Filaria specific antibody response profiling in plasma from anti-retroviral naïve Loa loa microfilaraemic HIV-1 infected people.

BACKGROUND: In West and Central Africa areas of endemic Loa loa infections overlap with regions of high prevalence of human immunodeficiency virus type 1 (HIV-1) infections. Because individuals in this region are exposed to filarial parasites from birth, most HIV-1 infected individuals invariably also have a history of filarial parasite infection. Since HIV-1 infection both depletes immune system and maintains it in perpetual inflammation, this can hamper Loa loa filarial parasite mediated immune modulation, leading to enhanced loaisis. METHODS: In this study we have assessed in plasma from asymptomatic anti-retroviral (ARV) naïve Loa loa microfilaraemic HIV-1 infected people the filarial antibody responses specific to a filariasis composite antigen consisting of Wbgp29-BmR1-BmM14-WbSXP. The antibody responses specific to the filariasis composite antigen was determined by enzyme linked immunosorbent assay (ELISA) in plasma from ARV naïve Loa loa microfilaraemic HIV-1 infected participants. In addition the filarial antigen specific IgG antibody subclass profiles were also determined for both HIV-1 positive and negative people. RESULTS: Both Loa loa microfilaraemic HIV-1 positive and negative individuals showed significantly higher plasma levels of IgG1 (P < 0.0001), IgG2 (P < 0.0001) and IgM (P < 0.0001) relative to amicrofilaraemic participants. A significant increase in IgE (P < 0.0001) was observed exclusively in Loa loa microfilaraemic HIV-1 infected people. In contrast there was a significant reduction in the level of IgG4 (p < 0.0001) and IgG3 (P < 0.0001) in Loa loa microfilaraemic HIV-1 infected individuals. CONCLUSIONS: Loa loa microfilaraemia in ARV naïve HIV-1 infected people through differential reduction of plasma levels of filarial antigen specific IgG3, IgG4 and a significant increase in plasma levels of filarial antigen specific IgE could diminish Loa loa mediated immune-regulation. This in effect can result to increase loaisis mediated immunopathology in antiretroviral naive HIV-1 infected people.

Dendritic cell targeted HIV-1 gag protein vaccine provides help to a recombinant Newcastle disease virus vectored vaccine including mobilization of protective CD8+ T cells.

INTRODUCTION: Recombinant Newcastle Disease virus (rNDV) vectored vaccines are safe mucosal applicable vaccines with intrinsic immune-modulatory properties for the induction of efficient immunity. Like all viral vectored vaccines repeated inoculation via mucosal routes invariably results to immunity against viral vaccine vectors. To obviate immunity against viral vaccine vectors and improve the ability of rNDV vectored vaccines in inducing T cell immunity in murine air way we have directed dendritic cell targeted HIV-1 gag protein (DEC-Gag) vaccine; for the induction of helper CD4+ T cells to a Recombinant Newcastle disease virus expressing codon optimized HIV-1 Gag P55 (rNDV-L-Gag) vaccine. METHODS: We do so through successive administration of anti-DEC205-gagP24 protein plus polyICLC (DEC-Gag) vaccine and rNDV-L-Gag. First strong gag specific helper CD4+ T cells are induced in mice by selected targeting of anti-DEC205-gagP24 protein vaccine to dendritic cells (DC) in situ together with polyICLC as adjuvant. This targeting helped T cell immunity develop to a subsequent rNDV-L-Gag vaccine and improved both systemic and mucosal gag specific immunity. RESULTS: This sequential DEC-Gag vaccine prime followed by an rNDV-L-gag boost results to improved viral vectored immunization in murine airway, including mobilization of protective CD8+ T cells to a pathogenic virus infection site. CONCLUSION: Thus, complementary prime boost vaccination, in which prime and boost favor distinct types of T cell immunity, improves viral vectored immunization, including mobilization of protective CD8+ T cells to a pathogenic virus infection site such as the murine airway.

Role of some biomarkers in placental malaria in women living in Yaoundé, Cameroon.

Despite intensive research on the immunpathology of placental malaria (PM), the role of some ß-chemokines known to attract inflammatory cells is less known. This study sought to determine the role of CXCL-10, IL-10, IL-19, IL-17A and IL-23 in placental malaria in women at delivery. Between 2010 and 2011, paired peripheral and placental blood specimens were collected from 139 Cameroonian women at delivery. Differential white blood cell counts and malaria parasitaemia were determined microscopically while the accumulation of parasites in the placenta was investigated through histological studies. Plasma levels of CXCL-10, IL-10, IL-17A, IL-19 and Il-23 were determined by ELISA. The cytokines IL-10, IL-17A and IL-23 were predominant in peripheral plasma from both infected and non-infected women. While IL-10 associated negatively with parity, IL-23 showed a positive correlation (p<0.05). The production of CXCL-10 was independent of parity and higher in placental plasma. There was an association between the plasma levels of IL-10 and CXCL-10 with malaria parasitaemia in the placenta impression smears, placental and peripheral blood and the presence of malaria pigments in the placenta tissue. Leukocyte accumulation into the intervillous space correlated positively with plasma levels of placental IL-17A (p<0.001). Parity also associated with peripheral IL-17A (p=0.016). The peripheral and placental plasma levels of CXCL-10 and IL-10 also correlated positively with monocyte counts (p=0.011-0.042) while a negative correlation was found with lymphocyte counts (p=0.017 to <0.001) of the impression smear. However, the levels of IL-10 in both peripheral and placental plasma and CXCL-10 in placental plasma only, were higher in low birth weight baby. With regards to IL-17A, its placental plasma level correlated positively with lymphocyte counts of placental blood (p=0.045). During PM, CXCL-10 might attract monocytes and lymphocytes into the placenta where they produce inflammatory cytokines such as IL-10 and IL-17A to modulate the disease, which affect baby weight.