To address a

possible role of ATF6 signaling in LCMV infection, we used cells deficient in site 2 protease (S2P), a metalloprotease required for the activation of ATF6. Cells deficient in S2P showed significantly lower levels of production of infectious virus during acute but not persistent infection, indicating a requirement for ATF6-mediated signaling for optimal virus multiplication. In summary, acute LCMV infection seems to selectively induce the ATF6-regulated branch of the UPR that is likely beneficial for virus replication and cell viability, but it avoids induction of PERK and IRE1, whose activation may be detrimental for virus and the host cell.”
“Since the membrane attack complex (MAC), an end product of the activated complement cascade, has been shown to play a role in neurodegeneration, we investigated to which extent MAC contributes to structural reorganization, neuronal cell buy DAPT death, and seizure development in two rat models for temporal lobe epilepsy. We used the electrically-induced status epilepticus (SE) model and the kindling model in C6-deficient rats (that are unable to form MAC) and wild-type (WT) PVG/c rats. Structural reorganization was investigated using hilar cell counts and mossy fiber sprouting. Seizure development was monitored

using electroencephalographic (EEG) recordings. 4 weeks after electrically stimulated SE, hilar cell counts in C6-deficient and WT post-SE rats were significantly decreased compared to an

unstimulated control group, but not different between C6-deficient and WT post-SE. Since seizure selleck chemicals development was unexpectedly absent in most post-SE rats we assessed epileptogenesis using the kindling rate as main parameter. Kindling development was slightly delayed in C6-deficient rats compared to WT rats. SCH772984 price The lack of effect of C6 deficiency on hilar cell death and mossy fiber sprouting after electrically-induced SE or kindling argues against a role of the terminal complement complex in neuronal cell death induced by SE or seizures. A small but significant delay of kindling epileptogenesis suggests a subtle role of MAC in seizure spread. Whether complement components upstream of MAC play a crucial role in neuronal death and/or epileptogenesis needs to be further investigated. (C) 2011 IBRO. Published by Elsevier Ltd. All rights reserved.”
“Antibody-dependent enhancement (ADE) is implicated in severe, usually secondary, dengue virus (DV) infections. Preexisting heterotypic antibodies, via their Fc-gamma receptor (Fc gamma R) interactions, may increase disease severity through enhanced target cell infection. Greater numbers of infected target cells may contribute to higher viremia and excess cytokine levels often observed in severe disease. Monocytes, macrophages, and immature and mature dendritic cells (DC) are considered major cellular targets of DV.