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The coxsackievirus B serogroup (CB) may be a causative agent in the development of human myocarditis and cardiovascular disease, and mice infected with CB3 develop autoimmune myocarditis. On page 393, Horwitz et al. show that CB3 infection of transgenic mice expressing IFN-g in their pancreatic b cells results in reduced viral replication and prevents chronic autoimmune myocarditis. The cover shows that transgenic expression of IFN-g in the pancreas activates resident macrophages (brown staining) to defend neighboring pancreatic acinar cells after viral infection.
In an attempt to broaden the current debate over proposed revisions to the Declaration of Helsinki, we define vulnerable subjects as those lacking basic rights, and examine the ethical risks inherent in research on such subjects. We then propose special ethical criteria for the conduct and publication of research on vulnerable subjects.
Global health problems require global solutions, and public–private partnerships are increasingly called on to provide these solutions. But although such partnerships may be able to produce the desired outcome, they also bring their own problems. A first-of-its kind workshop in April, hosted by the Harvard School of Public Health and the Global Health Council, examined the organizational and ethical challenges of partnerships, and ways to address them.
After a decade of unsuccessful attempts to correct one form of severe combined immunodeficiency using gene therapy, success has finally been achieved in another genetic type. Whether this success is due to the type of defect or to other factors, such as improved retroviral vectors or stem cell growth conditions, is not yet apparent.
Studies indicate that it is possible to achieve long-term gene transfer into hematopoietic stem cells and progenitor cells. But what needs to be done before we can take the final steps towards human stem cell gene therapy (pages 652–658)?
Elucidation of the mechanisms behind nuclear translocation of viral nucleic acids will lead to improvements in the design of anti-retroviral drugs and gene therapy vectors that are able to transduce non-dividing cells. A recent study has identified a triple stranded HIV cDNA intermediate of reverse transcription, or a ‘central DNA flap,’ as a component of HIV nuclear import.
A double mutation in the androgen receptor allows prostate cancer cells to become responsive to glucocorticoids. This discovery sheds light on a new pathway by which prostate cancer cells can escape androgen dependence (pages 703–706).
CD40 ligation serves as a powerful mediator of protective and therapeutic immunity against foreign invaders and cancer cells in vivo. A study now shows that agonistic antibodies against CD40 may also be useful in the treatment of a chronic autoimmune inflammatory disease ( pages 673–679).
Coxsackieviruses have long been associated with myocarditis. Recent studies have attempted to determine whether this autoimmune response to heart antigens is initiated by the virus itself, or by host antigens released during viral damage (pages 693–697).
Studies indicate that amyloid-A-induced upregulation of RAGE leads to a cell stress response in some cases of amyloidosis. Will RAGE blockade be the answer to the toxic effects of amyloid deposits ( pages 643–651)?