Infectious Bursal Disease Virus Changes the Potassium Current Properties of Chicken Embryo Fibroblasts

Rudolf-Buchheim-Institute of Pharmacology, Justus-Liebig-University, Giessen, Germany.
Virology (Impact Factor: 3.32). 08/1998; 246(2):362-9. DOI: 10.1006/viro.1998.9187
Source: PubMed


Infectious bursal disease virus (IBDV) is the causative agent of an economically significant poultry disease. IBDV infection leads to apoptosis in chicken embryos and cell cultures. Since changes in cellular ion fluxes during apoptosis have been reported, we investigated the membrane ion currents of chicken embryo fibroblasts (CEFs) inoculated with the Cu-1 strain of IBDV using the patch-clamp recording technique. Incubation of CEFs with IBDV led to marked changes in their K+ outward current properties, with respect to both the kinetics of activation and inactivation and the Ca2+ dependence of the activation. The changes occurred in a time-dependent manner and were complete after 8 h. UV-treated noninfectious virions induced the same K+ current changes as live IBDV. When CEFs were inoculated with IBDV after pretreatment with a neutralizing antibody, about 30% of the cells showed a normal K+ current, whereas the rest exhibited K+ current properties identical to or closely resembling those of IBDV-infected cells. Incubation of CEFs with culture supernatant from IBDV-infected cells from which the virus particles were removed had no influence on the K+ current. Our data strongly suggest that the K+ current changes induced by IBDV are not due to virus replication, but are the result of attachment and/or membrane penetration. Possibly, the altered K+ current may delay the apoptotic process in CEFs after IBDV infection.

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Available from: Henning J Draheim
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    • "Results of other investigations may indicate that the IBDV attachment molecule is composed of an N-glycosylated protein (Ogawa et al., 1998). As known for several other viruses, IBDV infection also changes the potassium current properties of chicken embryo fibroblasts (Repp et al., 1998). These might cause alterations of membrane permeability, thus affecting intracellular ion homeostasis and contributing to cytolysis and the death of the infected cells. "
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    • "Infectious bursal disease virus (IBDV), a member of the family Birnaviridae, induced apoptosis in chicken peripheral lymphocytes and embryo fibroblasts. IBDV incubation of several hours eliminated the inactivation of an outward delayed rectifier K + current and accelerated the opening phase of the current (Repp et al., 1998). The changes lasted for many hours, allowing a significant K + efflux. "
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    • "The lurcher gene-induced apoptosis in cerebellar Purkinje cells follows expression of Kv3.3 channels , implying a role for these K ϩ channels (Norman et al., 1995). Infection of chicken embryo fibroblasts with infectious bursal disease virus blocks inactivation of outward K ϩ currents, i.e., more K ϩ efflux, and is followed several hours later by apoptotic death (Repp et al., 1998). On the other hand, the apoptotic proteins Reaper and Grim induce inactivation of K ϩ currents; the authors suggested that Reaper and Grim may initiate apoptosis by blocking K ϩ channels (Avdonin et al., 1998). "
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