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Biomedical subjects

C A Mims

Publications and source records attributed to C A Mims.

At least 55 records · Page 3Linked to original sources
PubMed1981

Interaction of influenza virus with mouse macrophages.

Mouse peritoneal and alveolar macrophages differed substantially in their response to influenza in vitro. Immunofluorescent and infectious-center techniques showed that viral proteins were produced in only a small subpopulation (17%) of peritoneal macrophages and that these infected cells were removed from culture by 3 days postinfection. In contrast, alveolar macrophages were highly susceptible to influenza, and viral antigens were produced in all cells. This was accompanied by a cytopathic effect and cell death. However, no infectious virus was released and the infection was considered abortive. With mouse cytomegalovirus, however, both alveolar and peritoneal macrophages were equally restrictive, and viral antigens were produced in only 1 to 5% of either cell population. No significant differences were observed between mouse-virulent and -avirulent strains of influenza in their interaction with macrophages either in vitro or in vivo. In vivo, both strains induced an influx of cells to the alveolar spaces by 3 to 4 days postinfection, and this was reflected by a 5- to 10-fold increase in the number of "macrophages" in harvest fluids at this time. Many of these cells had an altered morphology compared with alveolar macrophages from uninfected mice, and the cell population as a whole was not susceptible to influenza. However, this resistance was lost by 7 days of in vitro culture.

Animals↗
PubMed1980

Murine cytomegalovirus: reactivation in pregnancy.

Murine cytomegalovirus (MCMV) may be rapidly and reproducibly attenuated by passage in tissue culture. A high proportion of CDI mice neonatally infected with the virulent strain of CMV can be shown to have replicating virus in the kidneys for up to 90 weeks p.i. and this high rate of isolation is not altered in pregnancy. A much lower rate of isolation from the kidneys is seen in CDI mice neonatally infected with the attenuated strain. However, this isolation rate was significantly increased during pregnancy and higher titres of virus were recovered.

Animals↗
PubMed1979

Reactivation of polyoma virus in kidneys of persistently infected mice during pregnancy.

Female mice infected at birth with 10(7) 50% tissue culture infective doses of polyoma virus were mated when at least 6 weeks old. Polyoma was not detected in any tissues of 27 female mice before mating except for trace amounts in the kidneys of 2 mice, but late in gestation polyoma virus could be found in the kidneys of 21 of 38 mice with titers of 10(3.7) to 10(6.2) 50% tissue culture infective doses per gram of kidney. The virus was not detected in the brain, salivary gland, lung, liver, spleen, ovaries, placenta, or fetuses during gestation. Nonpregnant females were injected with female sex hormones over a period of 17 days, and polyoma was then detected in kidneys of 4 of 18 mice. Treatment of cultures of mouse embryo fibroblasts with either sexhormones or a glucocorticosteroid resulted in approximately a threefold increase in the rate of infection of cells with polyoma virus.

Animals↗
PubMed1978

Splenic necrosis in mice infected with cytomegalovirus.

Necrosis of the spleen is seen in mice of certain strains after injection of large doses of murine cytomegalovirus. Necrosis begins in perifollicular areas containing infected cells which do not appear to be macrophages, and in severe cases the entire spleen is involved. Necrosis is first visible three days after infection and is not prevented by treatment of mice with corticosteroids, cyclophosphamide, or theta antiserum. There is a striking loss of nucleated cells from the spleen at two to four days after infection, in the absence of splenic necrosis. The pathogenesis of splenic necrosis, which is seen also in certain other viral infections, remains unexplained.

Age Factors↗
PubMed1978

The role of macrophages in mice infected with murine cytomegalovirus.

Quantitative studies were made of the infection of mouse peritoneal macrophages in vitro by cytomegalovirus, using virus assays and immunofluorescence. The efficiency of infection was low. Broth-induced peritoneal macrophages were about four times more resistant to infection than unstimulated macrophages and it was even more difficult to infect activated macrophages taken from mice 6 days after intravenous infection. Peritoneal macrophages (unstimulated) were infected at least 15 times more readily by tissue culture-passed (attenuated) virus than by salivary gland (virulent) virus, but macrophages prevented the spread of tissue culture virus to underlying susceptible mouse embryo fibroblasts, whereas they did so much less effectively with virulent salivary gland virus. The pathogenesis of infection was studied in intact mice by immunofluorescence, and the observations paralleled the in vitro findings. When large doses of salivary gland virus were injected intravenously, infected Kupffer cells (liver macrophages) were occasionally seen and the inoculated virus directly infected large numbers of hepatic cells. In similar experiments with tissue culture-passed virus, there was initial infection of occasional Kupffer cells, which only rarely gave rise to infected hepatic cells. Differences in the extend of Kupffer cell infection by the two strains of virus were not detected in these experiments. Salivary gland virus also usually failed to infect splenic or lymph node macrophages. Occasional infected mononuclear cells were seen in the blood, lung and bone marrow, but were not identified. Infected cells were very rarely seen in the thymus, even in suckling mice.

Animals↗
PubMed1978

General features of persistent virus infections.

Persistent virus infections are discussed from the virus point of view in terms of the bodily sites in which the infection persists. Glands and body surfaces are thought to be significant because they give the virus protection at the topographical level from immune forces, and because they are appropriate sites for the shedding of virus to the exterior. Germ cells are relevant sites because infection can thus be transmitted vertically from generation to generation in the host. The central nervous system, however, is generally a 'dead end' from which there is no shedding to the exterior. Persistance in blood may be relevant when continued arthropod transmission becomes possible. Most persistent viruses infect lymphoreticular tissues, and this is interpreted by suggesting that it results in an impaired immune response to the infecting virus, which in turn favours persistence. It is suggested that the biological function of virus transformation and the integration of viral into host cell DNA is that it enables the infection to persist in the host and undergo reactivation. Papovaviruses, adenoviruses and oncornaviruses are considered from this point of view.

Adenoviridae Infections↗
PubMed1977

Transplacental transmission of polyoma virus in mice.

When pregnant mice were inoculated on day 1 of gestation with polyoma, some of them exhibited total resorption or reduced litter size, the extent depending on the dose of virus. Virus was detected in 4 out of 11 mouse embryo fibroblast (MEF) cultures made from infected mothers. After maternal infection on day 5 or 10 of gestation, virus titers of up to 10(7) 50% tissue culture infectious doses (TCID50)/g of fetus were found in all pools of fetuses tested 5 days later, with the titers falling by day 6. Hemagglutination-inhibiting antibodies against polyoma appeared in maternal serum by day 6 and rose to a maximum by day 14. Immunoglobulin G class antibodies were detected by day 7, with titers rising rapidly to a maximum at day 14. After maternal infection later in gestation (day 15), one out of three litters of newborn mice was found to have 10(5) TCID50 polyoma virus per g in pooled kidney samples.

Animals↗
PubMed1975

The meaning of persistent infections in nature.

Viruses that cause persistent infections maintain themselves more effectively in nature than those causing acute and limited infections. There is a tendency for persistent viruses to evolve towards a state of minimal pathogenicity in the host. Vertical transmission, with integration of viral into host genome, represents the state of perfect parasitism.

Animals↗
PubMed1973

Parainfluenza virus Sendai infection in macrophages, ependyma, choroid plexus, vascular endothelium and respiratory tract of mice.

Immunofluorescent observations showed that after intranasal instillation of parainfluenza 1 (Sendai) virus into adult mice, infection is confined to the epithelial lining of the larger airways. Alveolar macrophages were not significantly involved, although they could be infected in vitro. In suckling mice, the infection was more acutely lethal and extended into the terminal air spaces. The intranasal susceptibility of adult mice was not reproducibly affected by treatment with potent antithymocyte serum, and there were no obvious pathogenic effects when heterologous antiserum was instilled intranasally into infected mice. Peritoneal macrophages were infected by intraperitoneally injected Sendai virus, with production of a highly viscous peritoneal exudate. Kupffer cells of the liver and endothelial cells in large veins and auricles were infected by intravenously injected virus. When injected intracerebrally, Sendai virus infected ependyma and choroid plexus epithelium. Adult mice often survived, in spite of ependymal destruction and changes in ventricular morphology. Astrocytes were activated but not infected.

Animals↗