Natural immune systems protect animals from dangerous foreign pathogens, including bacteria, viruses, parasites, and toxins. Their role in the body is analogous to that of computer security systems in computing. Although there are many differences between living organisms and computer systems, this article argues that the similarities are compelling and could point the way to improved computer security. Improvements can be achieved by designing computer immune systems that have some of the important properties illustrated by natural immune systems. These include multi-layered protection, highly distributed detection and memory systems, diversity of detection ability across individuals, inexact matching strategies, and sensitivity to most new foreign patterns. We first give an overview of how the immune system relates to computer security. We then illustrate these ideas with two examples.

Abstract. The use of different mathematical tools to study biological processes is necessary to capture effects occurring at different scales. Here we study as an example the immune response to infection with the bacteria Mycobacterium tuberculosis, the causative agent of tuberculosis (TB). Immune responses are both global (lymph nodes, blood, and spleen) as well as local (site of infection) in nature. Interestingly, the immune response in TB at the site of infection results in the formation of spherical structures comprised of cells, bacteria, and effector molecules known as granulomas. In this work, we use four different mathematical tools to explore both the global immune response as well as the more local one (granuloma formation) and compare and contrast results obtained using these methods. Applying a range of approaches from continuous deterministic models to discrete stochastic ones allows us to make predictions and suggest hypotheses about the underlying biology that might otherwise go unnoticed. The tools developed and applied here are also applicable in other settings such as tumor modeling.

Abstract — Visceral leishmaniasis is a parasitic disease that is usually fatal if untreated. Host resistance is thought to involve the accumulation of inflammatory cells into structures called granulomas. To date, the possible processes underlying granuloma formation are not fully understood. The importance of modelling in immunology is increasing particularly for dynamic processes that are hard to study in vivo over extended periods of time. Appropriate modelling can provide novel insights that might help deepen the understanding of phenomena and/or help guide experimental work. This paper discusses initial studies on the regulation of granuloma using a combination of UML like modelling and agent based simulation. I.

Abstract. Predicting the virulence of new Influenza strains is an important problem. The solution to this problem will likely require a combination of in vitro and in silico tools that are used iteratively. We describe the agent-based modeling component of this program and report preliminary results from both the in vitro and in silico experiments. 1

Research article Immune control of HIV-1 infection after therapy interruption: immediate versus deferred antiretroviral therapy

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WA 98195-3100. She holds an MPH in epidemiology, and will complete her PhD in biocultural anthropology in spring of 2010.

Strain specific transcriptional response in Mycobacterium tuberculosis infected macrophages

Modeling of leishmaniasis infection dynamics: novel application to the design of effective therapies

Many studies have been devoted to understand the mechanisms used by pathogenic bacteria to exploit human hosts. These mechanisms are very diverse in the detail, but share commonalities whose quantification should enlighten the evolution of virulence from both a molecular and an ecological perspective. We mined the literature for experimental data on infectious dose of bacterial pathogens in humans (ID50) and also for traits with which ID50 might be associated. These compilations were checked and complemented with genome analyses. We observed that ID50 varies in a continuous way by over 10 orders of magnitude. Low ID50 values are very strongly associated with the capacity of the bacteria to kill professional phagocytes or to survive in the intracellular milieu of these cells. Inversely, high ID50 values are associated with motile and fast-growing bacteria that use quorum-sensing based regulation of virulence factors expression. Infectious dose is not associated with genome size and shows insignificant phylogenetic inertia, in line with frequent virulence shifts associated with the horizontal gene transfer of a small number of virulence factors. Contrary to previous proposals, infectious dose shows little dependence on contact-dependent secretion systems and on the natural route of exposure. When all variables are combined, immune subversion and quorum-sensing are sufficient to explain two thirds of the variance in infectious dose. Our results show the key role of immune subversion in effective human infection by small bacterial populations. They also suggest that cooperative processes might be important for successful infection by bacteria