human
***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Background Human immunodeficiency virus type 1 ( HIV-1 ) infected children treated with highly active antiretroviral therapy ( HAART ) may develop a significant reduction of plasma viremia associated with an increase in CD4 + T-cell counts . Functional capacity of this reconstituted immune system in response to recall antigens is important to maintain protective immunity to vaccine-preventable diseases . We therefore determined cellular and humoral immune responses to tetanus toxoid ( TT ) booster in perinatally HIV-1-infected children and adolescents receiving HAART . Methods Immune responses were prospect ively evaluated pre- and post-tetanus booster using lymphocyte proliferation assay ( LPA ) stimulation index ( SI≥3.0 ) and tetanus antibody ( TAb≥0.15 ) in 15 patients . The median interval from primary tetanus immunization series was 6 years ( range 2–12 years ) . We compared patients by their virological response to HAART ( complete responders , CR , n=7 ; incomplete responders , ICR , n=8 ) . Results There were no significant differences in median age 12.6 years ( CR : 12.9 ; ICR : 10.6 ) or median CD4 T-cell pre-booster ( CR : 35%/819 ; ICR : 26%/429 ) between groups . Tetanus LPA responses were observed in one patient prior to booster and in seven patients post-booster . In contrast , 38 % of patients had protective TAb pre-booster , but 92 % developed protective TAb post-booster . All of the CR and 5/6 ICR patients developed protective TAb . Conclusions HIV-1-infected children and adolescents  had modest LPA responses to tetanus following booster , similar to HIV-1-infected adults . However , the majority of patients developed protective TAb levels after booster and maintained the response . Shorter intervals may need to be considered for TT immunization boosters in HIV-1-infected pediatric patients , as only 38 % had protective TAb at baseline Objective To evaluate the humoral response to routine childhood immunization of HIV-infected children . Design Response rate , antibody titres and persistence after polio and tetanus vaccination were compared in 72 children with HIV seropositivity at birth and divided according to HIV infection status as determined by clinical and laboratory tests . Methods Polio antibodies were titred in a microneutralization test ( positive titres , ≥1:4 ) , and antibody to tetanus toxoid with a passive haemagglutination method ( protective titres , ≥1:1024 ) . Results The response rates  to polio and tetanus vaccination ( > 80 and > 75 % ) were similar in the HIV-infected and non-infected children , as were antibody levels . In the subgroup with sera obtained some months after the last dose of vaccine , polio antibody levels decreased in all four HIV-infected and in three of the seven non-infected children ; protective tetanus antitoxin levels were detected in three of the six infected and in all three non-infected children . Conclusions This study demonstrates the ability of children with HIV infection to respond adequately to the two vaccines considered , although tetanus antitoxin levels were inferior , compared with those in the seroreverted children . The unsatisfactory antibody levels observed in the admittedly few HIV-positive children studied some months after the last vaccination could be the result of a lower initial protective level and not necessarily an expression of severely impaired immunocompetence . The administration of booster doses in addition to the traditional immunization schedule could be useful in children with HIV infection BACKGROUND We studied whether severely immunocompromised , human immunodeficiency virus (HIV)-infected children who were beginning highly active antiretroviral therapy ( HAART ) or changing HAART regimens could spontaneously respond to a recall antigen ( tetanus toxoid [ TT ] vaccine ) or respond to a recall antigen and neoantigen ( hepatitis A virus [ HAV ] vaccine ) after 3 vaccinations . METHODS A total of 46 children who had CD4 cell percentages < 15 % and who demonstrated a > 0.75-log reduction in plasma HIV RNA levels within 4 weeks of starting HAART were r and omized to receive vaccinations with either TT or HAV vaccines during the first 6 months of HAART . Study subjects then received the alternate vaccine during the next 6 months of HAART . RESULTS Despite the early decline in viremia and the later increase in the percentage of CD4 T cells , spontaneous recovery of cell-mediated immunity ( CMI ) was not seen for TT . Serologic responses to TT required 3 vaccinations and were comparable in both groups . Serologic responses to HAV were infrequent and of low titer , although the group that received HAV vaccine after receiving TT vaccine performed somewhat better . CMI to HAV was virtually absent . CONCLUSIONS Severely immunocompromised children who are receiving HAART develop CMI and antibody to a recall antigen independent of the timing of vaccination , but they require a primary series of vaccinations . Antibodies to a neoantigen , HAV , developed when vaccination was delayed after initiation of HAART . CMI to a neoantigen was difficult to establish . TRIAL REGISTRATION Clinical trials.gov identifier : NCT00004735/PACTG P1006 BACKGROUND Administration of pneumococcal conjugate vaccine ( PCV ) to HIV-infected children during infancy confers limited long-term protection in the absence of antiretroviral therapy . The objective of the present study was to determine the immune responses to PCV at 5 years of age in HIV-infected and HIV-uninfected children who had been primed with vaccine during infancy ( i.e. , previous vaccinees ) and in those receiving their first dose of vaccine ( i.e. , control subjects ) . METHODS Serotype-specific antibodies were quantified by enzyme immunoassay , and antibody functionality to serotypes 6B , 9V , and 19F were evaluated using an opsonophagocytic killing assay 1 month after vaccination . RESULTS Of the HIV-infected children , 19.7 % were receiving antiretroviral therapy , and 40.5 % had a CD4(+ ) cell percentage < 15 % .  Geometric mean concentrations of antibody and the proportion with a concentration 0.35 microg/mL after vaccination were greater among HIV-uninfected children than among HIV-infected children for both previous vaccinees and control subjects . Antibody concentrations after vaccination were lower for 3 of 7 serotypes among HIV-infected previous vaccinees than among control subjects . Detectable opsonophagocytic activity to all studied serotypes was lower among HIV-infected than among HIV-uninfected previous vaccinees and control subjects . Postvaccination antibody-mediated killing activity as determined by the opsonophagocytic killing assay was enhanced in control subjects compared with previous vaccinees among HIV-uninfected children . CONCLUSION HIV-infected vaccinees experience a partial loss of anamnestic responses to PCV . The optimal timing and frequency of booster vaccination as well as the responses to them among HIV-infected children need to be determined BACKGROUND Varicella can be a severe illness in human immunodeficiency virus (HIV)-infected children . The licensed , live attenuated varicella vaccine is safe and immunogenic in HIV-infected children with minimal symptoms and good preservation of CD4(+ ) T cells ( Centers for Disease Control and Prevention immunologic category 1 ) . METHODS To study the safety and immunogenicity of this vaccine in varicella-zoster virus (VZV)-naive , HIV-infected children with moderate symptoms and /or more pronounced past or current decreases in CD4(+ ) T cell counts , such children ( age , 1 - 8 years ) received 2 doses of vaccine 3 months apart . The children were observed in a structured fashion for adverse events . Blood was tested for VZV antibody and VZV-specific cell-mediated immunity ( CMI ) at baseline , 8 weeks after each dose , and annually for 3 years . Subjects who had no evidence of immunity 1 year after vaccination received a third dose and were retested . RESULTS The vaccine was well tolerated ; there were no vaccine-related , serious adverse events . Regardless of immunologic category , at least 79 % of HIV-infected vaccine recipients developed VZV-specific antibody and /or CMI 2 months after 2 doses of vaccine , and 83 % were responders 1 year after vaccination . CONCLUSIONS HIV-infected children with a CD4(+ ) T cell percentage of > or = 15 % and a CD4(+ ) T cell count of > or = 200 cells/ microL are likely to benefit from receiving varicella vaccine BACKGROUND Achieving the level of population immunity required for measles elimination may be difficult in regions of high human immunodeficiency virus type 1 ( HIV-1 ) prevalence , because HIV-1-infected children may be less likely to respond to or maintain protective antibody levels after vaccination . METHODS We conducted a prospect i ve study of the immunogenicity of st and ard-titer measles vaccine administered at 9 months of age to HIV-1-infected and uninfected children in Lusaka , Zambia . RESULTS From May 2000 to November 2002 , 696 children aged 2 - 8 months were enrolled . Within 6 months of vaccination , 88 % of 50 HIV-1-infected children developed antibody levels of > or=120 mIU/mL , compared with 94 % of 98 HIV-seronegative children and 94 % of 211 HIV-seropositive but uninfected children ( P=.3 ) . By 27 months after vaccination , however , only half of the 18 HIV-1-infected children who survived and returned for follow-up maintained measles antibody levels > or=120 mIU/mL , compared with 89 % of 71 uninfected children ( P=.001 ) and in contrast with 92 % of 12 HIV-1-infected children revaccinated during a supplemental measles immunization activity . CONCLUSIONS Although HIV-1-infected children showed good primary antibody responses to measles vaccine , their rapid waning of antibody suggests that measles vaccination campaigns may need to be repeated more frequently in areas of high HIV-1 prevalence BACKGROUND Previously , we demonstrated that measles antibody prevalence was lower at age 12 months among children infected with human immunodeficiency virus ( HIV ) than uninfected children following measles vaccination ( MV ) at ages 6 and 9 months . Among HIV-uninfected children , measles antibody prevalence was lower among 1- than 2-dose MV recipients . Here , we report results through age 24 months . METHODS Children born to HIV-infected mothers received MV at 6 and 9 months , and children of HIV-uninfected mothers were r and omized to MV at 6 and 9 months or MV at 9 months . We followed children through age 24 months . The child 's HIV status was determined and measles immunoglobulin G ( IgG ) level was measured by enzyme immunoassay ( EIA ) and by plaque reduction neutralization ( PRN ) on a subset . RESULTS Among HIV-uninfected children , the difference in measles antibody prevalence at age 12 months between one- and two-dose recipients reported previously by EIA was shown to be smaller by PRN . By age 24 months , 84 % and 87 % of HIV-uninfected children receiving 1 or 2 doses , respectively , were seroprotected . Only 41 % of 22 HIV-infected children were measles seroprotected at age 20 months . DISCUSSION Measles seroprotection persisted through age 24 months among HIV-uninfected children who received 1 or 2 doses of MV .  HIV-infected children demonstrated seroprotection through age 12 months , but this was not sustained BACKGROUND Hepatitis B virus ( HBV ) is an important cause of comorbidity in human immunodeficiency virus (HIV)-infected individuals . The immunogenicity of HBV vaccination in children receiving highly active antiretroviral therapy ( HAART ) was investigated . METHODS HIV-infected children receiving HAART who had low to moderate HIV loads and who had previously received 3 doses of HBV vaccine  were given an HBV vaccine booster . Concentrations of antibody to hepatitis B surface antigen ( anti-HBs ) were determined before vaccination and at weeks 8 , 48 , and 96 . A subset of subjects was administered a subsequent dose , and anti-HBs was measured before and 1 and 4 weeks later . RESULTS At entry , 24 % of 204 subjects were seropositive .  Vaccine response occurred in 46 % on the basis of seropositivity 8 weeks after vaccination and in 
    Output:
    
agent
***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Background Human immunodeficiency virus type 1 ( HIV-1 ) infected children treated with highly active antiretroviral therapy ( HAART ) may develop a significant reduction of plasma viremia associated with an increase in CD4 + T-cell counts . Functional capacity of this reconstituted immune system in response to recall antigens is important to maintain protective immunity to vaccine-preventable diseases . We therefore determined cellular and humoral immune responses to tetanus toxoid ( TT ) booster in perinatally HIV-1-infected children and adolescents receiving HAART . Methods Immune responses were prospect ively evaluated pre- and post-tetanus booster using lymphocyte proliferation assay ( LPA ) stimulation index ( SI≥3.0 ) and tetanus antibody ( TAb≥0.15 ) in 15 patients . The median interval from primary tetanus immunization series was 6 years ( range 2–12 years ) . We compared patients by their virological response to HAART ( complete responders , CR , n=7 ; incomplete responders , ICR , n=8 ) . Results There were no significant differences in median age 12.6 years ( CR : 12.9 ; ICR : 10.6 ) or median CD4 T-cell pre-booster ( CR : 35%/819 ; ICR : 26%/429 ) between groups . Tetanus LPA responses were observed in one patient prior to booster and in seven patients post-booster . In contrast , 38 % of patients had protective TAb pre-booster , but 92 % developed protective TAb post-booster . All of the CR and 5/6 ICR patients developed protective TAb . Conclusions HIV-1-infected children and adolescents  had modest LPA responses to tetanus following booster , similar to HIV-1-infected adults . However , the majority of patients developed protective TAb levels after booster and maintained the response . Shorter intervals may need to be considered for TT immunization boosters in HIV-1-infected pediatric patients , as only 38 % had protective TAb at baseline Objective To evaluate the humoral response to routine childhood immunization of HIV-infected children . Design Response rate , antibody titres and persistence after polio and tetanus vaccination were compared in 72 children with HIV seropositivity at birth and divided according to HIV infection status as determined by clinical and laboratory tests . Methods Polio antibodies were titred in a microneutralization test ( positive titres , ≥1:4 ) , and antibody to tetanus toxoid with a passive haemagglutination method ( protective titres , ≥1:1024 ) . Results The response rates  to polio and tetanus vaccination ( > 80 and > 75 % ) were similar in the HIV-infected and non-infected children , as were antibody levels . In the subgroup with sera obtained some months after the last dose of vaccine , polio antibody levels decreased in all four HIV-infected and in three of the seven non-infected children ; protective tetanus antitoxin levels were detected in three of the six infected and in all three non-infected children . Conclusions This study demonstrates the ability of children with HIV infection to respond adequately to the two vaccines considered , although tetanus antitoxin levels were inferior , compared with those in the seroreverted children . The unsatisfactory antibody levels observed in the admittedly few HIV-positive children studied some months after the last vaccination could be the result of a lower initial protective level and not necessarily an expression of severely impaired immunocompetence . The administration of booster doses in addition to the traditional immunization schedule could be useful in children with HIV infection BACKGROUND We studied whether severely immunocompromised , human immunodeficiency virus (HIV)-infected children who were beginning highly active antiretroviral therapy ( HAART ) or changing HAART regimens could spontaneously respond to a recall antigen ( tetanus toxoid [ TT ] vaccine ) or respond to a recall antigen and neoantigen ( hepatitis A virus [ HAV ] vaccine ) after 3 vaccinations . METHODS A total of 46 children who had CD4 cell percentages < 15 % and who demonstrated a > 0.75-log reduction in plasma HIV RNA levels within 4 weeks of starting HAART were r and omized to receive vaccinations with either TT or HAV vaccines during the first 6 months of HAART . Study subjects then received the alternate vaccine during the next 6 months of HAART . RESULTS Despite the early decline in viremia and the later increase in the percentage of CD4 T cells , spontaneous recovery of cell-mediated immunity ( CMI ) was not seen for TT . Serologic responses to TT required 3 vaccinations and were comparable in both groups . Serologic responses to HAV were infrequent and of low titer , although the group that received HAV vaccine after receiving TT vaccine performed somewhat better . CMI to HAV was virtually absent . CONCLUSIONS Severely immunocompromised children who are receiving HAART develop CMI and antibody to a recall antigen independent of the timing of vaccination , but they require a primary series of vaccinations . Antibodies to a neoantigen , HAV , developed when vaccination was delayed after initiation of HAART . CMI to a neoantigen was difficult to establish . TRIAL REGISTRATION Clinical trials.gov identifier : NCT00004735/PACTG P1006 BACKGROUND Administration of pneumococcal conjugate vaccine ( PCV ) to HIV-infected children during infancy confers limited long-term protection in the absence of antiretroviral therapy . The objective of the present study was to determine the immune responses to PCV at 5 years of age in HIV-infected and HIV-uninfected children who had been primed with vaccine during infancy ( i.e. , previous vaccinees ) and in those receiving their first dose of vaccine ( i.e. , control subjects ) . METHODS Serotype-specific antibodies were quantified by enzyme immunoassay , and antibody functionality to serotypes 6B , 9V , and 19F were evaluated using an opsonophagocytic killing assay 1 month after vaccination . RESULTS Of the HIV-infected children , 19.7 % were receiving antiretroviral therapy , and 40.5 % had a CD4(+ ) cell percentage < 15 % .  Geometric mean concentrations of antibody and the proportion with a concentration 0.35 microg/mL after vaccination were greater among HIV-uninfected children than among HIV-infected children for both previous vaccinees and control subjects . Antibody concentrations after vaccination were lower for 3 of 7 serotypes among HIV-infected previous vaccinees than among control subjects . Detectable opsonophagocytic activity to all studied serotypes was lower among HIV-infected than among HIV-uninfected previous vaccinees and control subjects . Postvaccination antibody-mediated killing activity as determined by the opsonophagocytic killing assay was enhanced in control subjects compared with previous vaccinees among HIV-uninfected children . CONCLUSION HIV-infected vaccinees experience a partial loss of anamnestic responses to PCV . The optimal timing and frequency of booster vaccination as well as the responses to them among HIV-infected children need to be determined BACKGROUND Varicella can be a severe illness in human immunodeficiency virus (HIV)-infected children . The licensed , live attenuated varicella vaccine is safe and immunogenic in HIV-infected children with minimal symptoms and good preservation of CD4(+ ) T cells ( Centers for Disease Control and Prevention immunologic category 1 ) . METHODS To study the safety and immunogenicity of this vaccine in varicella-zoster virus (VZV)-naive , HIV-infected children with moderate symptoms and /or more pronounced past or current decreases in CD4(+ ) T cell counts , such children ( age , 1 - 8 years ) received 2 doses of vaccine 3 months apart . The children were observed in a structured fashion for adverse events . Blood was tested for VZV antibody and VZV-specific cell-mediated immunity ( CMI ) at baseline , 8 weeks after each dose , and annually for 3 years . Subjects who had no evidence of immunity 1 year after vaccination received a third dose and were retested . RESULTS The vaccine was well tolerated ; there were no vaccine-related , serious adverse events . Regardless of immunologic category , at least 79 % of HIV-infected vaccine recipients developed VZV-specific antibody and /or CMI 2 months after 2 doses of vaccine , and 83 % were responders 1 year after vaccination . CONCLUSIONS HIV-infected children with a CD4(+ ) T cell percentage of > or = 15 % and a CD4(+ ) T cell count of > or = 200 cells/ microL are likely to benefit from receiving varicella vaccine BACKGROUND Achieving the level of population immunity required for measles elimination may be difficult in regions of high human immunodeficiency virus type 1 ( HIV-1 ) prevalence , because HIV-1-infected children may be less likely to respond to or maintain protective antibody levels after vaccination . METHODS We conducted a prospect i ve study of the immunogenicity of st and ard-titer measles vaccine administered at 9 months of age to HIV-1-infected and uninfected children in Lusaka , Zambia . RESULTS From May 2000 to November 2002 , 696 children aged 2 - 8 months were enrolled . Within 6 months of vaccination , 88 % of 50 HIV-1-infected children developed antibody levels of > or=120 mIU/mL , compared with 94 % of 98 HIV-seronegative children and 94 % of 211 HIV-seropositive but uninfected children ( P=.3 ) . By 27 months after vaccination , however , only half of the 18 HIV-1-infected children who survived and returned for follow-up maintained measles antibody levels > or=120 mIU/mL , compared with 89 % of 71 uninfected children ( P=.001 ) and in contrast with 92 % of 12 HIV-1-infected children revaccinated during a supplemental measles immunization activity . CONCLUSIONS Although HIV-1-infected children showed good primary antibody responses to measles vaccine , their rapid waning of antibody suggests that measles vaccination campaigns may need to be repeated more frequently in areas of high HIV-1 prevalence BACKGROUND Previously , we demonstrated that measles antibody prevalence was lower at age 12 months among children infected with human immunodeficiency virus ( HIV ) than uninfected children following measles vaccination ( MV ) at ages 6 and 9 months . Among HIV-uninfected children , measles antibody prevalence was lower among 1- than 2-dose MV recipients . Here , we report results through age 24 months . METHODS Children born to HIV-infected mothers received MV at 6 and 9 months , and children of HIV-uninfected mothers were r and omized to MV at 6 and 9 months or MV at 9 months . We followed children through age 24 months . The child 's HIV status was determined and measles immunoglobulin G ( IgG ) level was measured by enzyme immunoassay ( EIA ) and by plaque reduction neutralization ( PRN ) on a subset . RESULTS Among HIV-uninfected children , the difference in measles antibody prevalence at age 12 months between one- and two-dose recipients reported previously by EIA was shown to be smaller by PRN . By age 24 months , 84 % and 87 % of HIV-uninfected children receiving 1 or 2 doses , respectively , were seroprotected . Only 41 % of 22 HIV-infected children were measles seroprotected at age 20 months . DISCUSSION Measles seroprotection persisted through age 24 months among HIV-uninfected children who received 1 or 2 doses of MV .  HIV-infected children demonstrated seroprotection through age 12 months , but this was not sustained BACKGROUND Hepatitis B virus ( HBV ) is an important cause of comorbidity in human immunodeficiency virus (HIV)-infected individuals . The immunogenicity of HBV vaccination in children receiving highly active antiretroviral therapy ( HAART ) was investigated . METHODS HIV-infected children receiving HAART who had low to moderate HIV loads and who had previously received 3 doses of HBV vaccine  were given an HBV vaccine booster . Concentrations of antibody to hepatitis B surface antigen ( anti-HBs ) were determined before vaccination and at weeks 8 , 48 , and 96 . A subset of subjects was administered a subsequent dose , and anti-HBs was measured before and 1 and 4 weeks later . RESULTS At entry , 24 % of 204 subjects were seropositive .  Vaccine response occurred in 46 % on the basis of seropositivity 8 weeks after vaccination and in 
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