Viral safety evaluation of biopharmaceuticals and homoeopathic preparations of human or animal origin.

In order to meet the generally high quality requirements for the pharmaceutical manufacturing process, medicaments of animal or human origin specifically have to undergo a substantial viral safety test program. This procedure has been narrowly defined in numerous internationally valid guidelines; in addition, registration authorities are available in an advisory capacity. In order to bring about the experimental evidence, thorough planning, virological expertise and infrastructure, as well as close cooperation between process engineers and virologists, is necessary.

Virus inactivation of plasma-derived proteins by pasteurization in the presence of guanidine hydrochloride.

Background: Viruses, among them parvovirus B19 and other small, nonenveloped viruses, may be present in human blood and may contaminate plasma-derived therapeutics. Efficient inactivation or removal of such viruses, especially parvoviruses, represents a current problem and corresponding technologies are under investigation. In this report, such a technology is described.

Genotypic and phenotypic resistance to stavudine after long-term monotherapy. BMS-020 Spanish Study Group.

Protocol BMS 020 was a double-blind, prospective clinical trial in which two different doses of stavudine (20 and 40 mg twice daily) were compared in human immunodeficiency virus (HIV)-infected patients with previous exposure to zidovudine for longer than 16 weeks. Genotypic and phenotypic resistance to both zidovudine and stavudine were examined after at least 2 years of stavudine monotherapy. None of 35 tested individuals harboured the codon 50 and/or 75 mutations previously described to be associated with stavudine resistance.

Resistance mutations selected in vivo under therapy with anti-HIV drug HBY 097 differ from resistance pattern selected in vitro.

The quinoxaline derivative HBY 097, an orally active nonnucleoside inhibitor of HIV-1 reverse transcriptase (NNRTI), showed an efficient suppression of viral load in a dose-escalating phase I study with mean trough concentrations increasing from 137-1299 ug/l [Rübsamen-Waigmann et al., Lancet 349:1517]. Half-maximal inhibitory concentrations (IC50) for viruses grown from the patients at entry of the study were 0.