If the type and mode of action of mutations favored by natural selection in wild populations are similar to those that contribute to human diseases, then studies in evolutionary mutant models have the potential to identify novel genetic factors and gene-by environment interactions that affect human health and underlie human disease.”
“Post-traumatic stress disorder (PTSD) is a severely debilitating psychiatric condition. Although a lifetime trauma incidence of 40-90% has been reported in the general population, the overall lifetime prevalence for Fosbretabulin nmr PTSD ranges between 7-12%, suggesting individual-specific differences towards the susceptibility to PTSD. While studies investigating main genetic

effects associated with PTSD have yielded inconsistent findings, there is growing evidence supporting the role of gene environment (G x E) interactions in PTSD. The hypothalamus pituitary adrenal (HPA) axis is one of the main systems activated after exposure to a trauma and perturbations in this system are one of the more consistent neurobiological abnormalities observed in PTSD. Genes regulating the HPA-axis are therefore interesting candidates for G x E studies

in PTSD. This article will review the concept and initial results of G x E interactions with polymorphisms in these genes find more for PTSD. In addition, the use of alternate phenotypes and more complex interaction models such as G x G x E or G x E x E will be explored. Finally, putative molecular mechanisms for these interactions will be presented. The research presented in this article indicates that a combined analysis of environmental, genetic, endophenotype and epigenetic data will be necessary to better understand pathomechanisms in PTSD.

This article is part of a Special

Issue entitled ‘Post-Traumatic Stress Disorder’. (C) 2011 Elsevier Ltd. All rights reserved.”
“Retrovirus transmission via direct cell-cell contact is more efficient than diffusion through the extracellular milieu. This is believed to be due to the ability of viruses to efficiently coordinate several steps of the retroviral life cycle at cell-cell contact sites (D. C. Johnson et al., J. Virol. 76:1-8, 2002; D. M. Phillips, AIDS 8:719-731, 1994; Q. Sattenau, Nat. Rev. Microbiol. 6:815-826, 2008). Using the murine leukemia virus (MLV) as a model retrovirus, learn more we have previously shown that interaction between viral envelope (Env) and receptor directs viral assembly to cell-cell contact sites to promote efficient viral spreading (J. Jin et al., PLoS Biol. 7:e1000163, 2009). In addressing the underlying mechanism, we observed that Env cytoplasmic tail directs this contact-induced polarized assembly. We present here the viral determinants in the Env cytoplasmic tail and Gag that are important in this process. A tyrosine residue within the cytoplasmic tail of Env was identified, which directs polarized assembly.