33 The most common transmission pathways for these infections were multi-use drug vials (30.3%) and non-disposable capillary blood sampling devices (27.3%). An analysis of five HBV outbreaks in the USA during 1994 found that patients were infected through failures of isolation, serological screening and vaccination, and through sharing of staff, equipment and supplies between patients.34 Commonly used serological tests for HBV include those for HBsAg, antibody to HBsAg (anti-HBs), antibody
to hepatitis B core antigen (anti-HBc) and viral DNA (HBV DNA) by polymerase chain reaction (Table 1). In primary infection, there is an incubation period of 4–10 weeks Fer-1 duration, following which HBsAg appears in blood. Anti-HBc antibodies appear soon afterwards. In the acute phase, anti-HBc antibodies are principally of the immunoglobulin M class.35 HBV DNA levels are high from very early in acute infection. Usually the e antigen is detectable in the bloodstream a short time after anti-HBc becomes apparent.36 HBV DNA and hepatitis B e antigen (HBeAg) usually disappear before the clearance of HBsAg, which happens after 1–2 months. Anti-HBs antibodies are present from several weeks after the disappearance of HBsAg, and anti-HBc antibodies persist indefinitely, switching to IgG Idasanutlin after 6–24 months. The detection of anti-HBc and anti-HBs signifies previous infection.37 Anti-HBs antibodies at
a titre of >10 IU/L indicate immunity. In a proportion of patients infected by HBV, chronic infection
supervenes. Persistence is seen in 90% of perinatally infected infants, 20–30% of children infected between 1 and 5 years of age, 6% of those infected between STK38 5 and 15 years old, and only 1–5% of adults.4 An ‘immune-tolerant’ phase of chronic infection is typically seen in those infected as infants or children. There may be a brief ‘immune-tolerant’ phase in infected adults, but this is uncommon. During this period, HBsAg, HBeAg and HBV DNA are detectable, and the patient is usually asymptomatic, with normal transaminases and liver histology.38 Following this period, or immediately in adult infection, is an ‘immune-clearance’ phase. This is characterized by intermittent surges in serum transaminase levels, and may occasionally be accompanied by hepatic decompensation. Cirrhosis can develop as a consequence, but usually this phase culminates in the clearance of HBeAg and seroconversion to anti-HBe. HBV DNA falls to low levels (<2000 IU/L) and may disappear altogether, while HBsAg persists.39 There is a third ‘inactive residual’ phase during which HBV DNA levels remain low and a low rate of HBsAg seroclearance is seen (between 1–2% annually).40,41 Where HBsAg seroclearance occurs, and provided cirrhosis has not supervened, the prognosis is usually excellent. Occasionally, an ‘occult infection’ state remains in which HBsAg is undetectable, and anti-HBc is usually measurable, but a small quantity of HBV DNA persists.