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Easterhoff, David,Moody, M. Anthony,Fera, Daniela,Cheng, Hao,Ackerman, Margaret,Wiehe, Kevin,Saunders, Kevin O.,Pollara, Justin,Vandergrift, Nathan,Parks, Rob,Kim, Jerome,Michael, Nelson L.,O’Connell, Public Library of Science 2017 PLoS pathogens Vol.13 No.2
<▼1><P>The canary pox vector and gp120 vaccine (ALVAC-HIV and AIDSVAX B/E gp120) in the RV144 HIV-1 vaccine trial conferred an estimated 31% vaccine efficacy. Although the vaccine Env AE.A244 gp120 is antigenic for the unmutated common ancestor of V1V2 broadly neutralizing antibody (bnAbs), no plasma bnAb activity was induced. The RV305 (NCT01435135) HIV-1 clinical trial was a placebo-controlled randomized double-blinded study that assessed the safety and efficacy of vaccine boosting on B cell repertoires. HIV-1-uninfected RV144 vaccine recipients were reimmunized 6–8 years later with AIDSVAX B/E gp120 alone, ALVAC-HIV alone, or a combination of ALVAC-HIV and AIDSVAX B/E gp120 in the RV305 trial. Env-specific post-RV144 and RV305 boost memory B cell V<SUB>H</SUB> mutation frequencies increased from 2.9% post-RV144 to 6.7% post-RV305. The vaccine was well tolerated with no adverse events reports. While post-boost plasma did not have bnAb activity, the vaccine boosts expanded a pool of envelope CD4 binding site (bs)-reactive memory B cells with long third heavy chain complementarity determining regions (HCDR3) whose germline precursors and affinity matured B cell clonal lineage members neutralized the HIV-1 CRF01 AE tier 2 (difficult to neutralize) primary isolate, CNE8. Electron microscopy of two of these antibodies bound with near-native gp140 trimers showed that they recognized an open conformation of the Env trimer. Although late boosting of RV144 vaccinees expanded a novel pool of neutralizing B cell clonal lineages, we hypothesize that boosts with stably closed trimers would be necessary to elicit antibodies with greater breadth of tier 2 HIV-1 strains.</P><P><B>Trial Registration:</B> ClinicalTrials.gov NCT01435135</P></▼1><▼2><P><B>Author summary</B></P><P>Developing a successful HIV-1 vaccine remains a high global health priority. Several HIV-1 vaccine trials have been performed with only the RV144 vaccine trial showing vaccine efficacy, albeit modest. No broadly neutralizing antibody activity was identified in RV144 and inducing sterilizing immunity against a complex pathogen like HIV-1 remains a major challenge. Here we characterize the B cell responses after RV144 vaccine-recipients received two additional boosts severals years after the conclusion of the RV144 vaccine trial. Delayed and repetitive boosting of RV144 vaccine-recipients was capable of increasing somatic hypermutation of the Env-reactive antibodies and expanding subdominant pools of neutralizing B cell clonal lineages. These data are pertinent to HIV-1 vaccine-regimen design.</P></▼2>
Fernandez, Maria Luz,Jones, Jennifer J.,Ackerman, Daniela,Barona, Jacqueline,Calle, Mariana,Comperatore, Michael V.,Kim, Jung-Eun,Andersen, Catherine,Leite, Jose O.,Volek, Jeff S.,McIntosh, Mark,Kalyn The Korean Nutrition Society 2010 Nutrition Research and Practice Vol. No.
Both metabolic syndrome (MetS) and elevated LDL cholesterol (LDL-C) increase the risk for cardiovascular disease (CVD). We hypothesized that low HDL cholesterol (HDL-C) would further increase CVD risk in women having both conditions. To assess this, we recruited 89 women with MetS (25-72 y) and LDL-C ${\geq}$ 2.6 mmol/L. To determine whether plasma HDL-C concentrations were associated with dietary components, circulating atherogenic particles, and other risk factors for CVD, we divided the subjects into two groups: high HDL-C (H-HDL) (${\geq}$ 1.3 mmol/L, n=32) and low HDL-C (L-HDL) (< 1.3 mmol/L, n=57). Plasma lipids, insulin, adiponectin, apolipoproteins, oxidized LDL, Lipoprotein(a), and lipoprotein size and subfractions were measured, and 3-d dietary records were used to assess macronutrient intake. Women with L-HDL had higher sugar intake and glycemic load (P< 0.05), higher plasma insulin (P< 0.01), lower adiponectin (P< 0.05), and higher numbers of atherogenic lipoproteins such as large VLDL (P < 0.01) and small LDL (P<0.001) than the H-HDL group. Women with L-HDL also had larger VLDL and both smaller LDL and HDL particle diameters (P<0.001). HDL-C was positively correlated with LDL size (r=0.691, P<0.0001) and HDL size (r=0.606, P<0.001), and inversely correlated with VLDL size (r=-0.327, P<0.01). We concluded that L-HDL could be used as a marker for increased numbers of circulating atherogenic lipoproteins as well as increased insulin resistance in women who are already at risk for CVD.
Maria Luz Fernandez,Jennifer J Jones,Daniela Ackerman,Jacqueline Barona,Mariana Calle,Michael V Comperatore,Jung-Eun Kim,Catherine Andersen,Jose O Leite,Jeff S Volek,Mark McIntosh,Colleen Kalynych,Wad 한국영양학회 2010 Nutrition Research and Practice Vol.4 No.6
Both metabolic syndrome (MetS) and elevated LDL cholesterol (LDL-C) increase the risk for cardiovascular disease (CVD). We hypothesized that low HDL cholesterol (HDL-C) would further increase CVD risk in women having both conditions. To assess this, we recruited 89 women with MetS (25-72 y) and LDL-C ≥ 2.6 mmol/L. To determine whether plasma HDL-C concentrations were associated with dietary components, circulating atherogenic particles, and other risk factors for CVD, we divided the subjects into two groups: high HDL-C (H-HDL) (≥ 1.3 mmol/L, n = 32) and low HDL-C (L-HDL) (< 1.3 mmol/L, n = 57). Plasma lipids, insulin, adiponectin, apolipoproteins, oxidized LDL, Lipoprotein(a), and lipoprotein size and subfractions were measured, and 3-d dietary records were used to assess macronutrient intake. Women with L-HDL had higher sugar intake and glycemic load (P < 0.05), higher plasma insulin (P < 0.01), lower adiponectin (P < 0.05), and higher numbers of atherogenic lipoproteins such as large VLDL (P < 0.01) and small LDL (P < 0.001) than the H-HDL group. Women with L-HDL also had larger VLDL and both smaller LDL and HDL particle diameters (P < 0.001). HDL-C was positively correlated with LDL size (r = 0.691, P < 0.0001) and HDL size (r = 0.606, P < 0.001), and inversely correlated with VLDL size (r = -0.327, P < 0.01). We concluded that L-HDL could be used as a marker for increased numbers of circulating atherogenic lipoproteins as well as increased insulin resistance in women who are already at risk for CVD.