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Background: Live attenuated viruses are among our most potent and effective vaccines. For human immunodeficiency virus, however, a live attenuated strain could present substantial safety concerns. We have used the live attenuated rubella vaccine strain RA27/3 as a vector to express SIV and HIV vaccine antigens because its safety and immunogenicity have been demonstrated in millions of children. One dose protects for life against rubella infection. In previous studies, rubella vectors replicated to high titers in cell culture while stably expressing SIV and HIV antigens. Their viability in vivo, however, as well as immunogenicity and antibody persistence, were unknown. Results: This paper reports the first successful trial of rubella vectors in rhesus macaques, in combination with DNA vaccines in a prime and boost strategy. The vectors grew robustly in vivo, and the protein inserts were highly immunogenic. Antibody titers elicited by the SIV Gag vector were greater than or equal to those elicited by natural SIV infection. The antibodies were long lasting, and they were boosted by a second dose of replication-competent rubella vectors given six months later, indicating the induction of memory B cells. Conclusions: Rubella vectors can serve as a vaccine platform for safe delivery and expression of SIV and HIV antigens. By presenting these antigens in the context of an acute infection, at a high level and for a prolonged duration, these vectors can stimulate a strong and persistent immune response, including maturation of memory B cells. Rhesus macaques will provide an ideal animal model for demonstrating immunogenicity of novel vectors and protection against SIV or SHIV challenge. [ABSTRACT FROM AUTHOR]

An abstract of the conference paper "Design of an HIV Env antigen that binds with high affinity to antibodies against linear, conformational and broadly neutralizing epitopes within V1/V2," by L. Liao and colleagues are presented.

An abstract of the research paper on bacteriophage T4 head for delivering HIV-1 antigens and genes into dendritic cells by V. Rao colleagues at AIDS Vaccine 2012 in Boston, Massachusetts is presented.

An abstract of the research paper "Peripheral T follicular helper cells from H1N1/09 vaccine nonresponders fail to induce antigen-specific antibody production in vitro," by A. Parmigiani and colleagues is presented.

An abstract of the conference paper "Structural Analyses of Antigen Binding Similarities and Differences Between Rabbit and Human Anti-gp120 V3 mAbs," by R. Pan and colleagues is presented.

An abstract of the conference paper "HIV-1 capture and antigen presentation by dendritic cells: enhanced viral capture does not correlate with better T-Cell activation" by M. Rodriguez-Plata and colleagues is presented.

An abstract of the conference paper "Shaping humoral responses against mini-libraries of HIV env antigens via lipid nanoparticle vaccine delivery" by M. C. Hanson and colleagues is presented.

An abstract of the conference paper "PD-1, IL-10, IFN and IL-12 form a network to regulate HIV-1-specific CD4 T Cell and antigen-presenting cell function ," by F. Porichis and colleagues are presented.

An abstract of the conference paper "Infiltration of dendritic cells and antigen uptake in the muscle after injection of HIV-1 Env gp120 in adjuvant," by F. Liang and colleagues are presented.

Background Malaria is endemic in countries of sub-Saharan Africa where there is also a high prevalence of HIV-1 infection, with pregnant women being the population most at risk to both infections. Epidemiological data and indirect evidence have established a link between placental malaria and an increased risk for HIV-1 mother-to-child transmission (MTCT), by unknown mechanisms. Material and methods The placenta-derived choriocarcinoma cell line BeWo and monocyte-derived macrophages (MDM) were infected with varying doses of luciferase reporter HIV-1 pseudo-typed with the vesicular stomatitis virus protein G. A recombinant DBL3γ domain, derived from a placental Plasmodium falciparum Erythrocyte Membrane Protein 1 (PfEMP1) adhesin domain (DBL3γ-732), that binds to chondroitin sulfate A (CSA) and a non-CSA-binding PfEMP1 adhesin domain, DBL1α-varO domain were used to stimulate infected cells. In some experiments, DBL3γ-732 was preincubated with the Fab fragment of a specific or an irrelevant monoclonal antibodies (mAb) that inhibits, or not, binding to CSA. TNF-α was measured in the culture supernatants and luciferase activity was quantified at different time points in cell lysates to evaluate viral replication. Results Addition of DBL3γ-732 to BeWo cells, led to a dose-dependent increase of HIV-1 replication of up to 400 times the control level in the absence of DBL3γ-732. This enhancement was specific since it was inhibited by Fab fragment of an anti- DBL3γ-732 monoclonal antibody but not by the Fab of an irrelevant mAb. In contrast, the addition of DBL1α-varO domain does not increase viral replication. In MDM which presents surface CSA, both DBL domains strongly inhibit viral replication. The effect of DBL3γ-732 on HIV-1 replication is most likely mediated by TNF-α as this cytokine is significantly increased by DBL3γ-732 binding to BeWo cells and MDM. Conclusions This study shows, for the first time, a direct link between a P. falciparum antigen and an increase of HIV-1 replication in placental cells in vitro. If this is occuring in vivo, the presence of both infections could lead to a higher risk of HIV-1 in utero transmission. These data underline the importance of efficient malaria prophylaxis and antiretroviral interventions for pregnant women in areas where HIV-1 and malaria co-circulate. [ABSTRACT FROM AUTHOR]