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To escape from cells, vaccinia viruses are propelled on the tip of an actin-filled protuberance toward an opposing cell. The cover image shows an infected 3T3 cell in which the so-called actin tails are visible (green). Viral replication centers are shown in blue. In this issue, Kalman and colleagues show that Abl-family kinases (red) are required for release of the viruses from the actin tails and they find that inhibitors of Abl-family kinases can prevent the spread of virus and disable poxvirus pathogenesis in mice. Image courtesy of Daniel Kalman.
Traditional boundaries among basic research, clinical research and patient-oriented research are yielding to a single, continuous, bidirectional spectrum commonly termed 'translational research' or 'translational medicine.' These encompass (i) the definition of guidelines for drug development or for the identification and validation of clinically relevant biomarkers; (ii) experimental nonhuman and nonclinical studies conducted with the intent of developing principles for the discovery of new therapeutic strategies; (iii) clinical investigations that provide a biological foundation for the development of improved therapies; (iv) any clinical trial initiated in accordance with the above goals; and (v) basic science studies that define the biological effects of therapeutics in humans. Although these goals are essentially no different from those of traditional academic clinical research, translational research emphasizes strategies to expedite their successful implementation. Unfortunately, several barriers that delay this process need to be surmounted to make translational research more than just an interesting concept.
The tyrosine kinase inhibitor Gleevec, currently used to treat cancers such as chronic myeloid leukemia, can also function as an antiviral drug to treat poxvirus infections (pages 731–739).
Findings over the last year or so have built the case that microRNAs might contribute to cancer. Three studies now definitively show this to be the case and also suggest that these small RNAs could be used to categorize tumors.
Inflammatory signals strongly influence the generation of T-cell memory after infection or vaccination. Experimental manipulation of these signals shortens the interval of time between administration of a vaccine and a booster (pages 748–756).
Autoimmune processes that destroy insulin-producing cells in the pancreas cause type 1 diabetes. To prevent the disease, autoreactive immune cells need to be suppressed or eliminated without deleterious side effects. Results from a phase 2 clinical trial take steps in this direction.
Genome instability and DNA repair defects have been discovered in the premature aging disease Hutchinson-Gilford progeria syndrome. These findings provide the first hint of a molecular mechanism for a group of human conditions caused by defects in the nuclear structural protein lamin A (pages 780–785).
New vaccines protect monkeys from Ebola and Marburg virus infections after a single shot. The live vaccines are built using a virus platform that should allow widespread protection in people, if the approach holds up in later safety and efficacy studies (pages 786–790).
PPARα reduces fat accumulation and enhances insulin sensitivity, but exactly how it operates has been unclear. Work on mice suggests that newly synthesized fat—but not preexisting fat—activates this transcription factor.