Herpesvirus latency confers symbiotic protection from bacterial infection

All humans become infected with multiple herpesviruses during childhood. After clearance of acute infection, herpesviruses enter a dormant state known as latency. Latency persists for the life of the host and is presumed to be parasitic, as it leaves the individual at risk for subsequent viral reactivation and disease. Here we show that herpesvirus latency also confers a surprising benefit to the host. Mice latently infected with either murine gammaherpesvirus 68 or murine cytomegalovirus, which are genetically highly similar to the human pathogens Epstein-Barr virus and human cytomegalovirus, respectively, are resistant to infection with the bacterial pathogens Listeria monocytogenes and Yersinia pestis. Latency-induced protection is not antigen specific but involves prolonged production of the antiviral cytokine interferon-gamma and systemic activation of macrophages. Latency thereby upregulates the basal activation state of innate immunity against subsequent infections. We speculate that herpesvirus latency may also sculpt the immune response to self and environmental antigens through establishment of a polarized cytokine environment. Thus, whereas the immune evasion capabilities and lifelong persistence of herpesviruses are commonly viewed as solely pathogenic, our data suggest that latency is a symbiotic relationship with immune benefits for the host.     

Dynamics of Mid-Palaeocene North Atlantic rifting linked with European intra-plate deformations

The process of continental break-up provides a large-scale experiment that can be used to test causal relations between plate tectonics and the dynamics of the Earth's deep mantle. Detailed diagnostic information on the timing and dynamics of such events, which are not resolved by plate kinematic reconstructions, can be obtained from the response of the interior of adjacent continental plates to stress changes generated by plate boundary processes. Here we demonstrate a causal relationship between North Atlantic continental rifting at approximately 62 Myr ago and an abrupt change of the intra-plate deformation style in the adjacent European continent. The rifting involved a left-lateral displacement between the North American-Greenland plate and Eurasia, which initiated the observed pause in the relative convergence of Europe and Africa. The associated stress change in the European continent was significant and explains the sudden termination of a approximately 20-Myr-long contractional intra-plate deformation within Europe, during the late Cretaceous period to the earliest Palaeocene epoch, which was replaced by low-amplitude intra-plate stress-relaxation features. The pre-rupture tectonic stress was large enough to have been responsible for precipitating continental break-up, so there is no need to invoke a thermal mantle plume as a driving mechanism. The model explains the simultaneous timing of several diverse geological events, and shows how the intra-continental stratigraphic record can reveal the timing and dynamics of stress changes, which cannot be resolved by reconstructions based only on plate kinematics.     

Which Wisdom Can Change the World?

The thoughts that Michel Puech formulates on wisdom, technology and the art of living are timely at a moment when social, ecological and economic problems are pressing upon our societies and the speed of technological development seems to overwhelm our ability to integrate and adapt new technologies in our lives and societies. However, he restricts his concept of wisdom too much to a personal endeavor and overestimates the relevance of non-confrontation. I argue that his project can only be of value when it is embedded in a broader societal and political strategy for change.     

Introduction. Meaningfulness,Volunteers, Citizenship

This introductory article starts by describing the genesis of this special issue and the interconnection of its topics. The editors offer a variety of reading entries into the key-note articles and responses. The article reconstructs the research interests underpinning the idea of integrating meaningfulness, volunteers and citizenship. It highlights the explicit interdisciplinary design of the special issue, and shows how the key-note authors, and their respondents, weave connections between meaningfulness, volunteering and citizenship. And, finally, the editors bring the background understandings of the key-note papers to the foreground, and reconstruct a non-intentional meta-level discussion on two fundamental concepts and their interplay: self and world.     

Examining ecological consequences of feral horse grazing using exclosures

Although feral horses have inhabited western North America since the end of the 16th century, relatively little synecological research has been conducted to quantitatively characterize how they interact with ecosystem components. Because feral horses exhibit watering behavior markedly different from that of domestic cattle, it is particularly important to evaluate response of ecosystem elements near water sources to horse use. To assess this response, we performed live-trapping of small mammals and 2-tiered vegetative sampling in 2 mountain ranges in central Nevada in the interior Great Basin, USA. At low elevations, plots around horse-excluded springs exhibited notably greater plant species richness, percent cover, and abundance of grasses and shrubs, as well as more small mammal burrow entrances than plots at horse-grazed springs. At high elevations, meadows protected from grazing exhibited maximum vegetation heights 2.8 times greater than vegetation grazed by horses only and 4.5 times greater than vegetation grazed by horses and cattle. Species richness in quadrats was most different between the horse-and-cattle-grazed meadow and its ungrazed counterpart, suggesting the possibility of synergistic effects of horse and cattle grazing in the same location. This study, the first in the Great Basin to investigate quantitatively ecosystem consequences of feral horse use with exclosures, represents a preliminary step in identifying factors that determine the magnitude of horse grazing impacts.     

Inflammatory bowel disease: is it a primary immunodeficiency?

Inflammatory bowel diseases (IBD) such as ulcerative colitis and Crohn’s disease are chronic and relapsing conditions, characterized by abdominal pain, diarrhea, bleeding and malabsorption. IBD has been considered a hyperinflammatory state due to disturbed interactions between the immune system and the commensal bacterial flora of the gut. However, there is evidence that Crohn’s disease might be the consequence of a reduced release of pro-inflammatory cytokines and an impaired acute inflammatory response, thereby suggesting that IBD might be an immunodeficiency rather than an excessive inflammatory reaction. This theory has been supported by observations in patients with primary immunodeficiencies such as the Wiskott–Aldrich syndrome and IPEX (immunodysregulation, polyendocrinopathy, enteropathy, X-linked syndrome). In contrary, defects in the anti-inflammatory down-regulation of the immune response as they are seen in patients with Mendelian defects in the IL10 signaling pathway support the hyper-inflammatory theory. In this review, we describe and discuss primary immunodeficiencies associated with IBD and show that the bowel is a highly sensitive indicator of dysregulations, making IBD a model disease to study and identify key regulators required to balance the human mucosal immune system.     

Variation in interleukin 7 receptor alpha chain (IL7R) influences risk of multiple sclerosis

Multiple sclerosis is a chronic, often disabling, disease of the central nervous system affecting more than 1 in 1,000 people in most western countries. The inflammatory lesions typical of multiple sclerosis show autoimmune features and depend partly on genetic factors. Of these genetic factors, only the HLA gene complex has been repeatedly confirmed to be associated with multiple sclerosis, despite considerable efforts. Polymorphisms in a number of non-HLA genes have been reported to be associated with multiple sclerosis, but so far confirmation has been difficult. Here, we report compelling evidence that polymorphisms in IL7R, which encodes the interleukin 7 receptor alpha chain (IL7Ralpha), indeed contribute to the non-HLA genetic risk in multiple sclerosis, demonstrating a role for this pathway in the pathophysiology of this disease. In addition, we report altered expression of the genes encoding IL7Ralpha and its ligand, IL7, in the cerebrospinal fluid compartment of individuals with multiple sclerosis.