Positive selection on mammalian immune genes-effects of gene function and selective constraint.

Genome-wide analyses of various taxa have repeatedly shown that immune genes are important targets of positive selection. However, little is known about what factors determine which immune genes are under positive selection. To address this question, we here focus on the mammalian immune system and investigate the importance of gene function and other factors like gene expression, protein-protein interactions, and overall selective constraint as determinants of positive selection.

To what extent does surrounding landscape explain stand-level occurrence of conservation-relevant species in fragmented boreal and hemi-boreal forest? - a systematic review.

Background: Forestry and land-use change are leading causes of habitat loss, degradation, and fragmentation worldwide. The boreal forest biome is no exception, and only a small proportion of this forest type remains intact. Since forestry will remain a major land-use in this region, measures must be taken to ensure forest dependent biodiversity.

Cytosolic serpins act in a cytoprotective feedback loop that limits ESX-1-dependent death of -infected macrophages.

Unlabelled: Serine protease inhibitors (serpins) constitute the largest family of protease inhibitors expressed in humans, but their role in infection remains largely unexplored. In infected macrophages, the mycobacterial ESX-1 type VII secretion system permeabilizes internal host membranes and causes leakage into the cytosol of host DNA, which induces type I interferon (IFN) production via the cyclic GMP-AMP synthase (cGAS) and stimulator of IFN genes (STING) surveillance pathway, and promotes infection . Using the infection model, we show that ESX-1-mediated type I IFN signaling in macrophages selectively induces the expression of and , two cytosolic serpins of the clade A3.

The germ theory revisited: A noncentric view on infection outcome.

The germ theory states that pathogenic microorganisms are responsible for causing infectious diseases. The theory is inherently microbe-centric and does not account for variability in disease severity among individuals and asymptomatic carriership-two phenomena indicating an important role for host variability in infection outcome. The basic tenet of the germ theory was recently challenged, and a radically host-centric paradigm referred to as the "full-blown host theory" was proposed.