11 February 2007

Nature Cell Biology doi:10.1038/ncb1542

Human adult stem cells isolated from adult blood vessels are able to regenerate muscle in a mouse model of muscular dystrophy disease, according to a study published online this week in Nature Cell Biology.

The lure of a cure for muscle-wasting diseases has lead researchers to explore the regeneration potential of stem cells isolated from the walls of blood vessels. In a recent Nature paper, Giulio Cossu and colleagues showed that such cells isolated from young golden retrievers regenerated the muscles of dystrophic dogs when injected into their circulation. A new study by the same team demonstrates that cells with similar properties can be isolated from human juvenile and adult blood vessels.

The same researchers isolated this type of stem cells from juvenile dystrophic patients and grew them in cell culture. Muscular dystrophy is linked to a mutation in dystrophin, a gene required for muscle formation, and the authors genetically modified the stem cells to make them express the corrected version of the gene. After injection into the blood vessels of dystrophic mice, these cells found their way to skeletal muscle, which they were able to partly regenerate. Importantly, the cells were shown to reconstitute the muscle's own stem cell population. The authors suggest that the isolation of these stem cells raises hope for treating muscular dystrophy using the patient's own cells.

11 February 2007

Nature Cell Biology doi:10.1038/ncb1544

A number of retroviruses, including HIV, induce cells to form long bridges along which the virus particles move from infected cells to uninfected cells, according to a paper in the March issue of Nature Cell Biology.

Viral transmission has long been recognized to be more efficient between infected and target cells that are in direct contact with each other. Exactly how viruses move from one cell to another is unclear, although structures called virological synapses, which contain the virus particle and form between areas of cell-cell contact, are thought to be important in this process.

In the present study, Walther Mothes and colleagues describe a novel mode of cell-cell transmission for three retroviruses - murine leukaemic virus, human immunodeficiency virus and avian leucosis virus - along the outside of long, thin intercellular bridges. These bridges seem to be stabilized by an association between a viral protein expressed by the infected cell and a viral-receptor protein in the target cell. Mutants of these proteins that cannot interact destabilize the bridges and markedly reduce viral spreading from cell to cell. This mode of transmission is observed in a variety of different cells, suggesting that it may be a general mechanism of viral spreading.

Whether these intercellular viral highways represent a predominant mode of viral transmission, their relative importance for different viruses, and their relationship to virological synapses are open questions. However, interference with the bridge structures described by Mothes and colleagues may provide a new avenue to limit the infectivity of a number of key viral diseases.