Progressive Rubella Panencephalitis

Wolinsky, Jerry S.; Berg, Bruce O.; Maitland, Charles J.

doi:10.1001/archneur.1976.00500100056016

Cited by 74 publications

(18 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has been demonstrated that ontogenic changes in cultures of newborn brain parallel those seen in vivo (Nelson 1975;Block 1982). If our observations can be extrapolated to the in vivo condition, they may partially explain the increased susceptibility of the immature brain to autoimmune phenomena (Miller et al 1956;Stone and Lerner 1965;Currier et al 1974;Lublin et al 1981) and persistent viral infections (Kennedy 1968;Wolinsky et al 1976).…”

Section: Discussionsupporting

confidence: 53%

“…(d) Do glial cell responses to lymphocyte culture supernatants change with glial cell age? The latter two questions were posed because of the particular susceptibility of the immature nervous system to both autoimmune phenomena and persistent viral infection (Miller et al 1956;Stone and Lerner 1965;Kennedy 1968;Currier et al 1974;Wolinsky et al 1976;Lublin et al 1981).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Recognition of major histocompatibility complexantigens on murine glial cells

Birnbaum¹,

Clinchy²,

Widmer³

1986

Journal of Neuroimmunology

View full text Add to dashboard Cite

Recognition of autologous major histocompatibility complex (MHC) antigens by T cells is an essential step in the induction of an immunologic reaction to either endogenous or exogenous antigens. We investigated the ability of murine glial cells of different ages to stimulate clones of allospecific T lymphocytes. We also investigated the effects of supernatants from cultures of activated T cells on the immunologic recognition of MHC antigens on murine glial cells. Lymphocyte clones specific for Class I, Class II and non-MHC, background antigens were obtained from C57B1/6J-anti-DBA/2 mixed lymphocyte cultures. Glial cell cultures were prepared from newborn syngeneic (C57B1/6J) and allogeneic (DBA/2) mouse brains. Glial cultures 1-4 weeks of age were able to stimulate alpha-Class I-specific clones. No stimulation of alpha-Class II or alpha-background clones was noted. Incubation of glial cells with supernatants from cultures of alloantigen-activated spleen cells (C57B1/6J-anti-DBA/2) resulted in a decreased ability of glial cells to stimulate alpha-Class I responses. In contrast supernatant-treated cultures acquired the capacity to stimulate alpha-Class II-specific clones. No responses were noted in clones responsive to non-MHC antigens. The ability to stimulate alpha-Class II-specific clones was most prominent with one-week-old glial cultures and was lost by four weeks of culture. The increased susceptibility of younger glial cultures to the modulatory effects of lymphokines from activated T cells may be a factor in the increased susceptibility of the immature central nervous system to persistent viral infections and the development of autoimmune phenomena.

show abstract

Section: Discussionsupporting

confidence: 53%

Section: Introductionmentioning

confidence: 99%

Recognition of major histocompatibility complexantigens on murine glial cells

Birnbaum¹,

Clinchy²,

Widmer³

1986

Journal of Neuroimmunology

View full text Add to dashboard Cite

show abstract

“…This condition is characterized by progressive dementia, ataxia, choreiform movements, myoclonic seizures, and fine perimacular retinal pigmentation. Microscopical study of biopsied brain tissue in a patient revealed a picture similar to SSPE, but with perivascular deposits and without inclusion bodies [66,67]. SSPE also presents with various types of seizures, mainly myoclonic jerks, atonic and tonic-clonic seizures.…”

Section: Differential Diagnosismentioning

confidence: 88%

Subacute sclerosing panencephalitis

2008

View full text Add to dashboard Cite

Subacute sclerosing panencephalitis (SSPE) is a subacute encephalopathy of childhood and young adolescence. Infrequently, SSPE can occur in adults and pregnant women. It is caused by an aberrant measles virus, known as the SSPE virus. SSPE virus differs from wild-type measles viruses in the form of several mutations affecting the viral genome. The matrix gene is most commonly affected by these mutations. The characteristic clinical manifestations of SSPE include behavioral changes, cognitive decline, myoclonic jerks, seizures, abnormalities in vision, bilateral pyramidal signs and coma. Ocular changes may occur in up to 50% of patients. The most characteristic ophthalmological lesion is necrotizing retinitis. Cortical blindness can be the early feature of SSPE. The diagnosis of SSPE is often difficult in the early stages. In a typical case diagnosis is based on clinical, electroencephalographic, and cerebrospinal fluid findings. At present, there is no effective treatment to completely cure SSPE. Oral isoprinosine and intrathecal or intraventricular alpha-interferon may prolong survival to some extent. Immunization against measles is currently the most effective strategy against SSPE.

show abstract

“…Progressive rubella panencephalities may follow either congenital or postnatal acquired rubella infection [5][6][7], This disorder is rare. Symptoms and signs of de mentia and motor degeneration begin 4-14 years follow ing initial rubella infection.…”

Section: Discussion Of Clinical Findingsmentioning

confidence: 99%