Uncoupled surface and below-ground soil respiration in mangroves: implications for estimates of dissolved inorganic carbon export

Potential disparities between rates of surface and below-ground respiration were examined in seven mangrove forests of different topographic height in Timor Leste. Differences in surface respiration between air-exposed and inundated soils were inconsistent, but surface respiration rates increased, with tidal elevation. Net primary production (NPP) on air-exposed soils declined with increasing forest cover indicating light limitation beneath the canopy. NPP and respiration were linearly related under both air-exposed and inundated conditions. Rates of DIC release from the soil surface varied among forests, correlating only with soil carbon (TOC) and nitrogen (TN) and their stoichiometric ratios. Sulfate reduction was detected to maximum depth of unconsolidated soil, correlating only with TOC and TN content at discrete depth intervals. DIC concentrations in drainage channels were equivalent to porewater concentrations. The rate of carbon mineralized by sulfate reducers (SRC) was equivalent to rates of total carbon oxidation (TCO) measured at the soil surface in forests at tidal heights?≤0.5?m above mean sea-level (MSL). However, SRC was increasingly greater than TCO in forests residing from 1.0 up to 2.5?m above MSL. Most carbon mineralized in subsurface deposits appears to seep out of the forest via groundwater. Rates of surface respiration therefore underestimate rates of total benthic carbon mineralization in forests at topographic heights?≥0.5?m above MSL, suggesting that the amount of respiratory carbon exported from many mangrove forests has also been underestimated.     

Evidence for an increased risk of transmission of simian immunodeficiency virus and malaria in a rhesus macaque coinfection model

In sub-Saharan Africa, HIV-1 infection frequently occurs in the context of other coinfecting pathogens, most importantly, Mycobacterium tuberculosis and malaria parasites. The consequences are often devastating, resulting in enhanced morbidity and mortality. Due to the large number of confounding factors influencing pathogenesis in coinfected people, we sought to develop a nonhuman primate model of simian immunodeficiency virus (SIV)-malaria coinfection. In sub-Saharan Africa, Plasmodium falciparum is the most common malaria parasite and is responsible for most malaria-induced deaths. The simian malaria parasite Plasmodium fragile can induce clinical symptoms, including cerebral malaria in rhesus macaques, that resemble those of P. falciparum infection in humans. Thus, based on the well-characterized rhesus macaque model of SIV infection, this study reports the development of a novel rhesus macaque SIV-P. fragile coinfection model to study human HIV-P. falciparum coinfection. Using this model, we show that coinfection is associated with an increased, although transient, risk of both HIV and malaria transmission. Specifically, SIV-P. fragile coinfected macaques experienced an increase in SIV viremia that was temporarily associated with an increase in potential SIV target cells and systemic immune activation during acute parasitemia. Conversely, primary parasitemia in SIV-P. fragile coinfected animals resulted in higher gametocytemia that subsequently translated into higher oocyst development in mosquitoes. To our knowledge, this is the first animal model able to recapitulate the increased transmission risk of both HIV and malaria in coinfected humans. Therefore, this model could serve as an essential tool to elucidate distinct immunological, virological, and/or parasitological parameters underlying disease exacerbation in HIV-malaria coinfected people.     

Functional Characterization of Two scFv-Fc Antibodies from an HIV Controller Selected on Soluble HIV-1 Env Complexes: A Neutralizing V3- and a Trimer-Specific gp41 Antibody

HIV neutralizing antibodies (nAbs) represent an important tool in view of prophylactic and therapeutic applications for HIV-1 infection. Patients chronically infected by HIV-1 represent a valuable source for nAbs. HIV controllers, including long-term non-progressors (LTNP) and elite controllers (EC), represent an interesting subgroup in this regard, as here nAbs can develop over time in a rather healthy immune system and in the absence of any therapeutic selection pressure. In this study, we characterized two particular antibodies that were selected as scFv antibody fragments from a phage immune library generated from an LTNP with HIV neutralizing antibodies in his plasma. The phage library was screened on recombinant soluble gp140 envelope (Env) proteins. Sequencing the selected peptide inserts revealed two major classes of antibody sequences. Binding analysis of the corresponding scFv-Fc derivatives to various trimeric and monomeric Env constructs as well as to peptide arrays showed that one class, represented by monoclonal antibody (mAb) A2, specifically recognizes an epitope localized in the pocket binding domain of the C heptad repeat (CHR) in the ectodomain of gp41, but only in the trimeric context. Thus, this antibody represents an interesting tool for trimer identification. MAb A7, representing the second class, binds to structural elements of the third variable loop V3 and neutralizes tier 1 and tier 2 HIV-1 isolates of different subtypes with matching critical amino acids in the linear epitope sequence. In conclusion, HIV controllers are a valuable source for the selection of functionally interesting antibodies that can be selected on soluble gp140 proteins with properties from the native envelope spike.     

Recognition of Lyso-Phospholipids by Human Natural Killer T Lymphocytes

Natural killer T (NKT) cells are a subset of T lymphocytes with potent immunoregulatory properties. Recognition of self-antigens presented by CD1d molecules is an important route of NKT cell activation; however, the molecular identity of specific autoantigens that stimulate human NKT cells remains unclear. Here, we have analyzed human NKT cell recognition of CD1d cellular ligands. The most clearly antigenic species was lyso-phosphatidylcholine (LPC). Diacylated phosphatidylcholine and lyso-phosphoglycerols differing in the chemistry of the head group stimulated only weak responses from human NKT cells. However, lyso-sphingomyelin, which shares the phosphocholine head group of LPC, also activated NKT cells. Antigen-presenting cells pulsed with LPC were capable of stimulating increased cytokine responses by NKT cell clones and by freshly isolated peripheral blood lymphocytes. These results demonstrate that human NKT cells recognize cholinated lyso-phospholipids as antigens presented by CD1d. Since these lyso-phospholipids serve as lipid messengers in normal physiological processes and are present at elevated levels during inflammatory responses, these findings point to a novel link between NKT cells and cellular signaling pathways that are associated with human disease pathophysiology.     

Drosophila CK2 phosphorylates Hairy and regulates its activity in vivo

Hairy is a repressor that regulates bristle patterning, and its loss elicits ectopic bristles (neural hyperplasia). However, it has remained unknown whether Hairy is regulated by phosphorylation. We describe here the interaction of protein kinase CK2 and Hairy. Hairy is robustly phosphorylated by the CK2-holoenzyme (CK2-HoloE) purified from Drosophila embryos, but weakly by the catalytic CK2α-subunit alone, suggesting that this interaction requires the regulatory CK2β-subunit. Consistent with this, Hairy preferentially forms a direct complex with CK2-HoloE. Importantly, we demonstrate genetic interactions between CK2 and hairy (h). Thus, flies trans-heterozygous for alleles of CK2α and h display neural hyperplasia akin to homozygous hypomorphic h alleles. In addition, we show that similar phenotypes are elicited in wild-type flies upon expression of RNAi constructs against CK2α/β, and that these defects are sensitive to h gene dosage. Together, these studies suggest that CK2 contributes to repression by Hairy.     

Biogeochemistry of inter-reef sediments on the northern and central Great Barrier Reef

The deposition and cycling of carbon and nitrogen in carbonate sediments located between coral reefs on the northern and central sections of the Great Barrier Reef were examined. Rates of mass sediment accumulation ranged from 1.9 kg m⁻² year⁻¹ (inshore reefs) to 2.1–4.9 kg m⁻² year⁻¹ (between mid-shelf reefs); sedimentation was minimal off outer-shelf reefs. Rates of total organic carbon decomposition ranged from 1.7 to 11.4 mol C m⁻² year⁻¹ and total nitrogen mineralization ranged from 77 to 438 mmol N m⁻² year⁻¹, declining significantly with distance from land. Sediment organic matter was highly reactive, with mineralization efficiencies ranging from 81 to 99% for organic carbon and 64–100% for nitrogen, with little C and N burial. There was no evidence of carbonate dissolution/precipitation in short-term incubation experiments. Rates of sulfate reduction (range 0–3.4 mmol S m⁻² day⁻¹) and methane release (range 0–12.8 μmol CH₄ m⁻² day⁻¹) were minor or modest pathways of carbon decomposition. Aerobic respiration, estimated by difference between total O₂ consumption and the sum of the other pathways, accounted for 55–98% of total carbon mineralization. Rates of ammonification ranged from 150 to 1,725 μmol NH₄ m⁻² day⁻¹, sufficient to support high rates of denitrification (range 30–2,235 μmol N₂ m⁻² day⁻¹). N₂O release was not detected and rates of NH₄ ⁺ and NO₂ ⁻ + NO₃ ⁻ efflux were low, indicating that most mineralized N was denitrified. The percentage of total N input removed via denitrification averaged ≈75% (range 28–100%) with little regenerated N available for primary producers. Inter-reef environments are therefore significant sites of energy and nutrient flow, especially in spatially complex reef matrices such as the Great Barrier Reef.