Multiple sclerosis (MS) is a chronic, demyelinating disease of the CNS in which autoimmunity to myelin plays a role in pathogenesis. The epidemiology of MS indicates that it may be triggered by a virus infection before the age of adolescence, but attempts to associate a specific virus with MS have produced equivocal results. Many studies of the aetiology of MS have postulated that a persistent virus infection is involved, but transient virus infection may provide a plausible alternative mechanism that could explain many of the inconsistencies in MS research. The most studied animal model of MS is chronic relapsing experimental autoimmune encephalomyelitis (CREAE), which is induced in susceptible animals following injection of myelin components. While CREAE cannot provide information on the initiating factor for MS, it may mimic disease processes occurring after an initial trigger that may involve transient virus infection. The disease process may comprise separate triggering and relapse phases. The triggering phase may involve sensitisation to myelin antigens as a result of damage to oligodendrocytes or molecular mimicry. The relapse phase could be similar to CREAE, or alternatively relapses may be induced by further transient virus infections which may not involve infection of the CNS, but which may involve the recrudescence of anti-myelin autoimmunity. Although current vaccines have a high degree of biosafety, it is suggested that the measles-mumps-rubella vaccine in particular could be modified to obviate any possibility of triggering anti-myelin autoimmunity.

Animals↗

PubMedDate not supplied

Colocalisation of human immunodeficiency virus and human cytomegalovirus infection in brain autopsy tissue from AIDS patients.

We have examined 26 human AIDS brains obtained at post mortem for infection by human immunodeficiency virus (HIV) and human cytomegalovirus (HCMV), and for dual infection of cells by both viruses. The techniques used were enzyme-linked immunocytochemistry for HCMV and in situ hybridisation using a cDNA probe for HIV. Using these techniques, HCMV infection was detected in 14 brains, HIV infection in 14 brains, and coinfection with HIV and HCMV in 7 brains. Four case of dual HIV/HCMV infection were found where no colocalisation could be detected. In randomly chosen dually infected areas 19.2% of infected cells were coinfected with both viruses. Although cells identified morphologically as macrophages were the most common infected cell type, astrocytes and neurons were both singly and doubly infected with HIV and HCMV. Complete clinical data were available for 4 of the 7 cases with coinfection and each had AIDS dementia complex.

AIDS-Related Opportunistic Infections↗

PubMedDate not supplied

Morphometric analysis of growth retardation in fetal lambs following experimental infection of pregnant ewes with border disease virus.

The onset of growth retardation was investigated in fetal lambs following experimental infection of pregnant ewes with Border Disease virus (BDV) on day 53 of pregnancy. Fetuses from control and infected ewes were harvested at weekly intervals between day 60 and day 95 of gestation and morphometric studies were completed on tibial radiographs and tibial growth cartilage metaphyseal junctions. Mean tibial areas were significantly reduced (P < 0.01) in fetuses from infected ewes at 35 and 42 days after infection and growth cartilage metaphyseal junctions were less mature in fetuses from infected ewes at 42 days after infection. Positive immunostaining for BDV antigen was demonstrated in the brains of all fetuses from infected ewes between 14 and 42 days after infection. Attempts to demonstrate BDV antigen in bone proved unsuccessful. It is concluded that intrauterine growth retardation is an early manifestation of BDV infection in lambs and that the process is initiated shortly following infection of the fetus.

Animals↗

PubMedDate not supplied

The pathogenicity of louping ill virus for mice and lambs.

Mice and lambs were infected with the LI/I, LI/31 or MA54 strain of louping ill virus (LIV) to provide information relevant to testing the efficacy and biosafety of a new generation of flavivirus vaccines based on a Semliki Forest virus (SFV) vector. Whereas clinical signs and neuropathological lesions were consistently severe in mice, the majority of lambs showed lesions of moderate severity and only lambs with severe lesions were clinically affected. For both species, dispersal of viral antigen occurred along neuronal cell processes, and neuronal degeneration and death were confirmed as central events after infection with LIV. In contrast to lambs, in which most lesions remained localized, mice showed widely dispersed lesions which were associated with less intense leucocytic infiltrates. Among the infiltrating cells, histiocytes predominated and apoptotic forms were prominent in severely affected animals. The intranasal route of infection provided an efficient avenue for entry of LIV into the brain and resulted in lesions which were more severe than those produced by subcutaneous or intraperitoneal inoculation.

Animals↗