INTERFERON INDUCTION BY VIRUSES .23. INTERFERON INDUCTION AS A QUASI-SPECIES MARKER OF VESICULAR STOMATITIS-VIRUS POPULATIONS

Citation
Pi. Marcus et al., INTERFERON INDUCTION BY VIRUSES .23. INTERFERON INDUCTION AS A QUASI-SPECIES MARKER OF VESICULAR STOMATITIS-VIRUS POPULATIONS, Journal of virology, 72(1), 1998, pp. 542-549
Citations number
50
Categorie Soggetti
Virology
Journal title
ISSN journal
0022538X
Volume
72
Issue
1
Year of publication
1998
Pages
542 - 549
Database
ISI
SICI code
0022-538X(1998)72:1<542:IIBV.I>2.0.ZU;2-J
Abstract
The interferon (IFN)-inducing capacity of different isolates of vesicu lar stomatitis virus (VSV) of the Indiana (IN) and New Jersey (NJ) ser otypes were measured to assess the extent of variability of this pheno type. Over 200 preparations of wild-type field isolates, laboratory st rains, and plaque-derived subpopulations were examined. Marked heterog eneity was found in the ability of these viruses to induce IFN, coveri ng a 10,000-fold range. A good fit to a normal distribution for the lo g of the IFN yields suggests a continuum of incremental changes in the viral genome may govern the IFN-inducing capacity of consensus popula tions derived from independently arising infections. A broad range in the magnitude of these changes, skewed towards inducers of high IFN yi elds, is consistent with a comparable series of ribonucleotide changes in the VSV genome, a sine qua non of a quasispecies population. Plaqu e- or vesicle-derived populations displayed standard deviations less t han the mean IFN yields, though skewed to higher yielders, whereas pop ulations from field and laboratory samples which differed widely in ti me and origin of isolation gave standard deviations greater than the m eans. The plaque isolation of IFN-inducing particles of VSV-IN, normal ly masked in populations by the predominance of non-IFN-inducing parti cles that suppress IFN induction, and the isolation of potent wild-typ e IFN-inducing VSV-IN from cows during an outbreak of vesicular stomat itis in a region that had yielded only virus expressing the non-IFN-in ducing phenotype in prior and subsequent years, supports the view that genetic bottlenecks are operative in the natural transmission of this disease.