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<jats:p> Virus-specific CD4 <jats:sup>+</jats:sup> T helper lymphocytes are critical to the maintenance of effective immunity in a number of chronic viral infections, but are characteristically undetectable in chronic human immunodeficiency virus–type 1 (HIV-1) infection. In individuals who control viremia in the absence of antiviral therapy, polyclonal, persistent, and vigorous HIV-1–specific CD4 <jats:sup>+</jats:sup> T cell proliferative responses were present, resulting in the elaboration of interferon-γ and antiviral β chemokines. In persons with chronic infection, HIV-1–specific proliferative responses to p24 were inversely related to viral load. Strong HIV-1–specific proliferative responses were also detected following treatment of acutely infected persons with potent antiviral therapy. The HIV-1–specific helper cells are likely to be important in immunotherapeutic interventions and vaccine development. </jats:p>

<jats:p> Analysis of a continuous sedimentary record taken in the Maldives indicates that strong primary production fluctuations (70 to 390 grams of carbon per square meter per year) have occurred in the equatorial Indian Ocean during the past 910,000 years. The record of primary production is coherent and in phase with the February equatorial insolation, whereas it shows diverse phase behavior with δ <jats:sup>18</jats:sup> O, depending on the orbital frequency (eccentricity, obliquity, or precession) examined. These observations imply a direct control of productivity in the equatorial oceanic system by insolation. In the equatorial Indian Ocean, productivity is driven by the wind intensity of westerlies, which is related to the Southern Oscillation; therefore, it is suggested that a precession forcing on the Southern Oscillation is responsible for the observed paleoproductivity dynamics. </jats:p>

<jats:p>Surface current patterns were used to map dispersal routes of pelagic larvae from 18 coral reef sites in the Caribbean. The sites varied, both as sources and recipients of larvae, by an order of magnitude. It is likely that sites supplied copiously from “upstream” reef areas will be more resilient to recruitment overfishing, less susceptible to species loss, and less reliant on local management than places with little upstream reef. The mapping of connectivity patterns will enable the identification of beneficial management partnerships among nations and the design of networks of interdependent reserves.</jats:p>

<jats:p> Methyl–coenzyme M reductase (MCR), the enzyme responsible for the microbial formation of methane, is a 300-kilodalton protein organized as a hexamer in an α <jats:sub>2</jats:sub> β <jats:sub>2</jats:sub> γ <jats:sub>2</jats:sub> arrangement. The crystal structure of the enzyme from <jats:italic>Methanobacterium thermoautotrophicum</jats:italic> , determined at 1.45 angstrom resolution for the inactive enzyme state MCR <jats:sub>ox1-silent</jats:sub> , reveals that two molecules of the nickel porphinoid coenzyme F <jats:sub>430</jats:sub> are embedded between the subunits α, α′, β, and γ and α′, α, β′, and γ′, forming two identical active sites. Each site is accessible for the substrate methyl–coenzyme M through a narrow channel locked after binding of the second substrate coenzyme B. Together with a second structurally characterized enzyme state (MCR <jats:sub>silent</jats:sub> ) containing the heterodisulfide of coenzymes M and B, a reaction mechanism is proposed that uses a radical intermediate and a nickel organic compound. </jats:p>

<jats:p>Retroviral vectors containing CD4 and an appropriate chemokine receptor were evaluated for the ability to transduce cells infected with human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV). These CD4–chemokine receptor pseudotypes were able to target HIV- and SIV-infected cell lines and monocyte-derived macrophages in a manner that corresponded to the specificity of the viral envelope glycoprotein for its CD4–chemokine receptor complex. This approach could offer a way to deliver antiviral genes directly to HIV-infected cells in vivo and could provide an additional treatment strategy in conjunction with existing antiviral therapies.</jats:p>

<jats:p>Tiam1 encodes an exchange factor for the Rho-like guanosine triphosphatase Rac. Both Tiam1 and activated RacV12 promote invasiveness of T lymphoma cells. In epithelial Madin–Darby canine kidney (MDCK) cells, Tiam1 localized to adherens junctions. Ectopic expression of Tiam1 or RacV12 inhibited hepatocyte growth factor–induced scattering by increasing E-cadherin–mediated cell-cell adhesion accompanied by actin polymerization at cell-cell contacts. In Ras-transformed MDCK cells, expression of Tiam1 or RacV12 restored E-cadherin–mediated adhesion, resulting in phenotypic reversion and loss of invasiveness. These data suggest an invasion-suppressor role for Tiam1 and Rac in epithelial cells.</jats:p>

<jats:p> The bacterial Sec and signal recognition particle ( <jats:italic>ffh</jats:italic> -dependent) protein translocation mechanisms are conserved between prokaryotes and higher plant chloroplasts. A third translocation mechanism in chloroplasts [the proton concentration difference (ΔpH) pathway] was previously thought to be unique. The <jats:italic>hcf106</jats:italic> mutation of maize disrupts the localization of proteins transported through this ΔpH pathway in isolated chloroplasts. The <jats:italic>Hcf106</jats:italic> gene encodes a receptor-like thylakoid membrane protein, which shows homology to open reading frames from all completely sequenced bacterial genomes, which suggests that the ΔpH pathway has been conserved since the endosymbiotic origin of chloroplasts. Thus, the third protein translocation pathway, of which HCF106 is a component, is found in both bacteria and plants. </jats:p>

<jats:p> CCR5 and CD4 are coreceptors for immunodeficiency virus entry into target cells. The gp120 envelope glycoprotein from human immunodeficiency virus strain HIV-1(YU2) bound human CCR5 (CCR5 <jats:sub>hu</jats:sub> ) or rhesus macaque CCR5 (CCR5 <jats:sub>rh</jats:sub> ) only in the presence of CD4. The gp120 from simian immunodeficiency virus strain SIVmac239 bound CCR5 <jats:sub>rh</jats:sub> without CD4, but CCR5 <jats:sub>hu</jats:sub> remained CD4-dependent. The CD4-independent binding of SIVmac239 gp120 depended on a single amino acid, Asp <jats:sup>13</jats:sup> , in the CCR5 <jats:sub>rh</jats:sub> amino-terminus. Thus, CCR5-binding moieties on the immunodeficiency virus envelope glycoprotein can be generated by interaction with CD4 or by direct interaction with the CCR5 amino-terminus. These results may have implications for the evolution of receptor use among lentiviruses as well as utility in the development of effective intervention. </jats:p>