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Nine HBeAg+ and 24 anti-HBe+ subjects with chronic hepatitis B virus (HBV) infection were studied for HBV DNA in the serum by molecular hybridization, for HBcAg in the liver by immunofluorescence, and for histologic evidence of liver disease. All HBeAg+ patients had underlying chronic liver disease (chronic persistent hepatitis, chronic active hepatitis, or cirrhosis with or without hepatocellular carcinoma), and all were found positive for both HBV DNA in the serum and HBcAg in the nucleus of hepatocytes. Of the 24 anti-HBe+ individuals, 18 had various forms of chronic liver disease. Six HBsAg+/anti-HBe+ patients had normal liver histology except for numerous "ground-glass" hepatocytes with abundant cytoplasmic HBsAg. All six were negative for nuclear HBcAg and serum HBV DNA, but three showed HBV DNA which appeared to be integrated into unique sites in host liver DNA by hybridization analysis. In contrast, 14/18 (78%) of HBsAg+/anti-HBe' patients with chronic liver disease were positive for nuclear HBcAg, serum HBV DNA, or both of these markers of HBV replication. It is suggested that in long-term HBsAg carriers with serum anti-HBe and normal liver histology, viral replication is suppressed or inactive and HBV potential infectivity is presumably very low or absent. However, when viral replication is present in HBsAg+/anti-HBe+ carriers (as demonstrated by serum HBV DNA and/or nuclear HBcAg) active liver disease is often found. In these individuals, active chronic liver disease appears to be related to continued replication and secretion of HBV and may occur in a much higher proportion of HBsAg+/anti-HBe+ carriers than was previously suspected.It is generally accepted that in chronic hepatitis B virus (HBV) infection, the presence of circulating antibodies to HBe antigen (anti-HBe) reflects a state of low or absent HBV replication and presumably of low HBV infectivity (1-3). However, a significant number of antiHBe+ patients with chronic HBV infection have been found recently to have demonstrable HBcAg in many hepatocytic nuclei (Hadziyannis, S. J. et al., Hepatology 1982; 2:179, Abstract). Similarly, HBV DNA sequences

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The prevalence of occupational low-back pain was investigated in 407 female nurses in a large tertiary health care unit in Athens, Greece. Work-related back pain within the previous 2 weeks was reported by 63% of respondents and within the previous 6 months by 67%. Prevalence was higher (66% in the previous 2 weeks) in the wards with physically heavy duties than in the rest (52%, P = 0.003), but all grades of nursing staff were affected equally. The specific factors which claimed to be responsible for causing back pain included moving heavy items (36%), lifting patients onto trolleys (32%) or in bed (29%), helping patients out of bed (24%) and bending to lift objects from the floor (24%). Absence from work because of back pain in the previous 2 weeks was reported by 28% of the sample.

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