Immunology of infants through adolescents: responses to emulate for HIV vaccines

Jaspan, Heather B.; Hanekom, Willem A.

doi:10.1097/coh.0b013e3282e1c633

Cited by 2 publications

(2 citation statements)

References 99 publications

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“…Neonatal innate, humoral, and cellular immunity differ to that of adults [13]. It is thought that neonates are poor type 1 T-helper (Th1) cytokine producers due to a lack of interleukin (IL)-12 production by dendritic cells [14–16].…”

Section: Introductionmentioning

confidence: 99%

In-utero exposure to maternal HIV infection alters T-cell immune responses to vaccination in HIV-uninfected infants

Kidzeru

Hesseling

Passmore

et al. 2014

Aids

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Objective In sub-Saharan Africa, HIV-exposed uninfected (HEU) infants have higher morbidity and mortality than HIV-unexposed infants. To evaluate whether immune dysfunction contributes to this vulnerability of HEU infants, we conducted a longitudinal, observational cohort study to assess T-cell immune responses to infant vaccines (Mycobacterium bovis BCG and acellular pertussis) and staphylococcal enterotoxin B (SEB). In total, 46 HEU and 46 HIV-unexposed infants were recruited from Khayelitsha, Cape Town. Methods Vaccine-specific T-cell proliferation (Ki67 expression) and intracellular expression of four cytokines [interferon-γ, interleukin (IL)-2, IL-13 and IL-17] were measured after whole blood stimulation with antigens at 6 and 14 weeks of age. Results HEU infants demonstrated elevated BCG-specific CD4+ and CD8+ T-cell proliferative responses at 14 weeks (P = 0.041 and 0.002, respectively). These responses were significantly increased even after adjusting for birth weight, feeding mode and gestational age. Similar to BCG, increased CD4+ and CD8+ T-cell proliferation was evident in response to SEB stimulation (P = 0.004 and 0.002, respectively), although pertussis-specific T cells proliferated comparably between the two groups. Within HEU infants, maternal CD4+ cell count and length of antenatal antiretroviral exposure had no effect on T-cell proliferation to BCG or SEB. HIV exposure significantly diminished measurable cytokine polyfunctionality in response to BCG, Bordetella pertussis and SEB stimulation. Conclusion These data show for the first time, when adjusting for confounders, that exposure to HIV in utero is associated with significant alterations to CD4+ and CD8+T-cell immune responses in infants to vaccines and nonspecific antigens.

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Section: Introductionmentioning

confidence: 99%

In-utero exposure to maternal HIV infection alters T-cell immune responses to vaccination in HIV-uninfected infants

Kidzeru

Hesseling

Passmore

et al. 2014

Aids

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“…In particular, for developing a neonatal vaccine against HIV breastmilk transmission, it is essential to evaluate safety, immunogenicity and efficacy of candidate vaccine strategies in nonhuman primate infants whose immune system development and vaccine responses most accurately reflect those of human infants (reviewed in [11–13]. Using this infant macaque model, we have previously demonstrated that intramuscular administration of attenuated poxvirus-based SIV vaccines (ALVAC-SIV and modified vaccine virus Ankara [MVA]-SIV) to infant macaques during the first 4 weeks after birth was immunogenic and partially protective against infection when animals were exposed repeatedly at 4 weeks of age to low doses of virulent SIVmac251 [14]; this partial resistance to infection was still evident when uninfected immunized animals were rechallenged orally with virulent SIV 16 months later.…”

Section: Introductionmentioning

confidence: 99%

Immunogenicity of viral vector, prime-boost SIV vaccine regimens in infant rhesus macaques: Attenuated vesicular stomatitis virus (VSV) and modified vaccinia Ankara (MVA) recombinant SIV vaccines compared to live-attenuated SIV

Rompay¹,

Abel²,

Earl³

et al. 2010

Vaccine

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In a previously developed infant macaque model mimicking HIV infection by breast feeding, we demonstrated that intramuscular immunization with recombinant poxvirus vaccines expressing simian immunodeficiency virus (SIV) structural proteins provided partial protection against infection following oral inoculation with virulent SIV. In an attempt to further increase systemic but also local antiviral immune responses at the site of viral entry, we tested the immunogenicity of different orally administered, replicating vaccines. One group of newborn macaques received an oral prime immunization with a recombinant vesicular stomatitis virus expressing SIVmac239 gag, pol and env (VSV-SIVgpe), followed 2 weeks later by an intramuscular boost immunization with MVA-SIV. Another group received two immunizations with live-attenuated SIVmac1A11, administered each time both orally and intravenously. Control animals received mock immunizations or non-SIV VSV and MVA control vectors. Analysis of SIV-specific immune responses in blood and lymphoid tissues at 4 weeks of age demonstrated that both vaccine regimens induced systemic antibody responses and both systemic and local cell-mediated immune responses. The safety and immunogenicity of the VSV-SIVgpe +MVA-SIV immunization regimen described in this report provide the scientific incentive to explore the efficacy of this vaccine regimen against virulent SIV exposure in the infant macaque model.

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Immunology of infants through adolescents: responses to emulate for HIV vaccines

Cited by 2 publications

References 99 publications

In-utero exposure to maternal HIV infection alters T-cell immune responses to vaccination in HIV-uninfected infants

In-utero exposure to maternal HIV infection alters T-cell immune responses to vaccination in HIV-uninfected infants

Immunogenicity of viral vector, prime-boost SIV vaccine regimens in infant rhesus macaques: Attenuated vesicular stomatitis virus (VSV) and modified vaccinia Ankara (MVA) recombinant SIV vaccines compared to live-attenuated SIV

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