Abstract: The invention provides monocytes expressing CD16 and CD163 and experimental system for drug screening or evaluating drug candidates where the modulation of CD16 and CD163 is desired.

Abstract: The invention provides monocytes expressing CD16 and CD163 and experimental system for drug screening or evaluating drug candidates where the modulation of CD16 and CD163 is desired.

Abstract: Provided is a method of detecting mild neurocognitive disturbance (MNCD) or HIV associated dementia (HAD) in a patient comprising detecting the level of acetyl spermine and/or acetyl spermidine from a cerebrospinal fluid test sample of the patient; and comparing the level of acetyl spermine and/or acetyl spermidine in the test sample to the level of the acetyl spermine and/or acetyl spermidine in a cerebrospinal fluid control sample or to a control value for lack of neurocognitive impairment, MNCD or HAD; wherein an elevated level of acetyl spermine and/or acetyl spermidine in the test sample as compared to the level in the control sample or a control value for lack of neurocognitive impairment, or a level of acetyl spermine and/or acetyl spermidine that is similar to that of a control value for MNCD or HAD, indicates that the patient suffers from MNCD or HAD. Also provided are methods for measuring the progression of an HIV-1-associated neurocognitive disorder, as well as methods for staging such a disorder.

Abstract: Provided is a method of detecting mild neurocognitive disturbance (MNCD) or HIV associated dementia (HAD) in a patient comprising detecting the level of acetyl spermine and/or acetyl spermidine from a cerebrospinal fluid test sample of the patient; and comparing the level of acetyl spermine and/or acetyl spermidine in the test sample to the level of the acetyl spermine and/or acetyl spermidine in a cerebrospinal fluid control sample or to a control value for lack of neurocognitive impairment, MNCD or HAD; wherein an elevated level of acetyl spermine and/or acetyl spermidine in the test sample as compared to the level in the control sample or a control value for lack of neurocognitive impairment, or a level of acetyl spermine and/or acetyl spermidine that is similar to that of a control value for MNCD or HAD, indicates that the patient suffers from MNCD or HAD. Also provided are methods for measuring the progression of an HIV-1-associated neurocognitive disorder, as well as methods for staging such a disorder.

Abstract: The invention provides a method for detecting CD163+/CD16+ cell population in peripheral blood mononuclear cells in a biological sample from a subject infected with HIV-1 which comprises contacting the biological sample with an anti-CD163 antibody, so that levels of CD163+/CD16+ peripheral blood mononuclear cells in the biological sample can be quantified.

Abstract: The invention provides a method for detecting CD163+/CD16+ cell population in peripheral blood mononuclear cells in a biological sample from a subject infected with HIV-1 which comprises contacting the biological sample with an anti-CD163 antibody, so that levels of CD163+/CD16+ peripheral blood mononuclear cells in the biological sample can be quantified.

Abstract: Macrophage colony-stimulating factor (M-CSF) is important for human immunodeficiency virus-type 1 (HIV-1) infection, replication and survival of infected cells. The mechanism(s) by which HIV-1 infection increases M-CSF production are, however, poorly understood. Here, we report that HIV-1 Vpr enhances M-CSF promoter activity and production in primary human monocytes and macrophages. Vpr activates M-CSF transcription through four C/EBP beta binding sites present within the M-CSF promoter, possibly through increased phosphorylation of C/EBP beta. RU486 (mifepristone) blocked Vpr-mediated up-regulation of M-CSF, suggesting that Vpr activates M-CSF promoter activity via the glucocorticoid pathway. The invention provides new avenues for therapeutic interventions in HIV-1 infection and other diseases involving M-CSF dysregulation (including malignancy, osteoporosis, autoimmune disorders, arthritis, and obesity) using glucocorticoid antagonists and modulators of C/EBP beta activity.

Abstract: This invention relates to retroviral regulatory proteins or fragments thereof, or interferon alpha protein or fragments thereof, which are carboxymethylated. This chemical modification leads to new proteins or fragments which are biologically inactive but preserve their immunogenicity (toxoids). These proteins or fragments thereof, or interferon alpha or fragments thereof, can be utilized in the treatment and prevention of retroviral infections. The invention also relates to a pharmaceutical composition comprising at least one carboxymethylated protein or fragment of the invention, together with a pharmaceutically acceptable carrier. The invention also relates to a vaccine comprising at least one of the carboxymethylated proteins or fragments of the invention, together with an immunologically acceptable carrier. The invention also relates to a process for obtaining an immunogenic yet not toxic retroviral regulatory protein or fragment, or interferon alpha or fragment.

Abstract: The present invention provides a Tat protein wherein all the cysteine residues of the cysteine-rich domain have been replaced with another amino acid, preferably with serine, nucleic acids encoding it, and methods of using it to elicit a humoral and cellular immune responses in a mammal. The Tat protein of the invention is therefore useful, inter alia, for prophylactic and/or therapeutic anti-HIV use as well as raising anti-native Tat antibodies in mammals.

Abstract: The invention concerns a viral regulation protein or a viral regulation protein fragment or the alpha interferon or the alpha interferon fragment which is carboxymethylated. The invention also concerns the preparation method and the use of the resulting product in a therapeutic method for treating the human or animal body, a pharmaceutical and vaccine composition containing, as active principle, one at least of the carboxymethylated proteins or fragments.

Abstract: A method for evaluating the inhibitory effect of a substance on tat-protein TAR RNA binding is described. A test system for determining the association of tat-protein with TAR RNA is also included within the scope of the invention.