Proviral DNA has been demonstrated by in situ hybridization in foci of cells of a lamb infected with the RNA slow virus visna. A few of these cells also contain the major virion structural antigen p30. This restriction in virus gene expression in the infected animal provides a mechanism for persistence of virus in this chronic infection.

A survey of carers belonging to the Alzheimer's Disease and Related Disorders Society (ADARDS) had three aims: (i) to investigate the process of health professionals providing information to patients and carers: (ii) to determine the nature of problems burdening carers; and (iii) to examine factors associated with institutional placement. Carers reported on deficiencies in the provision of information and indicated their preferences as to how the information should be given. ADARDS, general practitioners and other health professionals were reportedly helpful, with each appearing to have a role in providing information about dementia. Multiple problem behaviours were reported by most carers, especially difficulties with communication, the need for constant supervision and disruption to personal life. Institutional care was most highly correlated with dependency problems, severity of dementia and a non-spouse carer. Implications include the need for training of doctors in communication and education about dementia with particular attention to management of dependency problems.

The pathogenesis of the persistent progressive diseases of sheep (visna-maedi) and goats (arthritisencephalitis) is dependent on continuous replication of the causative lentiviruses. One subgroup of these viruses, Icelandic visna virus, accomplishes this form of replication by undergoing antigenic mutation. Mutant viruses arising late in the infection escape neutralization by antibodies directed to the parental virus. In contrast, we show here that viruses obtained from persistently infected sheep and goats with natural disease in this country do not induce virus-neutralizing antibodies, although antibodies to virus core proteins were produced. The lack of neutralizing antibodies was not overcome by hyperimmunization of animals with concentrated preparations of live or inactivated virus. Thus, failure to produce these specific antibodies was not due to lack of sufficient antigen or interference with the immune response because of the ability of these viruses to infect macrophages. The hyporesponsive state, however, was overcome by immunization of animals with virus and large amounts of inactivated Mvcobacteriimn tubericulosis. Induction of agglutinating and neutralizing antibodies by this method was probably due to a unique form of antigen processing by macrophages activated by M. tubercu(losis. Neutralizing antibodies were produced for the first time against the caprine arthritis-encephalitis virus by this method. These antibodies have similar biological properties to those induced by Icelandic visna virus. They belong to the immunoglobulin Gl subclass, they are effective against a narrow range of caprine arthritis-encephalitis viruses, and they identify (for the first time) antigenic variants among these caprine agents.

CSF lymphocyte subpopulations of eight patients with neurosarcoidosis were examined. CSF or CT was abnormal in all. The CSF T4/T8 (helper/suppressor) ratio was elevated at 6.8 and 7.6 in two patients; in one, there were only CSF T4 cells. The ratio was normal in five patients.

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