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The complete infective virion is a 42nm particle comprising an inner core of 27 nm surrounded by an outer envelope of surface protein HBsAg. This surface coat is produced in excess by the infected hepatocytes and can exist separately form the whole virion in the serum and the body as 22nm particle. The genome of HBV is a partially double stranded circular DNA molecule with a unique In that all regions of the viral genome encode protein sequences. HBsAG contains a major “a” antigenic determinant as well as several subtypes: “d” “y” “w” and “r”.
Combinations of these sub-determinants ( e:g adr, adw, ayw, and ayr) are used to classify HBV genotypes A-H of which the main types are type A(35%) B(225) (31%) and D(10%). There is a strong correlation between genotypes and geographical areas. Genotype A is mainly seen in North west Europe, North America, North America and central Africa; B in south East Asia; C in south East Asia D; in southern Europe, India and the middle East; E in west Africa; F in south and central America, in American Indians and in Polynesia.
G in France and the USA; and H in central and south America. The core is formed of core protein (HBcAg) containing incompletely double stranded circular DNA and DNA polymerase/reverse transcriptase. One strand is almost a complete circle and contains overlapping genes that encode both structural proteins (pre-S, surface (s), core (s)) and replicative proteins (polymerase and x). The other strand is variable in length synthesis during the viral replication. If there is an acute clinical episode the virus is cleared in approximately 90% of patients as there is a good immune reaction.
There is serum sickness-like immunological syndrome see urticaria or maculopapular rash and polyathritis affecting small joints and occurring in up to 25% of case in the subclinical period. There is increase of temperature. Extrahepatic immune
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