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Biomedical subjects

J A Winkelstein

Publications and source records attributed to J A Winkelstein.

At least 109 records · Page 6Linked to original sources
PubMed1981

Genetically determined deficiency of the third component of complement in the dog.

A genetically determined deficiency of the third component of complement (C3) has been identified in a colony of Brittany spaniels. Immunochemical methods show no detectable C3 in the serum of the affected dogs, and there is no evidence of an inhibitor of C3 in the serum. The C3 deficiency appears to be transmitted as an autosomal recessive trait.

Animals↗
PubMed1981

Host modification of Sindbis virus sialic acid content influences alternative complement pathway activation and virus clearance.

Previous studies have shown that Sindbis virus, an enveloped alphavirus of the togavirus group, activates the alternative complement pathway in the absence of detectable antiviral immunoglobulin. The present studies examined the role of the host-determined sialic acid content of Sindbis virus on activation of the alternative complement pathway. Purified Sindbis virus grown in baby hamster kidney (BHK-SV) and in mosquito (MOSQ-SV) cells yielded virus with 10.2 and less than 2.0 nmol sialic acid/mg viral protein, respectively. Sindbis virus deficient in sialic acid (2.0 nmol sialic/mg) was also produced by treating the BHK-SV with neuraminidase (NANase-SV). When MOSQ-SV or NANase-SV was incubated in either C4DGPS or C2DHS, each consumed significantly more C3 than did BHK-SV, indicating that the ability of Sindbis virus to activate the alternative pathway is inversely related to its sialic acid content. Studies in vivo showed that virus deficient in sialic acid (MOSQ-SV) was cleared from the blood of mice much more efficiently than was virus rich in sialic acid (BHK-SV), after i.v. inoculation. Furthermore, when animals were depleted of C3 through C9 by cobra venom factor (CoVF) treatment, no differences in the clearance of high and low sialic acid-containing viruses were observed. Thus both the activation in vitro and complement-dependent clearance in vivo are significantly affected by the host-determined sialic acid content of Sindbis virus.

Animals↗
PubMed1981

Immunologic studies of cartilage-hair hypoplasia in the Amish.

The immunologic status of 18 Old Order Amish persons with cartilage-hair hypoplasia and 9 unaffected sibs was studied. Although none of the subjects had a history suggestive of persistent immune dysfunction, the subjects with cartilage-hair hypoplasia had significantly lower lymphocyte mitogenic and allogeneic cell stimulation responses when compared to unaffected sibs and unrelated control subjects. The abnormalities of cellular immune function found in the 18 affected subjects were similar to those reported in Finnish subjects with cartilage-hair hypoplasia.

Adolescent↗
PubMed1981

The fixation of C3b to pneumococcal cell wall polymers as a result of activation of the alternative complement pathway.

The present study was performed in order to determine the identity of the pneumococcal cell wall polymer(s) to which C3b becomes fixed after activation of the alternative pathway. Purified pneumococcal autolysin was used to solubilize pneumococcal cell walls to which C3b had been fixed via activation of the alternative pathway. The resulting soluble cell wall polymers were then examined for the presence of C3b. Chromatographic separation of cell wall digests containing either radiolabeled teichoic acid or radiolabeled C3b demonstrated that although the elution profiles of the 2 radiolabels were similar, they were not identical. In addition, when teichoic acid-containing polymers were removed from solution by immunoabsorption with TEPC-15 myeloma, only 43 to 65% of the C3b was removed. These results demonstrate that C3b activated via the alternative pathway fixes both to teichoic acid-containing pneumococcal cell wall polymers and to other cell wall constituents and/or serum proteins bound to the cell wall.

Animals↗
PubMed1980

Chronic rotavirus infection in immunodeficiency.

The characteristics of rotavirus infection in 23 children with a variety of primary immunodeficiency diseases were studied. Stools and sera were tested for rotavirus by means of the enzyme-linked immunosorbent assay and the enzyme-linked fluorescent assay, respectively. Four immunodeficient patients had diarrhea during the study period and all had rotavirus infection; rotavirus was not detected in the stools of the 19 asymptomatic immunodeficient patients. Forty-six control children with diarrhea were tested and 22 had rotavirus infection; rotavirus was not detected in 39 asymptomatic control children. One immunodeficient patient with X-linked agammaglobulinemia and one with severe combined immunodeficiency had chronic, symptomatic rotavirus infection with rotavirus excretion lasting more than six weeks. The other two immunodeficient patients and eight control children eliminated the rotavirus from their stools in periods ranging from two to 12 days. Rotavirus antigen was detected in the sera of three of the four immunodeficient patients; none of the 14 control infants tested had rotavirus antigen detected in their sera. This study indicates that rotavirus may produce a chronic infection in immunodeficient children.

Adolescent↗
PubMed1980

The role of complement in viral infections. II. the clearance of Sindbis virus from the bloodstream and central nervous system of mice depleted of complement.

The following studies were performed to investigate the mechanism(s) by which the complement system limits Sindbis virus infection in the central nervous system of mice. After the intracerebral inoculation of Sindbis virus, no differences in mortality or viral growth in the central nervous system were observed between normal mice and mice depleted of complement by treatment with cobra venom factor. In addition, animals that had been inoculated subcutaneously with Sindbis virus and depleted of complement after the viremic phase had ended did not show any differences in mortality or viral growth in the central nervous system. In contrast, it was found that after the intracardiac inoculation of virus, complement-depleted mice demonstrated a defect in the clearance of infectious virus from the blood. These studies suggest that the increased growth of virus in the brains of complement-depleted mice after the subcutaneous inoculation of Sindbis virus is due to a defect in clearance of infectious virus from the bloodstream rather than to a primary defect within the central nervous system.

Animals↗
PubMed1980

Activation of the alternative complement pathway by Histoplasma capsulatum.

The present study was performed to determine whether Histoplasma capsulatum (yeast phase) is able to activate the alternative complement pathway. H. capsulatum yeasts were shown to consume C3 in C4-deficient guinea pig serum. Immunoelectrophoretic conversion of alternative pathway component factor B confirmed that C3 consumption was mediated by activation of the alternative pathway. These results demonstrate that H. capsulatum is able to activate the alternative complement pathway.

Animals↗
PubMed1979

Early complement component depletion and mixed cryoglobulinemia in a "healthy" family.

A family containing two apparently healthy brothers with profound early complement component depletion (C1, C4, C2) and mixed IgG-IgM polyclonal cryoglobulins was studied. The cryoglobulins possessed rheumatoid factor activity and depleted early complement components in normal human serum. Circulating immune complexes could not be detected by utilizing standard methods. The phenomenon was not HLA-linked. This study demonstrates the familial occurrence of a chronic hypocomplementemic state associated with cryoglobulinemia in clinically normal subjects.

Adult↗