Key result
The L and P proteins of the SSPE virus Kobe-1 strain suppressed viral RNA polymerase activity, restricting cell-surface F protein expression and attenuating neuropathogenicity to enable persistent infection.
Why the study?
The molecular mechanisms underlying the establishment and maintenance of persistent measles virus infection in the brain are unclear because isolating viruses before clinical signs appear is impractical.
Population
Suckling mice and cell lines infected with recombinant measles viruses
Comparison
Recombinant measles viruses harboring L and P… vs Recombinant measles viruses harboring wild-type…
Design
Preclinical
Follow-up
21 days (mice), 48-72 hours (cells)
Authors
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Hyperfusogenic MV mutations drive cell-to-cell spread in SSPE; leaves open whether fusion inhibitors could modify persistent brain infection.
Suppression of viral RNA polymerase activity by mutations in the L and P proteins is necessary for the establishment of persistent measles virus infection in the brain during transformation into SSPE virus.
Sakamoto et al. (2023) studied Subacute sclerosing panencephalitis (SSPE). Recombinant measles virus with SSPE virus Kobe-1 strain L and P genes vs. Wild-type measles virus (ICB strain) was evaluated on Viral RNA polymerase (RdRp) activity and neuropathogenicity. The L and P proteins of the SSPE virus Kobe-1 strain suppressed viral RNA polymerase activity, restricting cell-surface F protein expression and attenuating neuropathogenicity to enable persistent infection.
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