Astrocytic growth through the autocrine/paracrine production of IL-1β in the early infectious phase of fowl glioma-inducing virus.

Abstract

Fowl glioma is characterized morphologically by multiple nodular astrocytic growth with disseminated non-suppurative encephalitis. The disease is caused by fowl glioma-inducing virus (FGV) and its variants, belonging to subgroup A of avian leukosis virus (ALV-A). Fifty-seven FGV variants have so far been isolated from Japanese fowls and these variants have a variable degree of glioma inducibility. However, how these ALVs induce glioma with different degrees and frequencies has not been fully elucidated. In this study, we investigated the relationship between intracerebral viral replication and astrocytic growth in the early infectious phase. Replication abilities of two ALV strains, Sp-53 (a FGV variant) and ALV-based replication-competent vector RCAS(A) without glioma inducibility, were compared in the brains of C/O specific pathogen free chickens at 35 days of age. Sp-53 replicated faster than RCAS(A), and the histological score and the level of interleukin (IL)-1β in brains increased depending on the level of intracerebral viral RNA. Up-regulation of IL-1β was also demonstrated in primary cultured astrocytes. These results suggest that the astrocytic growth in this phase is enhanced through the autocrine/paracrine production of IL-1β in the FGV-infected astrocytes.