The stabilities of hepatitis A virus (HAV) and of poliovirus type 2 were compared under strictly controlled, identical conditions of pH value, temperature, and salt concentration. Although the resistance of the viruses proved to be the same from pH 3 to 11, the temperature at which 50% of poliovirus particles became disintegrated during heating at pH 7.0 for 10 min (T50,10 = 43¤) differed significantly from that characteristic for HAV (T5010 = 61 °). In the presence of 1 MMgCl2, the T50,10 for poliovirus and for HAV shifted to 61 ° and 81°, respectively. Destabilization of the physical integrity of HAV by heating resulted in the release of viral RNA and, simultaneously, in the generation of several ‘empty’ capsid structures or dissociation products thereof. Empty capsids and further dissociation products were still serologically reactive with anti-HAV IgG contained in human convalescent sera. With further heating (> T50,10 = 67 ° or > T50,1 = 87°), however, they irreversibly lost this reactivity.
1. In a ten-year study 41 human permanent cell strains derived from 6 different cell lines and collected from 19 almost exclusively european laboratories were tested for contamination with parvoviruses. Two stable cell strains of porcine and rat origin, respectively, were likewise examined.2. Out of 43 cell strains tested 36 proved to be contaminated with parvoviruses belonging to 4 distinct serotypes I--IV.3. Human cell strains become accidentally contaminated in the laboratory, whereas the animal cell strain RT probably derives from the already infected rat host.4. Parvovirus type I, the most frequent contaminant of human cell strains, is supposed to be of porcine origin and is presumably transmitted to cell cultures by trypsin.
SUMMARYCanine parvovirus (CPV), feline panleukopenia virus (FPLV) and mink enteritis virus (MEV) were compared serologically, by determination of their host range in cell cultures, as well as by restriction enzyme analysis. Maps of the virus genomes were established using seven different restriction enzymes cutting at a total of 56 sites. MEV and FPLV gave maps which were identical except for one restriction site. The map of CPV is closely related to those of FPLV/MEV since their DNAs share about 80% of the restriction sites tested. However, CPV is clearly distinct from FPLV/MEV since either eight (German isolate) or nine (Belgian, Swiss and American isolates) restriction sites are different. The DNAs of six vaccine strains of FPLV and MEV were also analysed. They gave maps which closely resembled those of the respective wild-type strains. CPV and FPLV/MEV also differed with respect to antigenicity, as well as to host range in cell cultures.
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