: Refer to Fig 24-7/8 pp 186. As mentioned before there are three serological markers.

• HBsAg: This means there is LIVE virus in the body. It may be that the patient has acute, chronic, carrier state hepatitis. Anti-HBsAg means no virus is present, patient is free of all types of hepatitis.

• HBcAg: This can help in determining how long the patient has had hepatitis. Finding anti-HBcAg IgM means the patient has had infection for short time (NEW INFECTION). Finding anti-HBcAg IgG means the patient has had infection for long time (OLD INFECTION).

• HBeAg: This helps in determining the infectivity of a patient. Having this means the patient has active disease and is highly infectious. Having anti-HBeAg means patient is lowly infectious.

Treatment/Prevention: Prevention: 1) Screening blood donors, 2) education (sexual partners, contacts), 3) careful health care practices, 4) Immunisation: administer HBsAg to infants at birth, 2, 4, 15 months. Treatment: 1) antiviral drugs: lamivudine, famciclovir 2) IFN-alpha.

Category: Microbiology Notes