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. 2002 Nov 12;3(3):245–261. doi: 10.1016/0168-1702(85)90049-8

In vivo and in vitro models of demyelinating diseases

XII. Persistence and expression of corona JHM vims functions in RN2-2 Schwannoma cells during latency

Marion Coulter-Mackie 1,∗, Richard Adler 1,∗∗, Greame Wilson 1, Samuel Dales 1,∗
PMCID: PMC7134134  PMID: 3000100

Abstract

The coronavirus JHMV persistently infects rat Schwannoma cells RN2-2 at 32.5°C and enters a host-imposed reversible, latent state at 39.5°C. JHMV can remain up to 20 days in the latent state and about 14 days before the cultures lose the capacity to resume virus production upon return to 32.5°C.

Although persistently and latently infected RN2-2 cells display resistance to superinfection by a heterologous agent VSV, these cells do not release detectable soluble mediators (e.g., interferon) of the antiviral state. Nevertheless, RN2-2 cells are competent to synthesize and release interferon when treated with the appropriate inducers. These observations suggest that interferon does not play any role or may not be the major factor in the control of latency in the Schwannoma cell.

Hybridization with virus-specific cDNAs shows that all viral mRNAs are present during latency and that viral mRNAs are present in the polysomes of infected cells at 39.5°C. Western immunoblotting with hybridoma antibodies demonstrates that viral specific proteins are produced at the restrictive temperature. These results

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