The hypernetted-chain integral equation is used to calculate the ion–ion pair correlation functions and the thermodynamic properties of models for aqueous alkali halides based on an ion–ion pair potential function having four terms: the usual Coulomb term, a core repulsion term of order r−9, a well-known dielectric repulsion term of order r−4, and a “Gurney” term to represent the effect of the overlap of the structure-modified regions, “cospheres,” about the ions when the ions come close together. The only parameter in the potential which is adjusted to fit excess free energy data for solutions is the coefficient Aij of the Gurney term for the interaction of ions of species i and j. This is scaled so it represents the molar free energy change of water displaced from the cospheres when they overlap. The corresponding entropy change Sij and volume change Vij are adjusted to fit, respectively, heat of dilution and apparent molal volume data. Some thermodynamic problems in this fitting process, due to the underlying McMillan–Mayer theory, are considered in detail. Good agreement is obtained between computed model properties and experiment for various sets of these parameters. Detailed results are given for one consistent set of Aij, Sij, and Vij parameters for all the alkali halide solutions for which the required data are available. The Aij parameters are in the range from 100 to − 200 cal/mole. Since this is small compared to RT, the thermodynamic data for these solutions can be interpreted without assuming rigid hydration of any of the ions, a conclusion previously reached by Rasaiah from the study of quite different models. The trends in A+− with variation of species do seem to reflect hydration and structure-breaking effects in the solutions. The sign of S+− is paradoxical, also in agreement with Rasaiah's results, while V+− and S+− seem to be mutually consistent.
The general theory of the calculation of the thermodynamic coefficients for electrolyte mixtures from the pair correlation functions for the mixtures is worked out. These correlation functions are computed for several models for aqueous LiCl-CsCl mixtures by means of the hypernetted-chain integral equation, and the theory is applied to them to obtain the free-energy mixing coefficients for these models. Special attention is given to a model having properties close to the experimental ones for this system. The computed results for this model seem to be accurate enough to be useful, judging by three self-consistency tests. The model exhibits three empirically established regularities about as well as experimental systems do. They are Harned's rule, Young's rule that certain mixing coefficients in a common-ion mixture are nearly independent of the common ion, and the rule that the sum of Harned's a coefficients depends linearly on the ionic strength. The model computations also elucidate the role of the mixture limiting law.
The sequences presented in this article have been submitted to the National Center for Biotechnology Information's Gene Expression Omnibus (www.ncbi.nlm.nih.gov/geo/) under accession number GSE164381.
Ebola virus (EBOV) infections are characterized by a pronounced lymphopenia that is highly correlative with fatalities. However, the mechanisms leading to T-cell depletion remain largely unknown. Here, we demonstrate that both viral mRNAs and antigens are detectable in CD4+ T cells despite the absence of productive infection. A protein phosphatase 1 inhibitor, 1E7-03, and siRNA-mediated suppression of viral antigens were used to demonstrate de novo synthesis of viral RNAs and antigens in CD4+ T cells, respectively. Cell-to-cell fusion of permissive Huh7 cells with non-permissive Jurkat T cells impaired productive EBOV infection suggesting the presence of a cellular restriction factor. We determined that viral transcription is partially impaired in the fusion T cells. Lastly, we demonstrate that exposure of T cells to EBOV resulted in autophagy through activation of ER-stress related pathways. These data indicate that exposure of T cells to EBOV results in an abortive infection, which likely contributes to the lymphopenia observed during EBOV infections.
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