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Biomedical subjects

C A Mims

Publications and source records attributed to C A Mims.

At least 19 recordsLinked to original sources
PubMed1995

Virology research and virulent human pandemics.

The possibility that a devastating human pandemic could arise, causing massive loss of human life, is discussed. Such a major threat to the human species is likely to be a virus, and would spread by the respiratory route. It need not necessarily cause massive loss of life, but if it caused serious illness or incapacity it would still have a major impact. A possible source is from an existing respiratory pathogen, but it would more probably arise from an infection that is maintained in an arthropod or vertebrate host, but which at present either does not infect humans, or if it does it fails to be effectively transmitted between them. More research should therefore focus on the pathogenetic factors and the viral determinants that promote respiratory transmission.

Disease Outbreaks↗
PubMed1992

The Zvonimir Dinter Memorial Lecture. New insights into the pathogenesis of viral infection.

Interesting recent highlights into the pathogenesis of viral infections have come from: (1) Studies of viruses that persist in cells and modify cell function without causing cell damage. (2) Transgenic mouse studies showing how tissue-specific transcriptional activators control virus expression and can determine viral tropism. (3) Studies of the influence of cell differentiation on viral expression. (4) The exploding world of cytokines, whose baffling complexity and multiple interactions are subjects of intense study. (5) Studies of the interaction of viruses with the immune system. In each case, no molecular studies are giving unprecedented insights into disease processes. However, even when viral genomes are sequenced and virulence genes identified there are additional daunting steps before we understand the role of a given gene product in pathogenesis.

Animals↗
PubMed1987

Genetic basis for Ia positivity and susceptibility to lactic dehydrogenase virus in macrophages of SJL/J mice.

SJL/J mice showed a higher elevation of serum lactic dehydrogenase after lactic dehydrogenase virus (LDV) infection, and a higher per cent of Ia positive and LDV infectable cultured macrophages, than several other mouse strains. Genetic studies suggested that these unique characteristics in SJL/J mice are closely linked and inherited as a single autosomal recessive trait, which is not within the H-2 gene complex.

Animals↗
PubMed1986

Infection of mice with lactic dehydrogenase virus prevents development of experimental allergic encephalomyelitis.

A significant reduction in the incidence of experimental allergic encephalomyelitis (EAE) in SJL/J mice was observed when mice were infected with lactic dehydrogenase virus (LDV) 14 days before, on day 0, or 3 days after immunization with spinal cord homogenate. These results are discussed in terms of the selective infection by LDV of I-region-associated antigen- (Ia) positive macrophages.

Animals↗
PubMed1986

Viral infection in patients with multiple sclerosis and HLA-DR matched controls.

Retrospective comparisons of the prevalence and age, where appropriate, of some childhood infectious illnesses and vaccinations, together with serological evidence for exposure to 16 viruses, many of which have previously been implicated in the aetiology of multiple sclerosis (MS) were made in 177 patients with acute optic neuritis, other recent isolated demyelinating episodes or established MS and 164 controls. The expected high frequency of HLA-DR2 in patients with demyelinating disease was matched by preselection of normal controls with this antigen (DR2+); the remaining individuals were classified as HLA-DR2 negative/DR3 positive (DR3+) or HLA-DR2 and 3 negative (DR2/3 -). Cases were compared with controls, collectively and in analyses restricted to each genetic group; these comparisons were repeated considering the three categories of patients with demyelination and two control populations separately. All DR2+, DR3+ and DR2/3 - individuals were compared in a single analysis to assess the effect of HLA type itself on the results. Patients with demyelinating disease had rubella and measles at a later age and reported mumps infection more frequently than controls. Age of typhoid vaccination and duration of exposure to domestic dogs was higher in all cases than controls. Age of measles and mumps, but not rubella, was higher in DR2+ cases than controls; but differences were not observed in the other genetic groups. Higher rubella antibody titres were present in all cases than controls and in analyses confined to DR2+ individuals in whom higher Epstein Barr virus antibody titres were also present. Measles haemagglutination inhibition and parainfluenza I antibody titres were increased and influenza A antibodies detected less frequently in all patients with optic neuritis and those with DR2 compared with appropriate controls; influenza B antibody titres were lower in all DR2+ cases than controls. Higher adenovirus and varicella zoster antibody titres were present in DR2/3- patients with demyelination and other neurological diseases compared with normal controls. Overall, older age of infection and higher antibody titres were observed more often in patients with optic neuritis, in particular DR2+ cases, than other individuals with demyelination or controls. Our serological results are consistent with the presence of abnormal HLA-immunological reactivity in patients with MS but cannot be explained only by an effect of DR type itself; age at which susceptible individuals develop some common childhood infections may also influence the subsequent development of the disease.

Adult↗
PubMed1986

Live lactate dehydrogenase-elevating virus (LDV) induces suppressor T cells that inhibit the development of delayed hypersensitivity to LDV.

A strong delayed-type hypersensitivity (DTH) response to lactate dehydrogenase-elevating virus (LDV) in mice was induced by immunization with u.v.- or heat-inactivated virus by the intravenous, intraperitoneal and especially the subcutaneous route. The peak DTH response was seen 7 days after immunization. Live virus, in contrast, did not induce a DTH response in young (1- to 3-month-old) mice irrespective of inoculation route, except after pretreatment with cyclophosphamide (CY), when the response peaked at 14 days. Live virus, however, induced a significant DTH response in old mice (greater than 8 months) without CY. The DTH response to inactivated virus was reduced when live virus was given intraperitoneally at the same time, but was partially restored when Ia-positive peritoneal cells were also given intravenously. The DTH response induced in infected mice pretreated with CY was suppressed by injection of spleen cells from infected or from normal 1- to 3-month-old mice. Suppression by normal spleen cells was abolished by treatment with anti-Thy1.2, anti-Lyt1 and anti-Lyt2 plus complement, whereas suppression by spleen cells from infected mice was prevented by anti-Thy1.2 and anti-Lyt2 plus complement. It is concluded that suppression of the DTH response was associated with induction of suppressor T cells and that severe depletion of Ia-positive cells may also have played a part.

Animals↗
PubMed1986

Subclass distribution of IgG and IgA responses to rubella virus in man.

Monoclonal anti-subclass antibodies were used in a micro-ELISA method to determine rubella-specific IgG subclass antibodies in serum from 22 subjects who had acute rubella or had been vaccinated, from 10 infants with congenital rubella, and in serum and synovial fluid samples from 21 patients with chronic arthritis. In nearly all samples IgG1 was the only type of IgG antibody detected. In acute infections it was present within 10 days of the onset of the rash. IgG4 antibody was detected in sera from two immune individuals. Rubella-specific IgA1 subclass antibody was detected by the same technique in sera from 6 of 12 subjects with acute rubella as early as 3 days but not later than 28 days after the appearance of the rash.

Adult↗
PubMed1985

Pattern of infection and selective loss of Ia positive cells in suckling and adult mice inoculated with lactic dehydrogenase virus.

Lactic dehydrogenase virus (LDV) infected cells were localised in cryostat sections of infected adult and suckling mice by fluorescent antibody staining. In almost every organ except brain and spinal cord, LDV infected cells were present in interstitial connective tissue, including dermis and submucosa of gastrointestinal and urinogenital tracts. They were also present in liver sinusoids and red pulp of spleen. The tissue distribution, shape, and fluorescence staining pattern of infected cells were similar in adult and suckling mice. The reactivity with monoclonal antibody to mouse macrophages (F4/80) and to Ia antigens indicated that infected cells were Ia antigen positive macrophages, and this was confirmed in double labelling experiments. Peak numbers of LDV infected cells were seen in every organ 12-18 hours post infection (p.i.), disappearing rapidly thereafter until at 48 hours p.i. they could no longer be detected. At the same time Ia positive cells fell to undetectable levels, although macrophages were still present in reduced numbers. At 7 days p.i. the total number of macrophages in sections had returned to normal, but the number of Ia positive cells remained at low levels. Macrophages recovered from peritoneal cavity and spleen of intraperitoneally infected mice were also studied. Ia positive cells had virtually disappeared from peritoneal cavity at 24-48 hours, and from spleen at 24-72 hours. Three weeks after infection the proportion of Ia positive cells was still low when compared with that of normal mice suggesting selective loss of these cells.

Animals↗