zqfang/GSEApy: gseapy-1.1.0

<h2>What's Changed</h2> <p>New:</p> <ul> <li>Add <code>gsva</code> module: This is the Rust implementation of <code>GSVA</code> algorithm. #226</li> </ul> <p>Fixed:</p> <ul> <li>#211, Now, <code>pheno_pos</code> and <code>pheno_neg</code> can define with</li> </ul> <pre><code class="language-python">from gseapy import GSEA gs = GSEA(data="./tests/extdata/Leukemia_hgu95av2.trim.txt", gene_sets='KEGG_2016', classes = "./tests/extdata/Leukemia.cls" ) # set here gs.pheno_pos = ... gs.pheno_neg = ... gs.run() </code></pre> <ul> <li>improvement for <code>barplot</code> #224. Specify colors for each group explicity</li> </ul> <pre><code class="language-python">barplot( ...., color= {'KEGG_2021_Human': 'salmon', 'MSigDB_Hallmark_2020':'darkblue'}) </code></pre> <p><strong>Full Changelog</strong>: https://github.com/zqfang/GSEApy/compare/v1.0.6...v1.1.0</p&gt

Immunogenicity of combined anti-HIV and anti-suppressive vaccine preparations

HIV-1 antigens generate in man both a humoral and cellular immune reaction. However, in ARC/AIDS patients, the cellular response is inhibited by HIV-1 which induces an antiproliferative (suppressive) effect on activated T cells. To overcome this inhibition and up-regulate the cellular response, we designed a new vaccine strategy directed both against HIV-1 and immunosuppression and we used an immunizing preparation composed of HIV-1 antigens combined with immunoregulatory peptides prepared in a biologically inactivated but immunogenic form. In mice, this preparation induced anti-HIV-1 antibodies and a cell-mediated cytotoxicity directed against H2 restricted cells carrying HIV-1 antigens. HIV-1 vaccine / immunosuppression / HIV-1 peptides. © 1992.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

One-year follow-up of vaccine therapy in hiv-infected immune-deficient individuals: A new strategy

Immunization of AIDS/ARC patients with autologous cells expressing HIV antigens, although providing clinical and biological benefits, fails to restore cellular immunity. The latter result is due partly to the antiproliferative effect of HIV-1 on activated T-cells (immune suppression), which leads to blockade of specific immune reactions. To overcome immune suppression, a new vaccine strategy was designed consisting of an immunization against HIV-1 combined with components of the T-cell-suppressive (antiproliferative) network. This new vaccine treatment proved to be innocuous in mice, monkeys, and two non-HIV-infected humans. A Phase I clinical trial was performed in six patients previously under cellular immunotherapy and still presenting a cellular immune defect. Preliminary results confirmed, after a 1-year follow-up of the patients, the safety of the new vaccine, which also partially restored the cellular immune response, including anti-HIV HLA-restricted cell-mediated cytotoxicity, delayed hypersensitivity to recall antigens, and proliferation of T-cells specifically activated by recall antigens. © 1992 Raven Press, New York.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

SARS-CoV-2 variants evolve convergent strategies to remodel the host response

SARS-CoV-2 variants of concern (VOCs) emerged during the COVID-19 pandemic. Here, we used unbiased systems approaches to study the host-selective forces driving VOC evolution. We discovered that VOCs evolved convergent strategies to remodel the host by modulating viral RNA and protein levels, altering viral and host protein phosphorylation, and rewiring virus-host protein-protein interactions. Integrative computational analyses revealed that although Alpha, Beta, Gamma, and Delta ultimately converged to suppress interferon-stimulated genes (ISGs), Omicron BA.1 did not. ISG suppression correlated with the expression of viral innate immune antagonist proteins, including Orf6, N, and Orf9b, which we mapped to specific mutations. Later Omicron subvariants BA.4 and BA.5 more potently suppressed innate immunity than early subvariant BA.1, which correlated with Orf6 levels, although muted in BA.4 by a mutation that disrupts the Orf6-nuclear pore interaction. Our findings suggest that SARS-CoV-2 convergent evolution overcame human adaptive and innate immune barriers, laying the groundwork to tackle future pandemics