Journal
JOURNAL OF VIROLOGY
Volume 83, Issue 3, Pages 1173-1183Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.02102-08
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Funding
- National Institutes of Health [R01 33506]
- NCRR [P40 RR0118604]
- National Science Foundation [IBN-9876754]
- American Cancer Society Eastern Division-Mercer Board [PF-08-26401-MBC]
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The attenuated pseudorabies virus (PRV) strain Bartha contains several characterized mutations that affect its virulence and ability to spread through neural circuits. This strain contains a small genomic deletion that abrogates anterograde spread and is widely used as a retrograde-restricted neural circuit tracer. Previous studies showed that the retrograde-directed spread of PRV Bartha is slower than that of wild-type PRV. We used compartmented neuronal cultures to characterize the retrograde defect and identify the genetic basis of the phenotype. PRV Bartha is not impaired in retrograde axonal transport, but transneuronal spread among neurons is diminished. Repair of the U(L)21 locus with wild- type sequence restored efficient transneuronal spread both in vitro and in vivo. It is likely that mutations in the Bartha U(L)21 gene confer defects that affect infectious particle production, causing a delay in spread to presynaptic neurons and amplification of infection. These events manifest as slower kinetics of retrograde viral spread in a neural circuit.
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