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Studies on a host range variant from different isolates of infectious pancreatic necrosis virus (IPNV)

1979; Wiley; Volume: 2; Issue: 5 Linguagem: Inglês

10.1111/j.1365-2761.1979.tb00389.x

1365-2761

B. L. Nicholson, G. W. THORNE, Caryle F. Janicki, Anne Hanson,

Blood groups and transfusion

Abstract. Eight isolates of infectious pancreatic necrosis virus (IPNV) propagated solely in RTG‐2 cells (RTG‐IPNV) were examined for ability to replicate in FHM cells. Seven isolates replicated in FHM cells; however, the plaque titres were 10‐ to greater than 100 000‐fold less than titres in RTG‐2 cells. The ability of IPNV to replicate in FHM cells was shown to result from the presence of a host range variant (FHM‐IPNV) that produced plaques in both cell types. Variant‐free preparations of two isolates differed in ability to generate FHM‐IPNV during a single replication cycle in RTG‐2 cells. One isolate did not generate the variant and failed to replicate in FHM cells even upon blind passage. IPNV propagated in AS cells (AS‐IPNV) was similar to RTG‐IPNV, producing equal numbers of plaques in RTG‐2 and AS cells but failing to form plaques in FHM cells. However, IPNV propagated in BF‐2 cells (BF‐IPNV) was similar to FHM‐IPNV in producing equal numbers of plaques in all three cell lines. RTG‐IPNV and FHM‐IPNV were identical in size, morphology and density in CsCl but differed in plaque size distribution and neutralization by specific antiserum. Restriction of the replication of RTG‐IPNV in FHM cells was partially explained by a reduction of 75% in adsorption to FHM cells. However, the synthesis of RTG‐IPNV antigens was reduced 90 to >99% in FHM cells.