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J. Virol., 07 1995, 4122-4126, Vol 69, No. 7
G Widmer
Some strains of the protozoan parasite genus Leishmania are persistently
infected with single-segmented double-stranded RNA viruses, which are
termed LRV. The function of these cytoplasmic viruses is unknown. In order
to address the question of whether LRV affects the parasite's phenotype,
pairs of isogenic LRV(+)-LRV- lines are required. Since the persistent
nature of these viruses precludes de novo infection of virus-negative
strains, LRV(+)-LRV- strains were transformed with a Leishmania expression
vector expressing the LRV capsid protein with the aim of determining if
LRV- promastigotes support capsid assembly and if LRV replication is
affected by excess capsid protein. I found that in LRV- promastigotes,
capsid protein was capable of self-assembly into virus-like capsids and
that capsid overexpression in a naturally infected LRV+ line resulted in a
progressive reduction in LRV copy number. Clonal lines derived from an LRV+
capsid overexpressor had no detectable levels of LRV. These results
demonstrate that LRV replication can be inhibited and that a significant
reduction of viral copy number has no effect on the parasite's viability in
liquid medium.
Copyright © 1995, American Society for Microbiology
Suppression of Leishmania RNA virus replication by capsid protein overexpression
Department of Comparative Medicine, Tufts University School of Veterinary Medicine, North Grafton, Massachusetts 01536, USA.
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