Premature termination or rapid degradation of the M protein may underlie the defectiveness of these three strains of SSPE virus.
M protein defects may underlie SSPE strain attenuation; leaves open human pathogenesis and therapeutic implications.
The nucleotide sequence has been determined for the matrix (M) protein gene of three strains, Niigata-1, ZH and Biken, of cell-associated subacute sclerosing panencephalitis (SSPE) virus. The M proteins of the Niigata-1 and ZH strains were found to terminate prematurely as a result of nonsense mutations at nucleotide positions 68 and 96 respectively. On the other hand it was predicted that the Biken strain would express M protein with 22 amino acid differences and eight additional amino acids at its C terminus in comparison to the M protein of the Edmonston strain of measles virus. Radiolabelling of cells carrying the Biken strain showed the production of an M protein with considerably altered immunoreactivity and a marked reduction in intracellular stability. Either premature termination or rapid degradation of the M protein may underlie the defectiveness of these three strains of SSPE virus.
No takes yet. Share an insight, caveat, or question.
Enami et al. (1989) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: