洪健清2006-07-262018-07-112006-07-262018-07-112005http://ntur.lib.ntu.edu.tw//handle/246246/23691A 4-year prospective longitudinal follow-up study was conducted to assess the immunogenicity of 23-valent pneumococcal polysaccharide vaccine (PPV) among 305 HIV-1 infected individuals who received PPV and HAART between June 2000 and June 2004. 89 randomly selected vaccinees were stratified into 3 groups based on their CD4 counts at baseline: Group 1 with CD4 counts less than 100 cells/µl; Group 2 with CD4 counts between 100 and 350 cells/µl; and Group 3 with CD4 counts higher than 350 cells/µl. Antibody responses to 3 capsular antigens (14, 19F, and 23F) were performed using home-made ELISA. Changes in these parameters from baseline to week 4, and every 6 months thereafter were determined and compared using Student’s t-test. Rates of response to vaccination in different groups of vaccinees were compared using χ2 test. Vaccinees with more than 2-fold increase in antibody responses were defined as vaccine responders. We found that immunization did not cause any significant changes in CD4 counts or plasma HIV-RNA load between vaccinees of different groups. For type 14, both the percentage of responders (27% v.s. 57% v.s. 54%) and the geometric mean fold-rise of reactive antibody (1.38 v.s. 2.89 v.s. 3.05) were significantly lower for Group 1 compared with Groups 2 and 3. The duration of antibody responses in responders was similar between groups. Among the 24 responders who had been followed for more than 3 years, more than 75% of them remained seropositive for type 14 irrespective of their baseline CD4 counts. Our findings suggest that antibody responses to 23-valent PPV are poorer in HIV-infected vaccinees with baseline CD4 counts less than 100 cells/µl compared with those with baseline CD4 counts higher than 100 cells/µl. The responses may last for more than 3 years in 75% of the vaccine responders who continue to receive HAART regardless of baseline CD4 + counts. Patients with HIV infection are at higher risk for invasive infections due to Streptococcus pneumoniae as compared with those without HIV infection. Rates of invasive pneumococcal infections among AIDS patients may be as high as 100-fold greater than in HIV-seronegative controls [1]. In the era of increasing rates of antimicrobial resistance among isolates of S. pneumoniae worldwide as well as an increased risk for developing invasive pneumococcal infections among HIV-infected patients, the US Centers for Disease Control and Prevention (CDC) has strongly recommended that pneumococcal vaccination be given to patients with HIV infection who are aged ≥2 years [2] and a CD4+ count ≥200 cells/µl [3]. In addition, revaccination is recommended when the CD4+ count increases to ≥200 cells/µl in patients with an initial CD4+ count of <200 cells/µl [3]. However, these recommendations are notwithstanding, clinical studies evaluating the benefits of pneumococcal vaccination among HIV-infected patients have yielded inconsistent results [4-7]. This inconsistency may be due to variations in the study populations or designs, the receipt of antimicrobial prophylaxis or antiretroviral therapy, or study end points and outcome measures. In retrospective studies conducted in the US [4,6,7], vaccination reduced the risk for invasive pneumococcal infections among HIV-infected patients before or after the introduction of highly active antiretroviral therapy (HAART). In Uganda where HIV-infected patients had no access to antiretroviral therapy (ART) [5], immunization with the 23-valent capsular polysaccharide pneumococcal vaccine (PPV) paradoxically increased the incidence of invasive pneumococcal infections and all-cause pneumonia. The reasons for such failure of pneumococcal vaccination to confer protection against invasive pneumococcal infections in Ugandan subjects remains unclear, although destruction of B-cell function resulting from polysaccharide vaccination in those patients without HAART or an increase of plasma HIV load has been proposed [5]. There remain several potential explanations for the failure of the immunity of HIV-infected patients to protect them from pneumococcal infections, including decreased serum opsonic activity against S. pneumoniae in HIV-infected patients [8], and a local effect of altered pulmonary immunoglobulin responses to penumococcal infection [9]. In the previous study [10], we have evaluated the impact of vaccination with the 23-valent PPV on HIV-infected patients who were receiving HAART. Our data suggested that vaccination with 23-valent PPV reduced risks for pneumococcal diseases and was associated with a lower risk for death among HIV-1-infected patients receiving HAART. Vaccination did not increase the risks of all-cause community-acquired pneumonia and HIV progression, and CD4+ continued to increase and PVL decrease among HIV-infected patients receiving HAART. Despite the clinical benefits, the serologic responses to the 23-valent PPV has rarely been studied among HIV-infected patients receiving HAART; whether antibody responses increase with immune reconstitution and when the booster vaccination should be administered in HIV-infected patients receiving HAART remain to be studied. In this study, we aim to evaluate the serial changes of anti-capsular antibodies in HIV-infected patients who underwent vaccination with 23-valent PPV and received HAART with increase of CD4+ counts.application/pdf47148 bytesapplication/pdfzh-TW國立臺灣大學醫學院內科[SDGs]SDG3reporthttp://ntur.lib.ntu.edu.tw/bitstream/246246/23691/1/932314B002086.pdf