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.

In order to understand the selective survival of temperature-sensitive (ts) mutants in persistent infection by HVJ (Sendai virus), an intracellular interaction between a ts 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 ts property at 39 degrees C, weak cytopathogenicity and faster electrophoretic mobility of P protein (P77K), but showed similar trypsin-activated growth to that of HVJo. When LLCMK2 cells were simultaneously infected with HVJo and HVJ cl.14 at 32 degrees C, synthesis of HVJo-derived P protein (P79K) 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 degrees C, HVJ cl.14 was rescued by coinfected HVJe at about 900- to 13 000-fold over single infection. This recovery was also shown by sequential synthesis of HVJ cl.14-derived P protein (P77K) following the earlier synthesis of HVJo-derived P polypeptide (P79K) in the mixed infection at 39 degrees 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 ts mutant and concomitant reduction of c.p.e. seemed to provide a general explanation for the preferable persistence of the ts mutant in the HVJ carrier cells.