We were able to initiate a persistent infection (PI) in HeLa cells with a temperature-sensitive ( ) mutant of rhinovirus type 2 (TS-1), but not with the corresponding wild-type () virus. The ability to initiate a PI may be related to the multiplicity of infection. Persistence was established at 37°C but not at 32°C and the virus isolated from the PI was no longer temperature-sensitive. Infectious virus was continually produced at low levels throughout the course of the PI and cell cultures underwent multiple episodes of partial destruction (crisis) and subsequent recovery. PI virus and the initiating virus were neutralized to the same extent by hyperimmune polyclonal TS-1 antiserum indicating that no significant change had occurred with respect to serological type. The presence of either interferon or virus-related interfering activity could not be demonstrated in the PI cultures. Superinfection experiments in cells that were ‘cured’ of PI virus indicated the selection of a cell population during persistence that could no longer support the growth of homologous-type virus. This effect became less pronounced upon further passage of the cured cells. When compared with the and viruses, the PI virus yielded comparable amounts of infectious virus in HeLa cells but with decreased synthesis of RNA.


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