A new species of Schäffer, 1897 (Collembola, Entomobryidae) from Altamira Caves (Cantabria, Spain).

This paper describes from the Altamira Caves, municipal district of Santillana del Mar (Cantabria, Spain), and five other caves near the coast of Cantabria (northern Spain). Its taxonomic position is discussed and differences and similarities among morphologically and geographically close species are highlighted. The new species can be identified by its five eyes, the basal and small inner paired teeth on the claw, and the length of the uncrenulated part of the distal dens.

A chromosomal investigation of some European Leiodidae (Coleoptera), with particular focus on Spanish subterranean Leptodirini.

Karyotypes are shown for Leiodes calcarata (Erichson, 1845), Catops coracinus Kellner, 1846, Cantabrogeus luquei (Salgado, 1993), Espanoliella luquei Salgado & Fresneda, 2005, Fresnedaella lucius Salgado, Labrada & Luque, 2011, Notidocharis uhagoni (Sharp 1872), Quaestus (Quaesticulus) pasensis Salgado, Labrada & Luque, 2010, all of which are shown to have a diploid number of 20 autosomes plus Xy (♂) or XX (♀) sex chromosomes, as well as an as yet undescribed triploid species of the genus Cantabrogeus Salgado, 2000. These results are contrasted with published information, all on Leptodirini, which lists 10 species as having diploid numbers of 22 + Xy or XX. It is shown that the higher chromosome number (n = 11 + X or y) previously reported refers exclusively to the more derived Leptodirini ("infraflagellates") whereas the lower number (n = 10 + X or y) refers to the less derived surface-dwelling forms and the less derived Leptodirini ("supraflagellates").

A surface groove essential for viral Bcl-2 function during chronic infection in vivo.

Antiapoptotic Bcl-2 family proteins inhibit apoptosis in cultured cells by binding BH3 domains of proapoptotic Bcl-2 family members via a hydrophobic BH3 binding groove on the protein surface. We investigated the physiological importance of the BH3 binding groove of an antiapoptotic Bcl-2 protein in mammals in vivo by analyzing a viral Bcl-2 family protein. We show that the gamma-herpesvirus 68 (gammaHV68) Bcl-2 family protein (gammaHV68 v-Bcl-2), which is known to inhibit apoptosis in cultured cells, inhibits both apoptosis in primary lymphocytes and Bax toxicity in yeast.

Age-dependent resistance to lethal alphavirus encephalitis in mice: analysis of gene expression in the central nervous system and identification of a novel interferon-inducible protective gene, mouse ISG12.

Several different mammalian neurotropic viruses produce an age-dependent encephalitis characterized by more severe disease in younger hosts. To elucidate potential factors that contribute to age-dependent resistance to lethal viral encephalitis, we compared central nervous system (CNS) gene expression in neonatal and weanling mice that were either mock infected or infected intracerebrally with a recombinant strain, dsTE12Q, of the prototype alphavirus Sindbis virus. In 1-day-old mice, infection with dsTE12Q resulted in rapidly fatal disease associated with high CNS viral titers and extensive CNS apoptosis, whereas in 4-week-old mice, dsTE12Q infection resulted in asymptomatic infection with lower CNS virus titers and undetectable CNS apoptosis.

Avian reoviruses cause apoptosis in cultured cells: viral uncoating, but not viral gene expression, is required for apoptosis induction.

The cytopathic effect evidenced by cells infected with avian reovirus S1133 suggests that this virus may induce apoptosis in primary cultures of chicken embryo fibroblasts. In this report we present evidence that avian reovirus infection of cultured cells causes activation of the intracellular apoptotic program and that this activation takes place during an early stage of the viral life cycle. The ability of avian reoviruses to induce apoptosis is not restricted to a particular virus strain or to a specific cell type, since different avian reovirus isolates were able to induce apoptosis in several avian and mammalian cell lines.

Modification of late membrane permeability in avian reovirus-infected cells: viroporin activity of the S1-encoded nonstructural p10 protein.

Infection of chicken embryo fibroblasts by avian reovirus induces an increase in the permeability of the host plasma membrane at late, but not early, infection times. The absence of permeability changes at early infection times, as well as the dependence of late membrane modification on both viral protein synthesis and an active exocytic route, suggest that a virus-encoded membrane protein is required for avian reovirus to permeabilize cells. Further studies revealed that expression of nonstructural p10 protein in bacterial cells arrested cell growth and enhanced membrane permeability.