Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
Genetic mitochondrial defects underlie a variety of neurodegenerative, muscular, cardiac and other diseases. On page 934 of this issue, Nakada et al. use a mouse model of mitochondrial disease to show that wild-type and mutant mitochondria can complement each other within a single cell both in vivo and in vitro. The cover depicts an electron micrograph of mouse cardiac muscle fibers that contain 88% pathogenic deletion mutant mitochondrial DNA. Staining of ultra-thin sections reveals fine organelle structures possibly representing mitochondrial fusion or fission. Magnification, x54,000.
Emerging data has indicated that supervised treatment interruption (STI) of highly active antiretroviral therapy might significantly augment immune responses in HIV-1-infected patients and slow disease progression. Here the authors discuss the rationale behind STI and future directions for study.
Obesity and insulin resistance enjoy a complex relationship that gives rise to a range of metabolic disorders, including type 2 diabetes, dyslipidemia and coagulation disorders. Teasing apart this relationship could yield new therapies to treat some of these conditions and two new reports point to the adipocyte-secreted protein, adiponectin, as a new molecular target. (pages 941–946 and pages 947–953)
A new study shows that a mouse model of cystic fibrosis has lower levels of liquid on the surface of its airway epithelium which suggests that thickened airway secretions might have a role in the disease process and that rehydrating the airways might be of benefit to patients.
Patients with hepatitis C constitute the highest proportion of candidates for liver transplantation. The lack of small animal models for the disease has been a major stumbling block in understanding how hepatitis C and liver damage develop and in testing possible treatments. The report of infection of a mouse model with the hepatitis C virus is a significant and welcome achievement. (pages 927–933)
Although systemic viral infection gives rise to robust responses from both CD8+ and CD4+ T cells, there are striking differences as well as similarities in the way the two classes of lymphocyte cells react. Insights into the patterns of response by each type of T cell could lead to the development of new therapeutics that enhance or suppress factors governing CD8+ and CD4+ T-cell immunity. (pages 913–919)
Although the tuberculosis bacterium is most renowned for its ability to cause pulmonary infection, the bacilli colonize many sites in the body in addition to the lungs. The recent identification of a key player in the dissemination of infection sheds light on the route by which tuberculosis spreads from the lungs and opens the way to assessing the significance of dissemination to the course of disease.
Unequivocal evidence for the dynamic nature of mammalian mitochondria has been hard to find. However, the successful development of a transgenic mouse model carrying pathogenic mtDNA as reported here will cause us to take a fresh look at these dynamic organelles. (pages 934–940)