Antibody Class and Subclass Responses to Pneumococcal Polysaccharides following Immunization of Human Immunodeficiency Virus-Infected Patients

Carson, Paul J.; Schut, Ronald L.; Simpson, Margaret; O'Brien, James; Janoff, Edward N.

doi:10.1093/infdis/172.2.340

Cited by 78 publications

(45 citation statements)

References 32 publications

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“…Furthermore, even children older than 2 years who have HIV infections and were vaccinated with the 23vPPV did not respond well to the polysaccharide antigen, when compared with controls. 16 Just six children were more than 2 years old at the time of data collection and none of them had been given the 23vPPV, already available at that time, confirming the published data that states that selective vaccination of high-risk groups is less efficient than vaccination of all children.…”

Section: Discussionsupporting

confidence: 71%

Doença pneumocócica invasiva em crianças e adolescentes soropositivos para HIV

Mattei¹,

Falleiros-Carvalho²,

Cavalcante³

2008

J. Pediatr. (Rio J.)

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Objective: Invasive pneumococcal disease (IPD) primarily affects children less than 5 years old, the elderly and certain at-risk groups; especially people infected by the human immunodeficiency virus (HIV). The objective of this study was to analyze invasive pneumococcal diseases (IPD) in children and adolescents infected by the human immunodeficiency virus (HIV), with relation to morbidity, the case fatality ratio, pneumococcus serotypes, susceptibility to penicillin and ceftriaxone and to the proportion of susceptible and resistant Streptococcus pneumoniae (Sp) included in the 7-valent pneumococcal conjugate vaccine that has already been licensed. Methods:A total of 19 cases of IPD were identified among HIV seropositive patients aged from 1 month to 20 years and hospitalized between 1993 and 2000. Data were recorded on standardized charts containing information on age, clinical diagnosis and progression, serotypes and the susceptibility to penicillin and ceftriaxone of the Sp strains identified in cultures. When the minimum inhibitory concentration was < 0.1 mcg/mL, Sp were defined as susceptible to penicillin (SpSPn), and all other strains were defined as not susceptible (SpNSPn). Results:Of the 19 HIV seropositive cases with IPD, 16 (84%) had pneumonia and three (16%), had meningitis; 13 (68%) cases were children less than 2 years old and 16 (84%) were less than 5 years old. The case fatality ratio was 10%. Seven (54%) of the 13 cases less than 2 years old were SpNSPn and 10 (77%) were caused by serotypes covered by the 7-valent pneumococcal conjugate vaccine. From the 10 isolated serotypes the most frequent were 14, 6B and 23F, all them susceptible to ceftriaxone. From the three patients with meningitis, two were caused by SpNSPn. Conclusion:In this study most of the IPD occurred in children less than 2 years old; 77% of the strains and 86% of the serotypes of SpNSPn were covered by the 7-valent pneumococcal conjugate vaccine.J Pediatr (Rio J). 2008;84(3):276-280: Pneumococcus, Streptococcus pneumoniae, children, adolescents, HIV seropositive, meningitis, pneumonia, invasive pneumococcal disease, antipneumococcal vaccine.

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Section: Discussionsupporting

confidence: 71%

Doença pneumocócica invasiva em crianças e adolescentes soropositivos para HIV

Mattei¹,

Falleiros-Carvalho²,

Cavalcante³

2008

J. Pediatr. (Rio J.)

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“…200 cells/mL after receipt of HAART and for those patients who have undergone pneumococcal polysaccharide vaccination 5 years earlier [13]. However, most studies conducted in patients not receiving HAART suggest that HIV-infected patients have a significantly lower frequency and magnitude of antibody response to vaccination with 23-valent PPV than those without HIV infection, and antibody titres [immunoglobulin G (IgG) or IgM] appear to be associated with CD4 cell count and decrease more rapidly in HIV-infected patients [14][15][16][17][18][19][20][21][22]. Interpretation of studies conducted in the HAART era is limited by different durations of and immunological and virological responses to HAART, different vaccination schedules and short-term observation of antibody responses [23][24][25][26][27].…”

Section: Discussionmentioning

confidence: 99%

“…Studies investigating short-term serological responses to 23-valent PPV in HIV-infected patients have not produced consistent results [14][15][16][17][18][19][20][21][22][24][25][26][27][30][31][32][33][34][35][36][37][38], and only one study assessed the rate of antibody decline for five consecutive HAART, highly active antiretroviral therapy; MSM, men who have sex with men; PVL, plasma HIV RNA load; SD, standard deviation.…”

Section: Discussionmentioning

confidence: 99%

A 5‐year longitudinal follow‐up study of serological responses to 23‐valent pneumococcal polysaccharide vaccination among patients with HIV infection who received highly active antiretroviral therapy^*

Chang

et al. 2009

HIV Medicine

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BackgroundLong-term antibody responses to 23-valent pneumococcal polysaccharide vaccine (PPV) among HIV-infected patients receiving highly active antiretroviral therapy (HAART) are rarely investigated. MethodsAntibody responses to three pneumococcal capsular polysaccharides [Pneumococcal polysaccharide (PPS) 14, 19F and 23F] were assessed among 169 HIV-infected patients who received HAART and 23-valent PPV. Patients were stratified into four groups according to CD4 count at vaccination: group 1, CD4o100 cells/mL (n 5 35); group 2, CD4 100-199 cells/mL (n 5 36); group 3, CD4 200-349 cells/mL (n 5 34); and group 4, CD4 ! 350 cells/mL (n 5 64). The proportion of patients who achieved increases in antibody titres of twofold or greater from baseline values (responders) was compared among the four groups of patients for five consecutive years after vaccination. ResultsThe proportion of responders to the three serotypes was significantly lower among patients in group 1 compared with those in the other three groups during yearly follow-up. Much faster loss of antibody responses was observed in group 1, although the rate of decline varied with the serotypes studied in the four groups. Compared with the nonresponders, more responders had CD4 counts 4100 cells/mL at vaccination and achieved better virological suppression throughout the 5-year period, while the absolute increases of CD4 cell counts after HAART were not statistically significantly different. ConclusionsDespite continued increases in CD4 cell counts after HAART, the proportion of HIV-infected patients who maintained antibody responses to PPV declined significantly over the 5-year follow-up period, especially among those who had CD4 counts o100 cells/mL at vaccination and who failed to achieve virological suppression. DOI: 10.1111/j.1468-1293.2009.00744.x HIV Medicine (2010 r 2009 British HIV Association 54 antiretroviral therapy (HAART) [1]. Although cohort or population-based surveillance studies suggest that the incidence of invasive pneumococcal infections or pneumococcal pneumonia declines among HIV-infected patients with access to HAART and appropriate antimicrobial prophylaxis [2,4,6,7], it remains significantly higher among HIV-infected patients than in the general population, with risk ratios ranging from 35 to 60 [2][3][4]. In observational studies conducted in several developed countries, vaccination with 23-valent pneumococcal polysaccharide vaccine (PPV) has been shown to decrease the risk of invasive pneumococcal infections among HIVinfected patients [5,[8][9][10][11][12]. According to U.S. Public Health Service/Infectious Diseases Society of America (USPHS/ IDSA) guidelines, it is recommended that patients with HIV infection who have CD4 lymphocyte counts of 4200 cells/mL should receive 23-valent PPV, and revaccination can be considered for those patients who have initial CD4 counts of o200 cells/mL and whose CD4 counts increase to ! 200 cells/mL after receipt of HAART and for those patients who have undergone pneumococcal polysaccharide v...

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“…We recently reported that up to a third of serum antibodies that are reactive with the polysaccharide capsule of an invasive mucosal Gram-positive organism, Streptococcus pneumoniae, are of the IgA class (14,15). The majority of this pathogen-specific IgA in serum is in the polymeric form (≥ 2 IgA molecules bound by a J chain) and remains polymeric long after immunization or infection (15), even though about 90% of the total IgA in serum is in the monomeric form (5).…”

Section: Introductionmentioning

confidence: 99%

“…S. pneumoniae may colonize the nasopharyngeal mucosa without sequelae but also commonly causes serious invasive clinical syndromes, including pneumonia, bacteremia, and meningitis in children and adults (16)(17)(18)(19). Natural infection and immunization elicit capsule-specific polymeric IgA (pIgA) responses in blood and at mucosal sites (14,15,(20)(21)(22). Thus, pIgA may play a functional role at both mucosal and systemic sites.…”

Section: Introductionmentioning

confidence: 99%

Killing of Streptococcus pneumoniae by capsular polysaccharide–specific polymeric IgA, complement, and phagocytes

Janoff¹,

Fasching²,

Orenstein³

et al. 1999

J. Clin. Invest.

131

129

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The role of IgA in the control of invasive mucosal pathogens such as Streptococcus pneumoniae is poorly understood. We demonstrate that human pneumococcal capsular polysaccharide-specific IgA initiated dose-dependent killing of S. pneumoniae with complement and phagocytes. The majority of specific IgA in serum was of the polymeric form (pIgA), and the efficiency of pIgA-initiated killing exceeded that of monomeric IgA-initiated killing. In the absence of complement, specific IgA induced minimal bacterial adherence, uptake, and killing. Killing of S. pneumoniae by resting phagocytes with immune IgA required complement, predominantly via the C2-independent alternative pathway, which requires factor B, but not calcium. Both S. pneumoniae-bound IgA and complement were involved, as demonstrated by a 50% decrease in killing with blocking of Fcα receptor (CD89) and CR1/CR3 (CD35/CD11b). However, IgA-mediated killing by phagocytes could be reproduced in the absence of opsonic complement by pre-activating phagocytes with the inflammatory products C5a and TNF-α. Thus, S. pneumoniae capsule-specific IgA may show distinct roles in effecting clearance of S. pneumoniae in the presence or absence of inflammation. These data suggest mechanisms whereby pIgA may serve to control pneumococcal infections locally and upon the pathogen's entry into the bloodstream.

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Antibody Class and Subclass Responses to Pneumococcal Polysaccharides following Immunization of Human Immunodeficiency Virus-Infected Patients

Cited by 78 publications

References 32 publications

Doença pneumocócica invasiva em crianças e adolescentes soropositivos para HIV

Doença pneumocócica invasiva em crianças e adolescentes soropositivos para HIV

A 5‐year longitudinal follow‐up study of serological responses to 23‐valent pneumococcal polysaccharide vaccination among patients with HIV infection who received highly active antiretroviral therapy^*

Killing of Streptococcus pneumoniae by capsular polysaccharide–specific polymeric IgA, complement, and phagocytes

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Antibody Class and Subclass Responses to Pneumococcal Polysaccharides following Immunization of Human Immunodeficiency Virus-Infected Patients

Cited by 78 publications

References 32 publications

Doença pneumocócica invasiva em crianças e adolescentes soropositivos para HIV

Doença pneumocócica invasiva em crianças e adolescentes soropositivos para HIV

A 5‐year longitudinal follow‐up study of serological responses to 23‐valent pneumococcal polysaccharide vaccination among patients with HIV infection who received highly active antiretroviral therapy*

Killing of Streptococcus pneumoniae by capsular polysaccharide–specific polymeric IgA, complement, and phagocytes

Contact Info

Product

Resources

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A 5‐year longitudinal follow‐up study of serological responses to 23‐valent pneumococcal polysaccharide vaccination among patients with HIV infection who received highly active antiretroviral therapy^*