Mary Lou Jelachich

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Theiler's murine encephalomyelitis virus (TMEV) persists in the mouse central nervous system principally in macrophages, and infected macrophages in culture undergo apoptosis. We have detected abundant apoptotic cells in perivascular cuffs and inflammatory, demyelinating lesions of SJL mice chronically infected with TMEV. T cells comprised 74% of apoptotic(More)
To evaluate critically the merit of utilizing a wound model for growing human tumors, a series of increasingly difficult human tumor types were tested for growth at sites of trauma in athymic nude mice. In vitro tumor lines as well as fresh tumors from the breast, colon, rectum, lung, and a metastasis from an unknown primary were intraperitoneally injected(More)
Theiler's murine encephalomyelitis virus (TMEV) produces a persistent central nervous system infection and chronic, inflammatory demyelinating disease in susceptible mice. TMEV antigen(s) and RNA genome have been detected in astrocytes, oligodendrocytes, and macrophages during persistence. Whether there is a predominant cell type in which TMEV persists has(More)
Theiler's murine encephalomyelitis viruses (TMEV), genus Cardiovirus, family Picorniviridae, are natural enteric pathogens of mice which cause central nervous system demyelination similar to that seen in multiple sclerosis. TMEV can be classified into two groups based on neurovirulence: a highly virulent group, e.g., GDVII virus, and a less virulent group,(More)
The human class I alleles HLA-A11 and HLA-A3 have a well-documented history of serological cross-reactivity. This cross-reactivity suggests that they are closely related, a suggestion which is supported by the fact that the HLA-A11 and HLA-A3 genes are distinguished from all other A-locus genes by a restriction fragment length polymorphism observed in Bam(More)
Theiler's murine encephalomyelitic virus (TMEV) preferentially replicates in macrophages in the central nervous system of mice during the persistent phase of infection. Macrophages accumulate in demyelinating lesions and are evidently the primary cell to harbor virus. To investigate TMEV-macrophage interactions, we studied GDVII infection of three cell(More)
Infection of susceptible mouse strains with BeAn, a less virulent strain of Theiler's murine encephalomyelitis virus (TMEV), results in immune system-mediated demyelinating lesions in the central nervous system (CNS) similar to those in multiple sclerosis. Since macrophages appear to carry the major detectable antigen burden in vivo, and purification of(More)
After an acute phase of virus growth in neurons (e.g. anterior horn cells), Theiler's murine encephalomyelitis virus (TMEV) persists as a chronic productive infection, largely in macrophages in the CNS white matter. TMEV replication in macrophages is highly restricted, probably as the result of host cell factors. The preponderance of evidence indicates that(More)
Supernatants from phorbol 12-myristate 13-acetate-activated cultures of the mouse EL4 thymoma, or of several mouse T-cell hybridomas stimulated either by their specific antigen or by concanavalin A, induced primary splenic B cells to proliferate and differentiate to antibody-secreting cells. This effect was not due to interleukin 2 and did not require the(More)
Infection of susceptible mice with the low-neurovirulence Theiler's murine encephalomyelitis virus strain BeAn results in an inflammatory demyelinating disease similar to multiple sclerosis. While the majority of virus antigen is detected in central nervous system macrophages (Mphis), few infiltrating Mphis are infected. We used the myelomonocytic precursor(More)