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Biomedical subjects

V G Pons

Publications and source records attributed to V G Pons.

22 records · Page 2Linked to original sources
PubMed1980

Influenza A/USSR/77 (H1N1) on a university campus.

An extensive outbreak of influenza caused by A/USSR/77 (H1N1) virus occurred in February, 1978, at the University of Maryland, College Park, Maryland, and the outbreak was studied by virus isolation, serology, clinical questionnaire and outpatient chart review. Among students who returned questionnaires, clinical attack rates were extraordinarily high (73.2% of those less than or equal to 23 years of age and 45.7% for those greater than 23 years (p less than 0.001)), and rates were higher in students who lived on campus (p less than 0.05). Employing the criterion of hemagglutination inhibition titer greater than or equal to 16, 89.8% of those less than or equal to 23 years of age had evidence of infection by March, 1978. Illness was generally mild, and no complications were reported. The extent and rapid spread of this outbreak suggested that only immunoprophylaxis or rapidly acting control measures such as chemoprophylaxis would be effective in this institutional setting with a highly susceptible population.

Adolescent↗
PubMed1979

Cell-mediated cytotoxicity following influenza infection and vaccination in humans.

Cell-mediated cytotoxic activity in circulating mononuclear cells from 31 volunteers challenged with live influenza A/Victoria virus, and 22 volunteers vaccinated with inactivated influenza vaccine, was examined employing target cells infected with several viruses by means of a 51Cr release assay. Effectors from infected volunteers, and from volunteers who manifested four-fold rises in serum HAI antibody after vaccination, demonstrated significantly elevated levels of cytotoxicity against targets infected with the homologous virus. Elevated cytotoxicity was seen by days 3 and 4 after challenge or vaccination and returned to baseline levels by day 9 to 10. In infected volunteers, cytotoxic activity was broadly directed, rising against targets infected with an antigenically distinct virus within the same influenza type (A), against targets infected with a serologically unrelated virus of a different influenza type (B), and also against cells infected with Newcastle disease virus, a paramyxovirus from another species. However, elevated levels of cytotoxicity were not observed when targets infected with herpes simplex virus, a member of an entirely different virus group, or when uninfected target cells were employed. In vaccinated volunteers, the rise in cytotoxicity was more restricted than after infection, since elevated cytotoxic activity was seen only against cells infected with the homologous virus and not against inflenza B-infected cells. Fractionation of mononuclear cell populations indicated that effector cell activity is associated with T-cell depleted fractions and can only partially be reduced by depletion of adherent cells. The rapid development, short duration, and broadly directed specificity of this cytotoxic response suggest that it may be involved in early events following acute influenza infection in humans.

Adolescent↗
PubMed1979

Decreased cell-mediated cytotoxicity against virus-infected cells in systemic lupus erythematosus.

Cell-mediated cytotoxicity, directed against virus-infected tissue culture cells, was studied with peripheral blood mononuclear cells from 11 patients with systemic lupus erythematosus (SLE) and 12 matched, normal subjects in a 51Cr release assay. Baseline (preimmunization) levels of cytotoxicity against target cells infected with influenza A/Victoria, influenza B/Hong Kong, Newcastle disease virus, and herpes simplex virus were significantly decreased in patients with SLE compared to normal subjects (P less than 0.001), although serum antibody levels to the respective viruses were similar in both groups. After intramuscular administration of inactivated influenza A/Victoria vaccine, SLE patients failed to generate elevated levels of cytotoxicity against A/Victoria-infected cells, in contrast to normal subjects. SLE patients responded with levels of serum hemagglutination-inhibition antibody which were similar to those of normal subjects. Thus, SLE patients manifest decreased cell-mediated cytotoxicity against virus-infected target cells, although humoral antibody responses appeared to be intact. Studies of SLE patients with influenza may help to define the role of cell-mediated immunity in the pathogenesis of certain viral infections.

Adolescent↗