Homologous interference inAedes aegypti cell cultures infected with sindbis virus

Temperature Sensitivity of a Sindbis Virus Mutant Isolated from Persistently Infected <i>Aedes aegypti</i> Cell Culture

“…The SV-W and SV-S plaques were readily distinguished by their different sizes [1], SV-S directed RNA synthesis. The ability of SV-S to interfere at 39.5 raised the question of whether interference was correlated with viral RNA synthesis at the nonpermissive temperature, /.<?., whether SV-S was RNA'.…”

“…Stocks of wild-type Sindbis virus (SV-W) and the mutant virus (SV-S) were prepared as previously outlined [1,5]. In most experiments, unless otherwise indicated, cells were infected at input multiplicities of approximately 10 PFU/cell.…”

Adaptation of an Aedes aegypti Mosquito Cell Line to Growth at 15 C and its Response to Infection by Sindbis Virus

“…The mechanism responsible for homologous interference is unknown. However, at least in one case, in SV infected A. aegypti cultures at 28 °C, interference was found to be associated with the appearance in the culture of a small plaque forming mutant SV-S (Peleg & Stollar, 1974). The fact that A. aegypti (c) cultures, even 130 days after inoculation with SV, did not yield such a mutant suggested that this might be the reason for the absence of homologous interference.…”

“…We hoped to obtain information about this by testing A. aegypti (c) cultures with interfering agents which are known to produce a similar effect in A. aegypti cultures at 28 °C. An agent having such a property is SV-S, which was isolated from persistently infected A. aegypti cultures at 28 °C (Peleg & Stollar, 1974).…”

“…These, or about Io-fold lower titres, continued to be produced over a I3O day test period without causing visible cell damage. Continuous virus proliferation and the yield of uniformly large plaque forming progeny viruses are the two most important features which differentiate infection with this virus in A. aegypti (c) cells from that of A. aegypti cells grown at 28 °C (Peleg & Stollar, 1974). Absence of homologous interference vis-h-vis cell-virus coexistence suggests that homologous interference is not a prerequisite for maintaining cell-virus coexistence.…”