Publications by authors named "Maria Abad-Fernandez"

Cross-reactive antibodies (Abs) to epitopes that span envelope proteins on the virion surface are hypothesized to protect against dengue. Here, we measured Abs targeting the quaternary envelope dimer epitope (EDE) as well as neutralizing and binding Abs and evaluate their association with dengue virus (DENV) infection, vaccine response, and disease outcome in dengue vaccinated and unvaccinated children (n=252) within a longitudinal cohort in Cebu, Philippines (n=2,996). Abs targeting EDE were prevalent and strongly associated with broad neutralization of DENV1-4 in those with baseline multitypic immunity.

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Recent work demonstrates the limitations of the standard dengue virus (DENV) neutralization assay to predict protection against dengue. We perform studies to compare how a commercial IgG ELISA, envelope domain III (EDIII) or non-structural protein 1 (NS1) binding antibodies, and titers from plaque reduction neutralization tests (PRNTs) using reference standard and clinical mature viruses are associated with dengue disease. Healthy children (n = 1,206) in Cebu, Philippines were followed for 5 years.

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During the early 1980s, the first 3 human retroviruses were identified: human T-lymphotropic virus 1 and 2 (HTLV-1 and HTLV-2) and human immunodeficiency virus (HIV) [...

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We developed a highly reproducible 32-marker mass cytometry panel able to measure all canonical immune lineages and perform detailed characterization of both CD4 and CD8 T cells in human peripheral blood mononuclear cells. In this panel, we identify six different T cell memory subsets, as well as markers of activation, cell cycling, and survival. In addition, this panel classifies all major CD4 T cell helper subsets.

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People living with HIV-1 and HTLV-2 concomitantly show slower CD4 T cell depletion and AIDS progression, more frequency of the natural control of HIV-1, and lower mortality rates. A similar beneficial effect of this infection has been reported on HCV coinfection reducing transaminases, increasing the spontaneous clearance of HCV infection and delaying the development of hepatic fibrosis. Given the critical role of CD8 T cells in controlling HIV-1 infection, we analysed the role of CD8 T cell-mediated cytotoxic activity in coinfected individuals living with HIV-1.

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The human immunodeficiency virus (HIV)-1 viral inhibition assay (VIA) measures CD8 T cell-mediated inhibition of HIV replication in CD4 T cells and is increasingly used for clinical testing of HIV vaccines and immunotherapies. Different VIAs that differ in length of CD8:CD4 T cell culture periods (6-13 days), purity of CD4 cultures [isolated CD4 T cells or CD8 depleted peripheral blood mononuclear cells (PBMCs)], HIV strains (laboratory strains, isolates, reporter viruses) and read-outs of virus inhibition (p24 ELISA, intracellular measurement of p24, luciferase reporter expression, and viral RNA) have been reported. Here, we describe multiple modifications to a 7-day VIA protocol, the most impactful being the introduction of independent replicate cultures for both HIV infected-CD4 (HIV-CD4) and HIV-CD4:CD8 T cell cultures.

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The HIV-1 viral inhibition assay (VIA) measures CD8 T cell-mediated inhibition of HIV replication in CD4 T cells and is increasingly used for clinical testing of HIV vaccines and immunotherapies. The VIA has multiple sources of variability arising from HIV infection and co-culture of two T cell populations. Here, we describe multiple modifications to a 7-day VIA protocol, the most impactful being the introduction of independent replicate cultures for both HIV infected-CD4 (HIV-CD4) and HIV-CD4:CD8 T cell cultures.

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Objectives: This study aims to analyze the association of the presence of common polymorphisms [single nucleotide polymorphisms (SNPs)] on Toll-like receptors (TLRs), such as TLR9-1635A/G, TLR2-1892A/C, TLR2-2258G/A, TLR4-899A/G, and TLR4-1196C/T, with the viral rebound after stopping antiretroviral treatment (ART). CCR5-Δ32 deletion and HLA-A/HLA-B alleles were also analyzed.

Design: Interruption of ART may be required to investigate the outcome of strategies aimed to achieve drug-free HIV remission or cure.

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HIV infection induces a robust T cell response that is sustained by high viremia, but falls following the onset of antiretroviral therapy (ART). Relatively little has been reported on the subsequent stability of the HIV-specific T cell response in individuals on durable therapy. Such data are critical for powering clinical trials testing T cell-based immunotherapies.

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A major limitation of current humanized mouse models is that they primarily enable the analysis of human-specific pathogens that infect hematopoietic cells. However, most human pathogens target other cell types, including epithelial, endothelial and mesenchymal cells. Here, we show that implantation of human lung tissue, which contains up to 40 cell types, including nonhematopoietic cells, into immunodeficient mice (lung-only mice) resulted in the development of a highly vascularized lung implant.

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Purpose Of Review: CMV-vectored vaccines expressing SIV antigens have mediated unprecedented levels of virus control following SIV challenge in rhesus macaques. Remarkably, protection was dependent on nonclassically restricted CD8 T cells. Here, we review the latest research in CMV-vectored vaccines in both humans and nonhuman primates as well as recent advances in the understanding nonclassically restricted T cells, particularly MHC-E-restricted CD8 T cells.

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Current efforts toward human immunodeficiency virus (HIV) eradication include approaches to augment immune recognition and elimination of persistently infected cells following latency reversal. Natural killer (NK) cells, the main effectors of the innate immune system, recognize and clear targets using different mechanisms than CD8 T cells, offering an alternative or complementary approach for HIV clearance strategies. We assessed the impact of interleukin 15 (IL-15) treatment on NK cell function and the potential for stimulated NK cells to clear the HIV reservoir.

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We analyzed the effect of interferon α (IFN-α) and ribavirin (RBV) therapy on cell-associated human T-lymphotropic virus type 2 (HTLV-2) DNA in HIV-1-coinfected patients receiving antiretroviral therapy. Sixty-one patients under suppressive antiretroviral therapy were included: 37 with hepatitis C virus (HCV) infection, 15 with sustained virologic response (N = 10), relapse (N = 2), or with nonresponse (N = 3) after IFN-α/RBV treatment, and 9 with spontaneous HCV RNA clearance. Patients who were treated with IFN-α/RBV or had spontaneous HCV clearance had lower level of cell-associated HTLV-2 DNA (P = 0.

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Objectives: The absence of direct clinical symptoms clearly associated to HTLV-2 infection may partially explain an underestimate of the real HTLV-2 prevalence rate and its effects in patients concurrently infected with HIV-1 and hepatitis C virus (HCV). Hence, to date, the influence of HTLV-2 on hepatic fibrosis has been poorly studied.

Design: Retrospective study to clarify the influence of HTLV-2 infection in HCV infection and hepatic fibrosis among patients co-infected with HIV-1.

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Background: Numerous studies have analyzed the effects of raltegravir intensification on HIV-1 viral replication in infected individuals receiving suppressive combined antiretroviral treatment (cART). Nevertheless, there are only two studies on the effect of raltegravir in HTLV-1 infection, and none in HTLV-2.

Objective: To study the effect of raltegravir on HTLV-2 infection in HIV-1-co-infected individuals.

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Objective: Antiretroviral therapy (ART) intensification has been shown to reduce the reservoir of latently infected CD4 T cells. However, it is currently unknown whether this effect is maintained after discontinuation of the intensifying drug.

Design: The effect of ART intensification during 48 weeks with maraviroc or raltegravir in chronically HIV-1-infected patients was assessed in two previous clinical trials.

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Background: HIV-1-infected individuals progressively loss CD4(+) T cells leading to immunosuppression and raising the risk of opportunistic infections. CD8(+) T-cells play an important role in the immune response against virus infections through their TCR.

Objective: To evaluate the CD8-TCR repertoire and immunologic markers in HIV-1-infected patients.

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Introduction: Microbial translocation (MT) has been proposed as one of the triggering mechanisms of persistent immune activation associated to HIV-1 infection. Our objectives were to determine the correlation between different measurements of MT in suppressed HIV-1-infected individuals and to evaluate its correlation with immune activation.

Methods: Eighteen suppressed HIV-1-infected patients with CD4+ T-cell count above 350 cells per cubic millimeter and undetectable plasma viral load, included in antiretroviral treatment intensification clinical trials, were evaluated.

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Objectives: HIV-infected subjects on antiretroviral therapy often fail to normalize the CD4/CD8 ratio despite CD4 count normalization. We aimed to analyze the biological significance of this finding.

Methods: Cross-sectional analysis in 20 HIV-infected subjects on stable triple-ART, plasma HIV RNA <40 copies/mL for at least 2 years and CD4 count >350 cells/mm(3).

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Objectives: The stability of the reservoir of latently infected memory CD4 T-cells may be associated with continuous replenishment from residual HIV-1, not completely eliminated by otherwise successful antiretroviral therapy (ART). Treatment intensification could help to control residual virus and to modify the latent reservoir. The objective of this work is to assess the effect of intensifying therapy with raltegravir on the HIV-1 cell reservoir.

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Background: Most of the non-B HIV-1 subtypes are predominant in Sub-Saharan Africa and India although they have been found worldwide. In the last decade, immigration from these areas has increased considerably in Spain. The objective of this study was to evaluate the prevalence of non-B subtypes circulating in a cohort of HIV-1-infected immigrants in Seville, Southern Spain and to identify drug resistance-associated mutations.

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