Santa Fe Institute

About: Santa Fe Institute is a nonprofit organization based out in Santa Fe, New Mexico, United States. It is known for research contribution in the topics: Population & Context (language use). The organization has 558 authors who have published 4558 publications receiving 396015 citations. The organization is also known as: SFI.

Dominant influence of HLA-B in mediating the potential co-evolution of HIV and HLA.

Abstract: The extreme polymorphism in the human leukocyte antigen (HLA) class I region of the human genome is suggested to provide an advantage in pathogen defence mediated by CD8+ T cells. HLA class I molecules present pathogen-derived peptides on the surface of infected cells for recognition by CD8+ T cells. However, the relative contributions of HLA-A and -B alleles have not been evaluated. We performed a comprehensive analysis of the class I restricted CD8+ T-cell responses against human immunodeficiency virus (HIV-1), immune control of which is dependent upon virus-specific CD8+ T-cell activity. In 375 HIV-1-infected study subjects from southern Africa, a significantly greater number of CD8+ T-cell responses are HLA-B-restricted, compared to HLA-A (2.5-fold; P = 0.0033). Here we show that variation in viral set-point, in absolute CD4 count and, by inference, in rate of disease progression in the cohort, is strongly associated with particular HLA-B but not HLA-A allele expression (P < 0.0001 and P = 0.91, respectively). Moreover, substantially greater selection pressure is imposed on HIV-1 by HLA-B alleles than by HLA-A (4.4-fold, P = 0.0003). These data indicate that the principal focus of HIV-specific activity is at the HLA-B locus. Furthermore, HLA-B gene frequencies in the population are those likely to be most influenced by HIV disease, consistent with the observation that B alleles evolve more rapidly than A alleles. The dominant involvement of HLA-B in influencing HIV disease outcome is of specific relevance to the direction of HIV research and to vaccine design.

Complexity and the Economy

Abstract: After two centuries of studying equilibria—static patterns that call for no further behavioral adjustments—economists are beginning to study the general emergence of structures and the unfolding of patterns in the economy. When viewed in out-of-equilibrium formation, economic patterns sometimes simplify into the simple static equilibria of standard economics. More often they are ever changing, showing perpetually novel behavior and emergent phenomena. Complexity portrays the economy not as deterministic, predictable, and mechanistic, but as process dependent, organic, and always evolving.

Effects of Body Size and Temperature on Population Growth

Abstract: For at least 200 years, since the time of Malthus, pop- ulation growth has been recognized as providing a critical link be- tween the performance of individual organisms and the ecology and evolution of species. We present a theory that shows how the intrinsic rate of exponential population growth, , and the carrying capacity, rmax K, depend on individual metabolic rate and resource supply rate. To do this, we construct equations for the metabolic rates of entire populations by summing over individuals, and then we combine these population-level equations with Malthusian growth. Thus, the theory makes explicit the relationship between rates of resource sup- ply in the environment and rates of production of new biomass and individuals. These individual-level and population-level processes are inextricably linked because metabolism sets both the demand for environmental resources and the resource allocation to survival, growth, and reproduction. We use the theory to make explicit how and why exhibits its characteristic dependence on body size and rmax temperature. Data for aerobic eukaryotes, including algae, protists, insects, zooplankton, fishes, and mammals, support these predicted scalings for . The metabolic flux of energy and materials also rmax dictates that the carrying capacity or equilibrium density of popu- lations should decrease with increasing body size and increasing tem- perature. Finally, we argue that body mass and body temperature, through their effects on metabolic rate, can explain most of the variation in fecundity and mortality rates. Data for marine fishes in the field support these predictions for instantaneous rates of mor- tality. This theory links the rates of metabolism and resource use of individuals to life-history attributes and population dynamics for a broad assortment of organisms, from unicellular organisms to mammals.

Email networks and the spread of computer viruses.

Abstract: Many computer viruses spread via electronic mail, making use of computer users' email address books as a source for email addresses of new victims. These address books form a directed social network of connections between individuals over which the virus spreads. Here we investigate empirically the structure of this network using data drawn from a large computer installation, and discuss the implications of this structure for the understanding and prevention of computer virus epidemics.

Parasites in food webs: the ultimate missing links

Abstract: Parasitism is the most common consumer strategy among organisms, yet only recently has there been a call for the inclusion of infectious disease agents in food webs. The value of this effort hinges on whether parasites affect food-web properties. Increasing evidence suggests that parasites have the potential to uniquely alter food-web topology in terms of chain length, connectance and robustness. In addition, parasites might affect food-web stability, interaction strength and energy flow. Food-web structure also affects infectious disease dynamics because parasites depend on the ecological networks in which they live. Empirically, incorporating parasites into food webs is straightforward. We may start with existing food webs and add parasites as nodes, or we may try to build food webs around systems for which we already have a good understanding of infectious processes. In the future, perhaps researchers will add parasites while they construct food webs. Less clear is how food-web theory can accommodate parasites. This is a deep and central problem in theoretical biology and applied mathematics. For instance, is representing parasites with complex life cycles as a single node equivalent to representing other species with ontogenetic niche shifts as a single node? Can parasitism fit into fundamental frameworks such as the niche model? Can we integrate infectious disease models into the emerging field of dynamic food-web modelling? Future progress will benefit from interdisciplinary collaborations between ecologists and infectious disease biologists.