Pediatric Viral Human Immunodeficiency Virus Type 1 RNA Levels, Timing of Infection, and Disease Progression in African HIV-1-Infected Children

Raffi, François; Sakarovitch, Charlotte; Msellati, Philippe; Elenga, Narcisse; Montcho, Crépin; Viho, Ida; Blanche, Stéphane; Rouzioux, Christine; Dabis, François; Leroy, Valériane

doi:10.1542/peds.112.4.e289

Cited by 63 publications

(46 citation statements)

References 39 publications

(38 reference statements)

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“…Both groups had similar increases in the magnitudes of HIV-1-specific IFN-␥ responses over their first year of life, an indication that infants infected in utero are not more immunosuppressed than infants infected peripartum and that both groups possess the capacity for continuing immune maturation. Infants infected in utero did not demonstrate higher peak viral loads than infants infected peripartum, as has also been described in the Abidjan ANRS 049 Ditrame Study (52). A primary report describing the bimodal disease progression in perinatally infected infants suggests that in utero infection may interfere with the maturation of the immune system and increase the rate of development of immunosuppression (5), something we do not show with our data.…”

Section: Vol 79 2005 Cd8 ϩ Ifn-␥ Elispot Responses In Hiv-1-infectesupporting

confidence: 67%

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Longitudinal Assessment of Human Immunodeficiency Virus Type 1 (HIV-1)-Specific Gamma Interferon Responses during the First Year of Life in HIV-1-Infected Infants

Lohman

Slyker

Richardson

et al. 2005

J Virol

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Section: Vol 79 2005 Cd8 ϩ Ifn-␥ Elispot Responses In Hiv-1-infectesupporting

confidence: 67%

“…Peak HIV-1 plasma load is an important marker of disease progression in HIV-1-infected infants (52). Peak viral load was defined as the highest viral load detected within 6 months postinfection.…”

Section: Concordance Between Peptide-stimulated Ifn-␥ Secretion and Dmentioning

confidence: 99%

Longitudinal Assessment of Human Immunodeficiency Virus Type 1 (HIV-1)-Specific Gamma Interferon Responses during the First Year of Life in HIV-1-Infected Infants

Lohman

Slyker

Richardson

et al. 2005

J Virol

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“…These assays are available as "standard" or "ultrasensitive" assays, and the lower limit of detection possible when using the ultrasensitive assays is in the range of 50 to 75 HIV-1 copies per mL of plasma. Numerous studies of the use of HIV-1 RNA assays for the diagnosis of HIV-1 infection in pediatric populations have been conducted, 52,59,[65][66][67][68][69][70][71][72][73][74][75] with the reported sensitivity of testing (Table 3) for such assays ranging from 25% to 50% within the first few days of life to 100% by 6 to 12 weeks of age. 65,67 HIV-1 RNA assays have been assessed to be at least as sensitive as, or more sensitive than, HIV-1 DNA assays among young infants.…”

Section: Hiv-1 Naatsmentioning

confidence: 99%

Diagnosis of HIV-1 Infection in Children Younger Than 18 Months in the United States

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2007

Pediatrics

118

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The objectives of this technical report are to describe methods of diagnosis of HIV-1 infection in children younger than 18 months in the United States and to review important issues that must be considered by clinicians who care for infants and young children born to HIV-1–infected women. Appropriate HIV-1 diagnostic testing for infants and children younger than 18 months differs from that for older children, adolescents, and adults because of passively transferred maternal HIV-1 antibodies, which may be detectable in the child's bloodstream until 18 months of age. Therefore, routine serologic testing of these infants and young children is generally only informative before the age of 18 months if the test result is negative. Virologic assays, including HIV-1 DNA or RNA assays, represent the gold standard for diagnostic testing of infants and children younger than 18 months. With such testing, the diagnosis of HIV-1 infection (as well as the presumptive exclusion of HIV-1 infection) can be established within the first several weeks of life among nonbreastfed infants. Important factors that must be considered when selecting HIV-1 diagnostic assays for pediatric patients and when choosing the timing of such assays include the age of the child, potential timing of infection of the child, whether the infection status of the child's mother is known or unknown, the antiretroviral exposure history of the mother and of the child, and characteristics of the virus. If the mother's HIV-1 serostatus is unknown, rapid HIV-1 antibody testing of the newborn infant to identify HIV-1 exposure is essential so that antiretroviral prophylaxis can be initiated within the first 12 hours of life if test results are positive. For HIV-1–exposed infants (identified by positive maternal test results or positive antibody results for the infant shortly after birth), it has been recommended that diagnostic testing with HIV-1 DNA or RNA assays be performed within the first 14 days of life, at 1 to 2 months of age, and at 3 to 6 months of age. If any of these test results are positive, repeat testing is recommended to confirm the diagnosis of HIV-1 infection. A diagnosis of HIV-1 infection can be made on the basis of 2 positive HIV-1 DNA or RNA assay results. In nonbreastfeeding children younger than 18 months with no positive HIV-1 virologic test results, presumptive exclusion of HIV-1 infection can be based on 2 negative virologic test results (1 obtained at ≥2 weeks and 1 obtained at ≥4 weeks of age); 1 negative virologic test result obtained at ≥8 weeks of age; or 1 negative HIV-1 antibody test result obtained at ≥6 months of age. Alternatively, presumptive exclusion of HIV-1 infection can be based on 1 positive HIV-1 virologic test with at least 2 subsequent negative virologic test results (at least 1 of which is performed at ≥8 weeks of age) or negative HIV-1 antibody test results (at least 1 of which is performed at ≥6 months of age). Definitive exclusion of HIV-1 infection is based on 2 negative virologic test results, 1 obtained at ≥1 month of age and 1 obtained at ≥4 months of age, or 2 negative HIV-1 antibody test results from separate specimens obtained at ≥6 months of age. For both presumptive and definitive exclusion of infection, the child should have no other laboratory (eg, no positive virologic test results) or clinical (eg, no AIDS-defining conditions) evidence of HIV-1 infection. Many clinicians confirm the absence of HIV-1 infection with a negative HIV-1 antibody assay result at 12 to 18 months of age. For breastfeeding infants, a similar testing algorithm can be followed, with timing of testing starting from the date of complete cessation of breastfeeding instead of the date of birth.

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“…Second, HIVinfected infants are more likely to possess nonprotective HLA alleles, since at least 50% of the infant's HLA genotype is shared with the mother, and high maternal viremia is a risk factor for perinatal HIV transmission (35). Finally, the infecting virus may be adapted to maternally and paternally inherited HLA genes (19,38). However, a minority of infants progress relatively slowly.…”

mentioning

confidence: 99%

Replicative Capacity of Human Immunodeficiency Virus Type 1 Transmitted from Mother to Child Is Associated with Pediatric Disease Progression Rate

Prado

Prendergast

Thobakgale

et al. 2010

J Virol

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Human immunodeficiency virus (HIV)-infected infants in the developing world typically progress to AIDS or death within the first 2 years of life. However, a minority progress relatively slowly. This study addresses the potential contribution of viral factors to HIV disease progression in eight infants selected from a wellcharacterized cohort of C clade HIV-infected infants, monitored prospectively from birth in Durban, South Africa. Three infants were defined as "progressors," and five were defined as "slow progressors." We observed that slow-progressor infants carry HIV isolates with significantly lower replicative capacity compared to virus from progressors. Furthermore, our data suggest a link between the attenuated viral phenotype and HLA-B* 57/5801 epitope-specific Gag mutational patterns of the transmitted virus and not to coreceptor usage or to the presence of Nef deletions or insertions. These data underline the importance of virus-host interactions and highlight the contribution of viral attenuation through Gag-specific CD8 ؉ T-cell escape mutations, among other factors, in the control of pediatric HIV infection.

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Pediatric Viral Human Immunodeficiency Virus Type 1 RNA Levels, Timing of Infection, and Disease Progression in African HIV-1-Infected Children

Cited by 63 publications

References 39 publications

Longitudinal Assessment of Human Immunodeficiency Virus Type 1 (HIV-1)-Specific Gamma Interferon Responses during the First Year of Life in HIV-1-Infected Infants

Longitudinal Assessment of Human Immunodeficiency Virus Type 1 (HIV-1)-Specific Gamma Interferon Responses during the First Year of Life in HIV-1-Infected Infants

Diagnosis of HIV-1 Infection in Children Younger Than 18 Months in the United States

Replicative Capacity of Human Immunodeficiency Virus Type 1 Transmitted from Mother to Child Is Associated with Pediatric Disease Progression Rate

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