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CD8 + T lymphocytes play a key role in controlling viremia during primary human immunodeficiency virus-1 and in maintaining disease-free infection. It has recently been shown that DNA immunization of rhesus monkeys can elicit strong, long-lived antigen-specific cytotoxic T lymphocyte (CTL) responses. In previous work, it was shown that macaque CTL responses to lipopeptide vaccination were...
It is speculated that a virus-encoded superantigen is involved in the pathogenesis of human and simian immunodeficiency virus infections and that the accessory protein Nef might be that superantigen. We are able to show, using a murine superantigen screening system, that Nef does not display features characteristic of a superantigen. Upon transfection into MHC class II expressing antigen-presenting...
The negative factor (Nef) is one of six accessory proteins from primate lentiviruses (HIV-1, HIV-2, and SIV). It leads to high levels of viremia and the progression to AIDS in monkeys and humans. In this study, we demonstrated that Nef from HIV-1 binds to the regulatory subunit (p85) of phosphatidylinositol-3-kinase (PI3K). This interaction depended on the C-terminus of p85 and Nef. Moreover, PI3K...
Human and simian immunodeficiency virus (HIV and SIV) may co-opt antigen capture and presentation functions of antigen presenting cells (APCs) to facilitate infection of CD4 + T-cells. To address whether the replicative capacity of SIV in the host may be associated with the extent of viral replication in response to APC–T-cell interactions, we compared the replicative phenotypes of cloned...
Nef, a multifunctional accessory protein of human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV), is important for disease progression. Nef downmodulates CD4 and MHC class I expression, alters host-cell signal transduction pathways, and enhances viral replication. We have identified a novel interaction between Nef and cAMP-dependent kinase (PKA). N-terminal serine residues Ser...
The Nef protein of Human Immunodeficiency Virus (HIV) and Simian Immunodeficiency Virus (SIV) is a pluripotent accessory protein that plays a critical role in disease progression. One analogous characteristic of Nef proteins from SIV and HIV is the ability to associate with cellular kinases. We have previously reported that the Nef protein from a macrophage-tropic neurovirulent SIV clone, SIV/17E-Fr,...
It has been demonstrated that the HIV-1 NL4-3 and IIIB Nef alleles downregulate HLA-A and -B but not -C or -E from the cell surface. It remained elusive, however, whether selective modulation of specific HLA molecules is conserved between different groups of human and simian immunodeficiency viruses, respectively. To address this, we analyzed a large panel of primate lentiviral Nef proteins and we...
CD8 + cytotoxic T lymphocytes (CTL) play an important role in controlling virus replication in HIV- and SIV-infected humans and monkeys, respectively. Three well-studied SIV CTL determinants are the two Mamu A ⁎ 01-restricted epitopes Gag CM9 and Tat SL8, and the Mamu B ⁎ 17-restricted epitope Nef IW9. Point mutations leading to amino acid replacements in these epitopes have...
Infection with Simian Immunodeficiency Virus (SIV) leads to high viral loads and progression to Simian AIDS (SAIDS) in rhesus macaques. The viral accessory protein Nef is required for this phenotype in monkeys as well as in HIV-infected humans. Previously, we determined that HIVNef binds HIVGagPol and Alix for optimal viral replication in cells. In this study, we demonstrated that these interactions...
Previous studies demonstrated that the nef gene is a critical determinant of the pathogenicity of simian immunodeficiency virus (SIV) in macaques. In the present study, we evaluated the effect of a spontaneous frameshift mutation in the C-terminus of the nef gene of the minimally pathogenic SIVsmH4i clone. This clone exhibited a single nucleotide deletion in the nef gene relative to pathogenic SIV...
HIV-1 NL4-3 Vpu induces downregulation of cell surface CD155, a ligand for the DNAM-1 activating receptor of NK and CD8+ T cells, to evade NK cell mediated immune response. Here we show that the conserved alanine residues at positions 10, 14 and 18 in the TM domain of Vpu are required for the efficient downregulation of cell surface CD155. In contrast, the CK-2 phosphorylation sites and the second...
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