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Biomedical subjects

S G Pahwa

Publications and source records attributed to S G Pahwa.

8 recordsLinked to original sources
PubMed1989

Detection of HIV-specific antibodies in infancy by isoelectric focusing and affinity immunoblotting.

Asymptomatic congenital HIV infection cannot be diagnosed in infants less than 15 mo by routine serologic techniques because of the presence of passively acquired maternal antibody in the infants' circulation. Possibly, infants who synthesize antibody to highly conserved HIV proteins may be recognized by the detection in serum of clonally distinct IgG antibodies to HIV. To test this hypothesis, isoelectric focusing in thin-layer agarose gels was combined with affinity immunoblotting to antigen-coated nitrocellulose membranes. In all 10 cases examined, the presence or absence of clonotypically distinct bands of IgG antibodies was concordant with infectious status. Thus, this technique may provide an accurate serologic approach to the diagnosis of congenital HIV infection.

Acquired Immunodeficiency Syndrome↗
PubMed1985

A classification of HTLV-III infection based on 75 cases seen in a suburban community.

Since 1981, 75 patients have been seen at our hospital with human T-cell lymphotropic virus type III (HTLV-III) infection. We have classified their clinical presentation into Groups 0 to 6. Groups 0 to 3 all have antibody to the Mr 41,000 protein of HTLV-III. Group 0 has no evident disease (9 patients), Group 1 has lymphadenopathy with or without exaggerated infection (16 patients), Group 2 has persistent lymphadenopathy with chronic hepatitis B surface antigenemia or profound hypergammaglobulinemia (7 patients), Group 3 has oral candidiasis with or without lymphadenopathy (7 patients). In Group 4 are acquired immunodeficiency syndrome (AIDS) adults or children (32 patients). Group 5 is a special classification for immunocompromised patients. Group 6 patients have lymphomas and Mr 41,000 protein antibody. Four children were classified separately. Three patients in Group 3 developed Group 4 disorders (AIDS). Four patients in Group 4 developed Group 6 disorders. HTLV-III infection spread in families (8 of 36), all from infected mothers to children. In 17 sexual partners, 6 were found to be infected. Five of 6 infected partners were homosexuals. We saw an inordinate number of transfusional AIDS (4 of 29) and 1 of 46 other disorders. Two infants also presented with severe intracranial defects, one with microcephaly and one with cranial calcifications and lucency. HTLV-III is spreading with alarming speed.

Acquired Immunodeficiency Syndrome↗
PubMed1979

T-lymphocyte differentiation in vitro in severe combined immunodeficiency. Defects of stem cells.

A study of T-lymphocyte differentiation was made on fractionated bone marrow cells from normal volunteers and from 11 patients with severe combined immunodeficiency (SCID) using normal thymic epithelial monolayers and their culture supernates as inducing agents. Normal marrow cells could regularly be induced to bear the human T-lymphocyte antigen (HTLA), to form rosettes with sheep erythrocytes (E rosettes), and to respond to the mitogen concanavalin A (Con A) after coculture with the thymic epithelial monolayers or their culture supernates. In contrast, studies of T-cell differentiation on the marrow cells of patients with SCID revealed varying defects, ranging from a complete "absence" of definable T-cell precursors to partial differentiation resulting in acquisition of one (HTLA) or two (HTLA and E rosettes) markers for T lymphocytes. Only in one patient was there induction of all three T-cell markers, namely, HTLA, E rosettes, and responsiveness to Con A. These observations indicate that SCID is a heterogeneous disorder in which defects of differentiation can occur at one or more multiple sites of differentiation leading the the clinical expression of T- and B-cell dysfunction. Further, our studies indicate that in T-cell differentiation, HTLA probably appears before the capacity to form E-rosettes, and development of the latter capacity is followed by a state of responsiveness to mitogens. A scheme of normal differentiation along with the defects of precursor T cells seen in SCID is presented.

Antigens, Surface↗
PubMed1978

Chemotactic defects in severe combined immunodeficiency.

Cellular and humoral components of leukotaxis were studied serially in four male infants with severe combined immunodeficiency disease. Two of the four, both lacking B and T cells initially, had a significant defect in neutrophil and monocyte chemotaxis. The other two, who had a high number of immunoglobulin-bearing cells (B cells), did not have these cellular abnormalities. It contrast, defective generation of chemotactic factor following endotoxin activation was observed in all patients. The defects were corrected coincident with or soon after successful engraftment of either bone marrow or fetal tissues. The reported deficiencies may be another manifestation of the heterogeneity in SCID.

B-Lymphocytes↗
PubMed1977

Cellular and humoral components of monocyte and neutrophil chemotaxis in cord blood.

Monocyte and polymorphonuclear neutrophil (PMN) chemotaxis was studied in cord blood from healthy term infants. Monocyte chemotaxis was normal to increased (115-126%) whereas PMN chemotaxis was decreased (79%) in comparison with that of healthy adult control subjects. Generation of chemotactic factors from cord sera was impaired, being 55% of that generated by pooled normal human serum (PNHS). Cord serum was less inhibitory than pooled adult human serum for adult monocytes when the cells were suspended in 10% serum and tested for chemotaxis. No inhibition of chemotactic factors by either cord or adult sera was observed. The dissociation of chemotactic response of the two different phagocytic cells may represent a protective mechanism whereby one cell can compensate for a defect in the response of the other.

Chemotaxis, Leukocyte↗