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Severe acute respiratory syndrome (SAR) emerged last year as a threat to global health. On page 290 of this issue, Haagmans et al. show that pegylated interferon-alpha is an effective prophylactic in a macaque model of respiratory infection by SARS coronavirus. The cover image shows a transmission electron micrograph of SARS coronavirus nucleocapsids (purple) in a type 1 alveolar pneumocyte from the lung of an infected macaque. Magnification, approximately x50,000.
Known for his drive and ability to drum up synergy, Otmar Wiestler is the natural choice to lead Germany's largest cancer research center. But can this non-clinician transform translational cancer research?
Several lines of evidence indicate that development of an effective vaccine for HIV-1 is going to be, at best, extremely difficult. The inability to solve fundamental scientific questions is the root cause for why a successful vaccine is not currently within our grasp. A renewed, organized, focused effort is needed to overcome these scientific obstacles.
Using stem cells to generate new neurons and replace those lost in diseases such as Parkinson and amyotrophic lateral sclerosis would be a major breakthrough, but significant hurdles remain before this goal can be realized. Instead, a more practical short-term approach may be to use stem cells to protect neurons dying in these diseases.
HIV mutates to avoid the pressure of the immune system. This process is balanced by the need of the virus to replicate efficiently. Two studies examine this dynamic as the virus infects new hosts (pages 275–281 and 282–289).
Aging is driven in part by an evolutionarily conserved hormone signaling pathway. A new study shows that this pathway is controlled by the p53 tumor suppressor, which exquisitely balances the need for cell proliferation against that for tumor suppression.
According to the 'hygiene hypothesis', viral infections prevent the development of asthma and other atopic diseases. Influenza virus appears now to enhance, rather than inhibit, the development of asthma and allergic responses.
A new anticancer compound interferes with aurora kinases, regulators of mitosis. We can now hope for the biology of these kinases to inform clinical trials (pages 262–267).
Upon injury, axons can send a message to the cell body to implement repair programs. This message is now shown to require a complex of the microtubule motor dynein and proteins that mediates nuclear-cytoplasmic transport.
Conditional removal of the putative tumor suppressor gene Aml1/Runx1 from the bone marrow of mice mimics a human familial platelet disorder (pages 299–304).
Heart researchers have had hints that a stress response protein, PKC-α, influences the progression to heart failure. The inner workings of this key regulator are now coming to light (pages 248–254).