The presence of pre-S1 proteins in serum and liver of individuals with acute and chronic hepatitis B virus infection was investigated in Western blots using antibodies against a fusion protein, containing amino acids 20-120 of the pre-S region. Pre-S1 proteins were present in 20 of 38 HBsAg-positive sera. All sera positive for pre-S1 proteins were also positive for hepatitis B virus DNA indicating the presence of hepatitis B virions, and 16 of these sera were also positive for HBeAg. In five sera positive for hepatitis B virus DNA, pre-S1 proteins were not found. In an additional study, pre-S1 proteins could be detected in 4 of 6 patients with acute hepatitis B virus infection during the first 2 weeks after admission to the hospital. The presence of pre-S1 proteins showed a good correlation with the detection of hepatitis B virus DNA. After seroconversion from HBeAg to anti-HBe, both hepatitis B virus DNA and pre-S1 proteins were no longer detectable. Pre-S1 proteins were present in three liver tissue specimens from two patients with acute hepatitis B virus infection and from one patient with cirrhosis of the liver. The proteins were not found in the liver of two HBsAg-positive patients with hepatocellular carcinoma (primary liver carcinoma), negative for HBeAg. Pre-S1 proteins can be detected in serum, positive for hepatitis B virus DNA and in liver tissue of hepatitis B virus-infected individuals. The presence of these proteins appears to correspond with the presence of hepatitis B virus DNA, both markers indicating hepatitis B virus replication.

DNA, Viral↗

PubMedDate not supplied

Signals regulating hepatitis B surface antigen transcription.

About 200 million people are chronic carriers of hepatitis B surface antigen (HBsAg), but since hepatitis B virus (HBV) cannot be propagated in vitro, HBsAg transcription has been studied only in cell lines containing HBV DNA integrated into chromosomes, and HBsAg-related mRNAs 2.0 to 2.5 kilobases (kb) long have been described. We have analysed the transcripts produced in an infected chimpanzee liver and in a rat cell line containing HBV DNA. In contrast to previous suppositions we report here that the major S gene transcript initiates close to the S gene, that is, within the 'pre-S' region and is processed/polyadenylated at a site situated within the core gene. The efficiency of processing/polyadenylation at this site varies between the chimpanzee liver and the rat cell line studied. The S gene promoter does not contain a TATA box but instead has a sequence homologous to that which positions the 5' ends of the major simian virus 40 (SV40) late transcript.

Animals↗

PubMedDate not supplied

Heat, cold and inflammation.

Although therapeutic heat and cold measures are widely used in rheumatic diseases, their application in joint inflammations is still broadly empirical. Animal experiments concerning the effects of systemic hyperthermia and of local heat and cold applications upon experimentally induced inflammations (dextran edema, formol edema, kaolin edema, carrageenan edema, adjuvant arthritis) show that some inflammations are significantly depressed, i.e. they are effected by a useful therapeutic influence, but that cold and heat can also act as enhancing inflammatory stimulus. Under certain conditions, whole-body hyperthermia has immuno-suppressive effects. Although the exact points of intervention of heat and cold investigations, acute exsudative inflammations seem to be better influenced by cold; on the contrary, chronic torpid and proliferous inflammations are better influenced by heat. Prostaglandin mediated inflammations can be aggravated by cold, because it stimulates the prostaglandin synthesis; acute exsudative inflammatory processes are most often aggravated by heat. These results show that both therapeutic agents should be applied within a well-defined range and with care.

Animals↗