The presence of hepatitis B surface antigen means actively replicating virus, and in the context of the history of recent needle-stick injury, this likely represents a hepatitis B infection. During the acute episode of disease, when there is active viral replication, large amounts of HBsAg and hepatitis B virus DNA can be detected in the serum, as can fully developed virions and high levels of DNA polymerase and HBeAg. Upon resolution of acute hepatitis B, HBsAg and HBeAg disappear from serum with the development of antibodies (anti-HBs and anti-HBe) against them. The development of anti-HBs is associated with elimination of infection and protection against reinfection. Anti-HBc is detected early in the course of disease and persists in serum for years. It is an excellent epidemiologic marker of infection, but is not protective. In patients with chronic hepatitis B, evidence of viral persistence can be found in serum. HBsAg can be detected throughout the active disease process, and anti-HBs does not develop, which probably accounts for the chronicity of the disease. However, anti-HBc is detected. Ref: Ray C.G., Ryan K.J. (2010). Chapter 13. Hepatitis Viruses. In C.G. Ray, K.J. Ryan (Eds), Sherris Medical Microbiology, 5e.