“…Although the majority of these individuals in a recent series (Woolf, Boyes, Jones, Whittaker, Tapp, MacSween, Renton, Stratton, and Dymock, 1974) showed some evidence of liver damage, there are some carriers with entirely normal liver histology. In these, HBsAg can be shown to be present in many hepatocytes (Hadziyannis, Vissoulis, Moussouros, and Afroudakis, 1972), which has led to the suggestion that the virus may not be cytopathic and that the destruction of infected cells in patients with acute virus B hepatitis and in those with chronic forms of liver damage is due to the development of an immune response to the infectious 'Present address: Department of Medicine, Columbia University College of Physicians and Surgeons, 630 West 168th Street, New York, NY 10032, USA Received for publication 21 April 1975. agent. Dudley, Fox, and Sherlock (1972) suggested that the persistence of HBsAg-whether or not liver disease was present-is related to a defect in cellular immunity and they found an impairment in lymphocyte response to phytohaemagglutinin (PHA), a T-cell mitogen, in patients with chronic liver disease and persistent antigenaemia as compared with normal controls (Giustino, Dudley, and Sherlock, 1972).…”