1887

Journal of General Virology header logo - Volume 55, Issue 2, 1981

Volume 55, Issue 2

Volume 55, Issue 2, 1981

  • Animal

      • An Intracellular Interaction Between a Temperature-sensitive Mutant and the Original Wild-type HVJ (Sendai Virus) is Responsible for the Establishment and Maintenance of HVJ Persistent Infection

        https://doi.org/10.1099/0022-1317-55-2-459
        SUMMARY

        In order to understand the selective survival of temperature-sensitive () mutants in persistent infection by HVJ (Sendai virus), an intracellular interaction between a clone (HVJ cl.14) isolated from HVJ carrier G2 cells and the original wild-type virus (HVJo) was studied. HVJ cl. 14 differed from HVJo mainly in its property at 39 °C, weak cytopathogenicity and faster electrophoretic mobility of P protein (P), but showed similar trypsin-activated growth to that of HVJo.

        When LLCMK2 cells were simultaneously infected with HVJo and HVJ cl.14 at 32 °C, synthesis of HVJo-derived P protein (P) was inhibited with concomitant reduction of cytopathic effect (c.p.e.) and more dominant growth of HVJ cl.14 was observed. For the analysis of progeny viruses in these mixed infections, another mutant of HVJo designated HVJe which formed plaques activated only by elastase was isolated and employed instead of HVJo. At 39 °C, HVJ cl.14 was rescued by coinfected HVJe at about 900- to 13000-fold over single infection. This recovery was also shown by sequential synthesis of HVJ cl.14-derived P protein (P) following the earlier synthesis of HVJo-derived P polypeptide (P) in the mixed infection at 39 °C. However, the u.v. inactivation of HVJe or HVJ cl.14 resulted in a loss of their activity on rescue or on c.p.e. reduction, suggesting the necessity of protein synthesis by opposite viruses for these interactions. The mechanisms involved in the predominant growth of the mutant and concomitant reduction of c.p.e. seemed to provide a general explanation for the preferable persistence of the mutant in the HVJ carrier cells.

    • Temperature-sensitive HVJ (Sendai Virus) with Altered P Polypeptide Derived from Persistently Infected Cell Lines

      https://doi.org/10.1099/0022-1317-55-2-469
      SUMMARY

      HVJ isolated from culture fluids of G2, THEL and GM2 cells persistently infected with HVJ (G2-HVJ, THEL-HVJ and GM2-HVJ) were characterized in comparison with wild-type HVJ (HVJo). Viral structural proteins were analysed by 10% SDS-polyacrylamide gel electrophoresis and it was found that only the P polypeptides of all the HVJ clones isolated from G2-HVJ cells had a smaller size mol. wt. of 77000 (77K), than that of HVJo with a mol. wt. of 79000 (79K). One of six clones from THEL-HVJ cells and one of ten clones from GM2-HVJ cells exhibited the same migration pattern of P polypeptide as that of the clones from G2-HVJ cells. However, the other structural proteins were not different from those of the wild-type virions. All the clones from these carrier cultures were temperature-sensitive and were blocked in early step(s) required for RNA synthesis. These results indicate that some mutations(s) associated with P polypeptide could occur during the course of HVJ persistent infection in cell cultures.

    • Correlation of Properties and Tumourigenicity of Hamster Kidney Cells Transformed by BK Virus

      https://doi.org/10.1099/0022-1317-55-2-481
      SUMMARY

      Hamster kidney cells transformed by BK virus (HKBK cells) were studied at low passage (about 30 subcultures) after transformation and at high passage (about 130 subcultures) after transforming. Several properties (rescue of virus, presence of T antigen, colony formation on plastic, in soft agar, on monolayers of normal cells, and serum dependency of growth) and tumourigenicity of these cells for newborn and adult hamsters were compared. HKBK cells at low passage showed high levels of T antigen, the growth properties of normal cells and low tumour-producing ability, while HKBK cells at high passage showed low levels of T antigen, the growth properties of transformed cells and high tumour-producing ability.

      These results may indicate that cellular transformation by BK virus is initiated, but not maintained, by the expression of genes regulating T antigen, and that the maintenance of the transformed state is due to complicated cellular and viral gene interactions occurring during the course of cell life.

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