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The cover photograph shows an HIV-infected T lymphocyte with viral particles budding from its surface. In this month's issue, three research articles explore different aspects of HIV pathology. On page 1217 of this issue, Wolf et al. elucidate a novel mechanism by which the HIV Nef protein prevents apoptosis. On page 1225, Scala and colleagues use phage-displayed envelope epitopes to elicit a partially protective antibody response in SHIV-89.6PD-challenged macaques. Finally, on page 1232, Margolis and colleagues investigate the effect of human herpesvirus 6 co-infection on the replication of HIV variants with different coreceptor requirements.
Systemic lupus erythematosus can cause various forms of central nervous system disorders, ranging from subtle cognitive dysfunction to life-threatening coma. How lupus autoantibodies target neurons and cause brain injury remains a mystery. New research suggests that a subset of autoantibodies to double-stranded DNA in lupus patients cross-reacts with the NMDA glutamate receptor, and produces neuronal injury and death. (pages 1189–1193)
The etiology of thrombotic thrombocytopenic purpura (TTP), a severe blood disorder resulting from increased platelet activation, has been an enigma. The identification of ADAMTS as a protease that cleaves von Willebrand factor and the demonstration of ADAMTS mutations in families with inherited TTP suggest a molecular mechanism for the disease.
Little was known about the function of T cells expressing the γδ–T-cell receptor, until these cells were shown to protect against skin cancer. But what is the mechanism mediating this activity?
Virologists and immunologists are all too aware of the ability of HIV to evade efforts by its human host to destroy it within the body. Now, two new pieces of evidence reveal yet more of HIV's survival abilities: the virus uses a single protein both to trigger and block apoptosis as the situation demands. (pages 1217–1224)
The finding that CD38 mediates a sustained calcium signal inside neutrophils, which directs their movement toward lung tissue infected with pneumococcus bacteria suggests a new mechanism by which the immune system prevents the spread of bacterial infection. (pages 1209–1216)
Holt–Oram syndrome has been associated with mutations in the T-box transcription factor TBX5, but little is known about the function of this protein or how mutations in it cause disease. A new mouse model of this syndrome will help to answer some of these questions.