University of Cambridge, UK

A zoologist traces flu across the globe.

In winter, everybody recognizes a stuffy nose, a fever and an achy body as influenza. But experts still grapple with where the flu virus goes during the summer. One theory has it that flu lays low, holding out until the following season in a small number of asymptomatic people. Another idea — that flu strains tend to become extinct locally but shift around geographically — carries more weight. A recent paper by Derek Smith of the University of Cambridge, UK, and his colleagues helped nail the latter hypothesis by plotting the results of antigen-binding assays and genetic sequencing of more than ten thousand viruses on a map (C. A. Russell et al. Science 320, 340–346; 2008).

The researchers call this approach 'antigenic cartography'. Their antigenic time charts contain data crunched from the portion of the World Health Organization's enormous 'Global Influenza Surveillance Network' database that details strains classified as 'H3N2' between 2002 and 2007. First, they confirm flu's source–sink dynamics by showing that winter flu strains are more closely related to (and thus more likely to have evolved from) strains found elsewhere than to last season's local contagion. Second, the team pinned down H3N2's spread. Temperate regions are regularly seeded by strains from east and southeast Asia, where many strains circulate continuously and asynchronously in a pattern probably driven by varying climatic conditions.

These findings suggest that close surveillance of emerging strains in east and southeast Asia could enable us to predict those that will later affect the rest of the world. Yet it also poses a question: why do flu strains not return to this region after spending time (and thus evolving) elsewhere? Now that we know where new strains come from, we need to find out why they never go back.

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Harvard Medical School, Boston, Massachusetts

An immunologist muses about inflammation through cell interactions.

I spend my lab hours trying to understand what prompts T cells — a type of white blood cell — to specialize. Some T cells produce soluble molecules that rattle the immune system into an inflamed state; other cells generate molecules that calm the system back down.

Upon infection, cells such as macrophages — another type of white blood cell — produce soluble molecules called interleukins that direct the fate of the responding T cells. An emerging curiosity in the field is which interleukins make certain T cells become pro-inflammatory, and which cause other T cells to become anti-inflammatory. This decision is crucial for determining whether an immune response induces or suppresses inflammation.

Recently, investigators have turned their attention towards an interleukin known as IL-27. This is produced by activated macrophages and was initially thought to induce IFN, a signalling molecule that activates macrophages even more.

But work by Nico Giraldi and his colleagues at Genentech in South San Francisco, and other groups, has recast IL-27 as a molecule that primarily directs T cells to suppress inflammation. In a paper published in March, Giraldi's team confirmed that IL-27 acts in this way because it causes CD4+ and CD8+ T cells to make the anti-inflammatory IL-10, and does not work through an alternative pathway (M. Batten et al. J. Immunol. 180, 2752–2756; 2008). Mice with Listeria infections or autoimmune tissue inflammation in their brains and spinal cords generated fewer IL-10-producing T cells when they lacked an IL-27 receptor. Whether an analogous interaction occurs in humans is not known, but, if it does occur, this research could become medically useful.

Posted by Maxine Clarke at 09:19 AM | Permalink | Comments (0) | TrackBacks (0)