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Biomedical subjects

M J Buchmeier

Publications and source records attributed to M J Buchmeier.

100 records · Page 6Linked to original sources
PubMed1978

Virus-induced immune complex disease: identification of specific viral antigens and antibodies deposited in complexes during chronic lymphocytic choriomeningitis virus infection.

Structural proteins of LCMV were identified and their role in the immune complex glomerulonephritis of LCMV carrier mice was examined. Purified LCMV contained three major polypeptides, a single nonglycosylated nucleoprotein with an estimated m.w. of 63,000, and two surface glycoproteins of 54,000 and 35,000. Deposition of nucleoprotein antigen in the glomeruli of LCMV carrier mice of several strains was demonstrated by immunofluorescent staining with a monospecific antibody. In addition, Ig eluted from kidneys of three strains of LCMV carrier mice was shown by immune precipitation to react against all of major viral polypeptides of LCMV. Antibody from normal mice, and from mice with immune complex disease unrelated to LCMV did not show deposition of LCMV antigen in glomeruli, and Ig eluted from the kidneys of these mice did not react against LCMV antigens. Hence, mice infected at birth with LCMV and persistently infected throughout their life make antibodies to all the known structural polypeptides of the virus.

Animals↗
PubMed1977

Variation between strains of hamsters in the lethality of Pichinde virus infections.

Infection by Pichinde virus, a member of the arenavirus group, was studied in Golden Syrian hamsters (Mesocricetus auratus) with regard to possible mechanisms of resistance to virus infection in adult hamsters. Two hamster strains were found to differ in their susceptibility to lethal Pichinde virus infection. LVG/Lak randomly bred hamsters were found to be 100% susceptible to low doses of Pichinde virus during the first 6 days of life, but after 8 days of life, mortality was uncommon. Peak virus titers in the serum of animals infected at 3 days of life were 4 logs greater than in animals infected at 12 days. MHA/Lak inbred hamsters, in contrast, were found to be susceptible to lethal virus infection both as newborns and as adults. Peak virus titers of greater than 10(8) plaque-forming units/ml were observed in serum 8 days after infection of adult MHA hamsters as compared with less than 10(3) plaque-forming units/ml in the serum of adult LVG hamsters. Cultured primary kidney cells and peritoneal macrophages from either hamster strain supported Pichinde virus replication equally well in vitro. Antibodies to the complement-fixing antigens and to antigens at the surface of virus-infected cells were produced by both strains of hamsters. Cyclophosphamide immunosuppression rendered adult LVG animals susceptible to lethal infections, and virus grew to high titers in the treated animals. These findings suggest that immunological factors that appear early in life in LVG hamsters and are deficient in MHA hamsters limit Pichinde virus infection. Unlike previously reported arenavirus diseases, the observations suggest that death is produced by a direct viral effect and not through immunopathological mechanisms.

Animals↗
PubMed1977

Antigens of Pichinde virus I. Relationship of soluble antigens derived from infected BHK-21 cells to the structural components of the virion.

Antigens detected by the complement-fixation (CF) test were prepared from BHK-21 cells infected with Pichinde virus. The preparations contained two antigens demonstrable by immunodiffusion. The antigen present in abundance was heat stable, Pronase resistant, and had a molecular weight of 20,000 to 30,000 as estimated by gel filtration. Polyacrylamide gel electrophoresis of purified antigen demonstrated two low-molecular-weight polypeptides. An identical antigenic determinant was found by disrupting purified virus with Nonidet P-40; however, none of the viral polypeptides co-migrated with the polypeptides derived from purified CF antigen. Pronase digestion of disrupted virus did not alter antigenicity but degraded the viral peptides to sizes similar to those associated with the major CF antigen. These observations suggest that the major CF antigen of Pichnide virus is a cleavage product of the structural proteins of the virus.

Antigens, Viral↗
PubMed1977

The reticuloendothelium as the target in a virus infection. Pichinde virus pathogenesis in two strains of hamsters.

The course of Pichinde virus infection in two strains of hamsters, LVG and MHA, was studied by sequential frozen-section immunofluorescence and light and electron microscopy. The major destructive effects of the infection were in the spleen and liver. In the spleen, primary target cells were macrophages in the marginal zone of the white pulp with subsequent spread into elements of the red pulp. In the liver, there was Kupffer cell and hepatocellular infection. The extent of involvement correlated with the outcome of infection; more extensive and progressive necrosis occurred in the fatally infected MHA than in the LVG strain in which infection was self-limiting. In neither strain of animal was there demonstrable infection of lymphoid cells. Similarly, lesion sites did not have mononuclear inflammatory infiltrations which are characteristic of most viral infections. These findings suggested that, in contrast to the situation in other rodent arenavirus infections, the lesions in these hamsters were probably not consequences of immunopathologic host response but rather were a result of direct viral effects in concert with a genetically determined host susceptibility.

Animals↗
PubMed1976

Inhibition of Pichinde virus replication by actinomycin D.

The yields of Pichinde virus, a member of the arenavirus group, were markedly inhibited when infected BHK 21 cells were incubated in the presence of 0.4 to 4 mug/ml of actinomycin D. Maximal inhibition was observed when actinomycin D was added after the adsorption of virus to cultures; however, addition of drug as late as 12 h after infection reduced the 24 h yield by 50%. Virus antigen synthesis, as measured by complement fixation and immunodiffusion, was not dramatically reduced by actinomycin D. The expression of virus antigens on the surface of infected cells was greater on cells treated with actinomycin D than on untreated cells. Putative defective particles with a density of Pichinde virus were not detected in fluids of cultures incubated with actinomycin D and 3H-amino acids. Actinomycin D appears to inhibit Pichinde virus late in the replicative cycle. The observations raise the possibility that the drug inhibits the synthesis of proteins of the host cell membrane which are required for virus maturation.

Antigens, Viral↗
PubMedDate not supplied

Longitudinal analysis of behavioral, neurophysiological, viral and immunological effects of SIV infection in rhesus monkeys.

A model is proposed in which a neurovirulent, microglial-passaged, simian immunodeficiency virus (SIV) is used to produce central nervous system (CNS) pathology and behavioral deficits in rhesus monkeys reminiscent of those seen in humans infected with human immunodeficiency virus (HIV). The time course of disease progression was characterized by using functional measures of cognition and motor skill, as well as neurophysiologic monitoring. Concomitant assessment of immunological and virological parameters illustrated correspondence between impaired behavioral performance and viral pathogenesis. Convergent results were obtained from neuropathological findings indicative of significant CNS disease. In ongoing studies, this SIV model is being used to explore the behavioral sequelae of immunodeficiency virus infection, the viral and host factors leading to neurologic dysfunction, and to begin testing potential therapeutic agents.

Animals↗
PubMedDate not supplied

High efficiency immunoaffinity purification of anti-peptide antibodies on thiopropyl sepharose immunoadsorbants.

Antibodies to peptides are routinely made by immunizing animals with peptide linked to a carrier protein such as keyhole limpet hemocyanin (KLH) or bovine serum albumin (BSA) via a disulfide bond. The majority of such a polyclonal antibody response is directed against the carrier protein. The presence of such background antibodies often complicates efforts to characterize the desired anti-peptide antibody; hence it is desirable to isolate the specific fraction of immunoglobulin reactive against the peptide of interest. We describe here a simple and efficient technique to purify anti-peptide antibodies from such sera using commercially available reagents. Peptide antigen with a carboxy or amino terminal cysteine is coupled to thiopropyl Sepharose via a disulfide linkage. The bond between peptide and propyl group on Sepharose was stable at neutral and acidic pHs, and affinity bound anti-peptide antibodies were eluted from the column at low pH (pH 3.0). This procedure permits purification of anti-peptide antibodies, separating them from usually high-titered antibodies to the carrier protein. We describe the application of this method for purification of antibodies to two peptides derived from the glycoprotein sequence of lymphocytic choriomeningitis virus, as well as sequences derived from the human acetylcholine receptor.

Amino Acid Sequence↗