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Biomedical subjects

A L Notkins

Publications and source records attributed to A L Notkins.

At least 253 records · Page 14Linked to original sources
PubMed1974

Production of chemotactic factor and lymphotoxin by human leukocytes stimulated with Herpes simplex virus.

Peripheral blood leukocytes (PBL) of 41 subjects were tested for their ability to be stimulated by herpes simplex virus antigens as measured by [(3)H]thymidine incorporation and lymphokine production (i.e., lymphocyte-derived chemotactic factor and lymphotoxin). The PBL of seronegative subjects failed to respond to viral antigens as measured by stimulation or lymphokine production. In contrast, PBL from seropositive subjects without clinical lesions of herpes labialis were stimulated by herpes simplex virus antigens and produced lymphokines. PBL from seropositive patients with clinical lesions of herpes labialis also produced lymphokines, but [(3)H]thymidine incorporation was slightly depressed. These findings suggest that lymphocytes from patients with a recent herpes simplex virus infection may respond less vigorously to in vitro stimulation by herpes antigens, but our study fails to show any basic defect in the responsiveness of the lymphocytes to account for recurrent herpetic episodes.

Animals↗
PubMed1974

Virus-induced diabetes mellitus. II. Relationship between beta cell damage and hyperglycemia in mice infected with encephalomyocarditis virus.

Infection of DBA 2 male mice with the M variant of encephalomyocarditis virus resulted in a diabetes-like syndrome. Histologic examination of the pancreas revealed damage to the beta cells with little involvement of the acinar cells. The severity of the hyperglycemia correlated closely with the degree of beta cell damage. By immunofluorescence, viral antigens could be detected in the beta cells during the first 10 days of the infection. In contrast to the response found in male DBA 2 mice, infection of DBA 2 female mice and male mice of several other strains resulted in little if any elevation of blood glucose concentration. Histologic examination of the pancreas of these animals revealed only minimal damage to the beta cells. It is concluded that differences in the severity of the hyperglycemia between DBA 2 males and females and among the different strains of male mice tested are directly related to the degree of beta cell damage produced by the viral infection.

Animals↗
PubMed1973

Virus-induced diabetes mellitus. I. Hyperglycemia and hypoinsulinemia in mice infected with encephalomyocarditis virus.

Infection of DBA/2N male mice with encephalomyocarditis virus resulted in a diabeteslike syndrome characterized by hyperglycemia, glycosuria, hypoinsulinemia, polydipsia, and polyphagia. Blood glucose levels were elevated within 4 days after infection and reached a maximum mean level of 320 mg/100 ml within 12 days. Approximately 60-80% of the animals developed a transient hyperglycemia while 10-15% of the animals remained hyperglycemic for well over 6 mo. The remaining animals failed to become hyperglycemic but many had abnormal glucose tolerance curves. Hyperglycemia was most pronounced when animals were allowed free access to food, and the incidence of byperglycemia was related both to the strain and sex of the animals, with few females developing hyperglycemia. The amount of immunoreactive insulin in the plasma of infected hyperglycemic mice was significantly lower than in appropriate controls, and injection of exogenous insulin resulted in a rapid drop in the blood glucose levels. Despite the fact that certain animals were hyperglycemic for many months, virus could not be recovered from the pancreas after the first 10 days of the infection.

Animals↗
PubMed1973

Prevention of cell-to-cell spread of herpes simplex virus by leukocytes.

Antibody to herpes simplex virus (HSV) plus complement destroyed HSV-infected cells but did not stop the spread of the infection. Studies on the relationship between the time of appearance of viral antigens on the cell surface, immunological destruction of the cells by antiviral antibody and complement, and transfer of the virus to adjacent cells showed that the virus spread from infected to uninfected cells before the infected cells were susceptible to immunological destruction. Incubation of infected monolayers with leukocytes, however, stopped the spread of the virus by nonspecifically damaging both infected and uninfected cells and by presumably breaking intercellular bridges. When leukocytes were removed from infected monolayers, viral plaques developed. If, however, antiviral antibody and complement were added to monolayers before the leukocytes were removed, the development of plaques was prevented. These findings suggest that both antibody and leukocytes are needed to cure HSV infections.

Animals↗
PubMed1973

Comparison of direct and indirect solid-phase microradioimmunoassays for the detection of viral antigens and antiviral antibody.

Viral antigens were fixed to the surface of microtiter wells, and serial dilutions of antiviral antibody were added. The amount of antiviral antibody bound to viral antigens was determined by measuring the extent to which the antiviral antibody either inhibited the specific binding of (125)I-labeled antiviral immunoglobulin G (IgG) (direct technique) or enhanced the specific binding of (125)I-labeled anti-IgG (indirect technique). Immune complexes composed of viral antigens and antiviral antibody (human) could be detected by the binding of (125)I-labeled rheumatoid factor. Specific binding was influenced by the concentration of protein in the diluents used during the different steps of the procedure. A high concentration of protein in the diluent used with the viral antigens decreased specific binding, whereas a high concentration of protein in the diluent used with (125)I-labeled anti-IgG increased specific binding by decreasing nonspecific attachment of the labeled anti-IgG. Under the conditions employed, the titer of a given antiviral serum was several hundredfold greater by the indirect than by the direct technique.

Animals↗
PubMed1973

Inhibition of replication of lactic dehydrogenase virus by actinomycin.

Lactic dehydrogenase virus replicated rapidly in monolayers of primary mouse embryo cells and reached a titer of 10(8) mean infective dose per ml within 18 h after infection. Despite the high virus yield, cytopathology was not observed. Examination of the tissue culture media failed to reveal any evidence of interferon, but the virus was found to be as sensitive to mouse interferon as vesicular stomatitis virus. Incubation of mouse embryo cells with actinomycin D markedly inhibited viral replication, whereas cytosine-beta-d-arabinofuranoside and 5-fluorodeoxyuridine had no effect on replication. These findings indicate that new DNA synthesis is not required but suggest that the intact function of cellular DNA may be required for lactic dehydrogenase virus replication.

Animals↗
PubMed1973

Incorporation of labeled precursors into the RNA and proteins of lactic dehydrogenase virus.

Lactic dehydrogenase virus was grown in primary mouse embryo cells and labeled with (3)H-uridine and (3)H-amino acids. Concentrated and purified virus was banded by isopycnic centrifugation in sucrose gradients, and infectivity and radioactivity were found to correspond at a density of 1.17 g/cm(3). The extracted viral RNA was resolved by electrophoresis in polyacrylamide-agarose mixed gels, and the mol wt was estimated to be 6.0 x 10(6).

Amino Acids↗