International Congress of NeuroImmunology Edinburgh, September 3 to 7, 2001

Approximately 1,000 scientists gathered in the Edinburgh International Conference Center for the Sixth International Congress of NeuroImmunology. The organizers were Angela Vincent, David Baker, John Fazakerley, John Greenwood, and Sandra Amor. The scientific program ranged from Alzheimer’s disease to prion diseases to multiple sclerosis (MS) and other autoimmune diseases of the central nervous system (CNS), neurodegeneration and repair, and infections of the CNS. The roles of cytokines, chemokines, inflammatory mediators, recruitment of peripheral and parenchymal cells to sites within the CNS, and intervention or therapeutics were all covered in plenary sessions, workshops and poster sessions. Wednesday, September 5, was the principal day on which infections and the CNS presentations were scheduled. The morning started with a session chaired by Christine Biron and John Fazakerley. Don Gilden (University of Colorado) discussed the molecular pathogenesis of varicella zoster virus infection and compared and contrasted this with other human herpesvirus infections. Diane Griffin (John Hopkins) provided evidence of regional differences in the mouse brain and spinal cord for the role of distinct components of the immune responses to the alphavirus Sindbis virus is more readily cleared from spinal cord and brainstem than from cortical neurons. Adriano Aguzzi (Zurich) discussed the immunobiology of prion diseases in the mouse model. He discussed the proposed entry of prions by the oral route to dendritic cells within the lymphatic system and ultimate spread to the CNS; he also showed evidence that neutralizing antibodies to the PrPsc form had profound beneficial effects in mice. In one of three simultaneous sessions which followed, Steve Jacobson (National Institutes of Health) and Rudi Dorries (Heidelberg) chaired a session devoted to the immune response to viral infections. Howard Gendelman (University of Nebraska) led off with a detailed exploration of the host–virus interaction in human immunodeficiency virus (HIV)-associated dementia (HAD) and presented a new animal host model with nod-scid mice reconstituted with human HLA-A2 cells developing CNS disease. He probed the mice for CD8 T cell-A2-tetramers and also examined hippocampal physiologic changes early in infection. Steve Miller (Northwestern University) discussed epitope spreading in mice infected with Theiler’s virus; his laboratory contributed a review to this journal in the last issue of Viral Immunology (13:227, 2001). The last speaker before lunch was Stanley Perlman (University of Iowa) who discussed his work on the coronavirus mouse hepatitis virus and the role of interferon-g (IFN-g) in demyelination in the Rag-1 knockout mouse reconstituted with wild-type MHV-immune T cells. He infected g-knockout mice and observed the formation of granulomas in the CNS that have CD41 T cells, neutrophils, and macrophages, in an attempt to associate cytokines and chemokines with the inflammatory responses. After lunch, during which we circulated among posters, there was a workshop organized by Hans van Noort (Lieden) and Ewe Liebert (Germany) on infectious and immunity. Hans van Noort started the session with a presentation on the putative role of viruses in the etiology of MS. He made cogent arguments that Epstein-Barr virus may have a causative role, inducing the stress protein a-B crystallin, which is closely linked to many human responses in the disease. Carol Reiss (New York University) described the complex