Effect of recurrent invasive pneumococcal disease on serum anti-pneumolysin IgG titres in HIV infected adults.

We measured serum anti-pneumolysin IgG concentrations in a prospective cohort of 34 HIV infected adults who developed recurrent pneumococcal bacteraemia, and compared baseline levels with HIV positive and HIV negative control subjects that remained free of pneumococcal disease. Anti-pneumolysin concentrations in HIV positive cases and controls were higher compared to HIV negative controls. There was no significant difference in levels between HIV positive subjects who did and did not subsequently develop pneumococcal bacteraemia (geometric means 849.1 U/ml vs. 564.6 U/ml, p=0.059). Anti-pneumolysin IgG titres before, and after the recurrent episode of pneumococcal bacteraemia did not differ significantly (p=0.95). High levels of anti-pneumolysin IgG do not predict protection from invasive pneumococcal disease or indicate that an effective immune response has occurred in HIV infected patients.

Lung fluid immunoglobulin from HIV-infected subjects has impaired opsonic function against pneumococci.

BACKGROUND: The incidence of pneumococcal pneumonia is greatly increased among human immunodeficiency virus (HIV)-infected subjects, compared with among non-HIV-infected subjects. Lung fluid levels of immunoglobulin G (IgG) specific for pneumococcal capsular polysaccharide are not reduced in HIV-infected subjects; therefore, we examined immunoglobulin subtypes and compared lung fluid IgG opsonic function in HIV-infected subjects with that in healthy subjects. METHODS: Bronchoalveolar lavage (BAL) fluid and serum samples were collected from 23 HIV-infected and 26 uninfected subjects. None of the subjects were receiving highly active antiretroviral therapy, and none had received pneumococcal vaccination. Pneumococcal capsule-specific IgG levels in serum and BAL fluid were measured by enzyme-linked immunosorbent assay, and IgG was concentrated from 40 mL of BAL fluid. Opsonization and opsonophagocytosis of pneumococci with serum, BAL fluid, and BAL IgG were compared between HIV-infected subjects and healthy subjects. RESULTS: The effect of type 1 pneumococcal capsular polysaccharide-specific IgG in opsonizing of pneumococci was significantly less using both serum and BAL IgG from HIV-infected subjects, compared with serum and BAL IgG from healthy subjects (mean level, 8.9 fluorescence units [95% confidence interval, 8.1-9.7 fluorescence units] vs. 12.1 fluorescence units [95% confidence interval, 9.7-15.2 fluorescence units]; P=.002 for lung BAL IgG). The opsonophagocytosis of pneumococci observed using BAL IgG from HIV-infected subjects was significantly less than that observed using BAL IgG from healthy subjects (37 fluorescence units per ng of IgG [95% confidence interval, 25-53 fluorescence units per ng of IgG] vs. 127 fluorescence units per ng of IgG [95% confidence interval, 109-145 fluorescence units per ng of IgG]; P<.001). CONCLUSION: HIV infection is associated with decreased antipneumococcal opsonic function in BAL fluid and serum.

Conjugate pneumococcal vaccine in HIV-infected Ugandans and the effect of past receipt of polysaccharide vaccine.

We investigated the immunogenicity of a 7-valent conjugate pneumococcal vaccine (CPV) in human immunodeficiency virus-infected Ugandan adults and measured the effect of past pneumococcal polysaccharide vaccine (PPV) receipt given as part of a controlled trial. Two doses of CPV, 4 weeks apart, were given to 54 past PPV recipients and 55 past placebo recipients (84% female; median CD4 cell count, 251 cells/ microL [range, 1-936 cells/ microL]). Postvaccination anticapsular immunoglobulin G (IgG) concentrations were directly correlated with CD4 cell count (P < .01 for all serotypes). There were significant increases in anticapsular IgG concentrations for all serotypes after the first dose (P < .01) and for all serotypes except 14 and 9V after the second dose. Past receipt of PPV did not affect vaccine response.