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: 3.28). 08/1998; 246(2):362-9. DOI: 10.1006/viro.1998.9187
Source: PubMed

ABSTRACT 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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    ABSTRACT: Alterations in the transmembrane gradients of several physiological ions may influence programmed cell death. In particular, recent data suggest that increases in intracellular calcium may either promote or inhibit apoptosis, depending on the level, timing and location, whereas loss of intracellular potassium promotes apoptosis.
    Current Opinion in Cell Biology 09/2001; · 8.74 Impact Factor
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    ABSTRACT: Abstract : We studied the novel hypothesis that an upmodulation of channels for outward delayed rectifier K+ current (Iκ) plays a key role in ceramide-induced neuronal apoptosis. Exposure for 6-10 h to the membrane-permeable C2-ceramide (25 μM) or to sphingomyelinase (0.2 unit/ml), but not to the inactive ceramide analogue C2-dihydroceramide (25 μM), enhanced the whole-cell Iκ current without affecting the transient A-type K+ current and increased caspase activity, followed by neuronal apoptosis 24 h after exposure onset. Tetraethylammonium (TEA) or 4-chloro-N,N-diethyl-N-heptylbenzenebutanaminium tosylate (clofilium), at concentrations inhibiting Iκ, attenuated the C2-ceramide-induced caspase-3-like activation as well as neuronal apoptosis. Raising extracellular K+ to 25 mM similarly blocked the C2-ceramide-induced cell death ; the neuroprotection by 25 mM K+ or TEA was not eliminated by blocking voltage-gated Ca2+ channels. An inhibitor of tyrosine kinases, herbimycin A (10 nM) or lavendustin A (0.1-1 μM), suppressed Iκ enhancement and/or apoptosis induced by C2-ceramide. It is suggested that ceramide-induced Iκ current enhancement is mediated by tyrosine phosphorylation and plays a critical role in neuronal apoptosis.
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