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Lamivudine (3TC) is a nucleoside analogue which inhibits replication of HIV and HBV and which is used in the treatment of chronic hepatitis B-infected patients with safety and efficacy. The activity of lamivudine was evaluated by the measurement of DNA-HBV concentration in plasma using a very sensitive assay (1,000 copies/mL) (Amplicor VHB Monitor. Roche). Ten patients chronically infected with hepatitis B (group A) and 24 patients with HIV-1 co-infection (group B) were enrolled. In 9 patients of group A, HBVDNA load was undetectable a median of 3.5 months after the beginning of treatment and remained negative for 2 years with hepatitis Be antigen disappearing and normal alanine aminotransferase concentration. In the last immunodeficient patient, the virus which had been resistant to three interferon treatments, was also resistant to lamivudine. In five patients of group B, HBV DNA load remained undetectable after 18 months with HBe antigen disappearing and baseline concentration of alanine aminotransferase. In the remaining 19 patients after a transient decrease of HBV DNA concentration for one year, HBV DNA load increased again without disappearing of HBe antigen and without decrease of alanine aminotransferase concentration showing lamivudine resistant hepatitis B virus. Mutations in the YMDD motif of the DNA polymerase gene were identified in 11 patients (3 with M550V/I mutation; 7 with M550V/I and L256M mutations; 1 with M550V/I, L526M and V519L mutations). In 6 of these patients, was found a M184V mutation in the VIH polymerase. No correlation could be observed between the mutations detected in the two viruses. Using a sensitive HBV-DNA assay, efficacy of lamivudine for a long time in HBV infected patients was proved. However, the prevalence of lamivudine resistance is related to duration of treatment and it may be necessary to use a multitherapy.

Experimental infection of mice by Toxoplasma gondii is the best way for antigen production or direct diagnosis. Early serological response from sera and peritoneal exudate of mice infected by T. gondii has been studied. In this report the authors show that specific antibodies (IgM) are found in the serum at 24 hours after intraperitoneal inoculation. Serological methods were unable to detect free antibodies in the peritoneal exudate. Specific antibodies coating the parasite surface were detected by direct immunofluorescence as soon as 48 hours post infection. Biochemical treatment usually used for antigen production (trypsin, pepsin) were unable to destroy this antibodies which where no longer detected after 2 mercapto-ethanol treatment. Control experiments showed that, in these conditions, 2 mercapto-ethanol treatment had no effect on the reactivity of surface antigens with antibodies. Therefore, this results show that checking for specific antibodies absorbed at the surface of T. gondii is a prerequisite of the use of antigen produced in vivo.

Amphotericin B (Am. B), a polyene heptaene, is an antifungal antibiotic substance produced by Streptomyces nodosus, a telluric actinomycetal from Venezuela. Although it is a very toxic substance and its pharmacokinetic is not completely known, Am. B is yet the former antifungal substance utilised against number of pathogenic agents of systemic mycoses. Am. B binds irreversibly to sterols of fungal cytoplasmic membranes causing a leak of potassium and other impairments leading the fungal cell to death. Further, Am. B might to induce an enhancement of humoral and cellular immunity. After intravenous perfusion, 95 per cent of Am. B binds to plasma lipoproteins. Only a low proportion of the Am. B serum level is detected in the CSF. Distribution of Am. B to extravascular inflammatory fluids and secretions might be letter. Am. B might be eliminated essentially by biliary way. Am. B toxic effects are very frequent. Generalized reactions are observed to the earlier doses. Toxic visceral, above all, nephrotoxic manifestations, appearing later. Recent results, from experimental and human infections suggest that Am. B encapsulated in liposomal vesicles is more active, less toxic and more easily administered.