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Query: UMLS:C0001175 (AIDS)
 120,706 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In vitro exposure of human blood monocyte-derived macrophages to T-cell tropic human immunodeficiency virus (HIV) isolates fails to establish a productive viral infection. Several studies have shown that such preferential HIV-1 replication in T cells or in mononuclear phagocytes (HIV tropism) may be determined by distinct viral characteristics. In the present study it was demonstrated that transforming growth factor-beta (TGF-beta), a factor known to be produced by platelets, macrophages, and other cells present at a wound site, can act as a mediator in overcoming the lymphocytotropic restriction of several well-characterized viral isolates of HIV-1 (i.e., LAV, Z84, pLAI, NY5). Macrophages infected with these isolates show cytopathic changes comparable to those seen upon infection with the monocytotropic isolate ADA. To achieve this effect with TGF-beta, the factor must be present after the infection period. The emerging virus retains its original cellular tropism. Based on these observations the authors propose a role for TGF-beta in the establishment and progression of HIV infection and disease.
AIDS Res Hum Retroviruses 1992 Apr
PMID:The replicative restriction of lymphocytotropic isolates of HIV-1 in macrophages is overcome by TGF-beta. 159 57

Human immunodeficiency virus (HIV-1) infected and replicated in primary cultures of normal human ileal and colonic epithelial cells. Monocyte-tropic strains (ADA, 24, and 36) were better able to replicate in the gastrointestinal (GI) cells than the T-cell-tropic HIV strain HTLV-IIIB. In some cultures, virus replication persisted through several months. Intestinal epithelium may be an initial target and reservoir for HIV and a vector for virus dissemination and transmission.
AIDS Res Hum Retroviruses 1990 Dec
PMID:Infection of human gastrointestinal cells by HIV-1. 207 18

The drug prescribing practices of dentists should be of interest to the dental profession, drug manufacturers, the medical profession and dental educators. This article presents an update on an earlier similar survey reported by the authors as well as information on current infection control procedures, the treatment of hepatitis and AIDS patients, and generic drug substitution. The classes of drugs that are important to the practitioner and the level of prescribing activity have not changed appreciably since the earlier study. There has been, however, a significant change in nonopioid analgesic drug preference with ibuprofen overtaking aspirin and acetaminophen by a wide margin. That age affects the character of practice was confirmed: far fewer older practitioners report prescribing drugs than do their younger counterparts. A very gratifying finding was the high level of compliance with ADA recommendations regarding infectious diseases although fears over treating AIDS patients remain high.
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PMID:A survey of dentists' drug prescribing practices. 253 30

Cytokines such as tumour necrosis factor-alpha (TNF-alpha) and IL-1 beta may play a role in immunopathogenesis of AIDS. We studied early effects (0.5-48 h) of monocytotropic (ADA) or lymphotropic (IIIB) strains of HIV-1 on TNF-alpha and IL-1 beta mRNA expression in primary human macrophages by a semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) assay. Three-day-old monocyte-derived macrophages were exposed either to tissue culture supernatants containing virus (at multiplicity of infection (m.o.i.) of 0.05) or to control supernatants free of virions and gp120. ADA strain, but not IIIB, replicated in primary tissue culture-differentiated macrophages (TCDM). Soluble CD4 (sCD4) was used to inhibit binding of both strains to macrophages. We found that TNF-alpha and IL-1 beta gene expression was induced by both strains 0.5-3 h after addition of virus, and that enhanced expression of both cytokines was inhibited by sCD4. We conclude that CD4-dependent binding to the cell surface is sufficient to enhance TNF-alpha and IL-1 beta mRNA, whereas productive viral replication in primary human macrophages is not required. Therefore, similar pathways regulate gene expression of TNF-alpha and IL-1 beta by macrophages during initial infection by HIV-1 in vitro.
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PMID:HIV-1 induces tumour necrosis factor and IL-1 gene expression in primary human macrophages independent of productive infection. 751 Oct 77

Cellular CD4 is the primary membrane molecule that binds HIV-1 through interaction with viral gp120. Membrane glycolipids and cell adhesion molecules have also been noted to be involved in the interaction of HIV-1 with cells and in syncytium formation in infected cells. The purpose of this study was to determine the role of the cell adhesion molecule CD44 in HIV-1 infection of cells. Both normal blood monocytes and lymphocytes expressed CD44 as determined by flow cytometry using the anti-CD44 antibody A3D8. Anti-CD44 monoclonal antibodies A3D8, A1G3, and 5F12 [ascites, purified IgG, and F(ab')2] inhibited infection of monocytes and peritoneal macrophages with HIV-1-BaL and HIV-1-ADA, but had no effect on HIV-1-IIIB infection of mitogen-stimulated lymphocytes, or cells of a T lymphocyte line. CD44 monoclonal antibodies were not toxic for monocytes, and the observed inhibitory effect of CD44 monoclonal antibodies was not dependent on complement. These results suggest that CD44 may be a determinant of HIV-1 infection of mononuclear phagocytes in vitro.
AIDS Res Hum Retroviruses 1995 May
PMID:Inhibition of HIV type 1 infection of mononuclear phagocytes by anti-CD44 antibodies. 757 9

Adenosine deaminase (adenosine aminohydrolase, EC 3.5.4.4; ADA) activity is widely distributed in human tissues and is highest in lymphoid tissues. Two ADA isozymes are known as ADA1 and ADA2. Human tissue extracts contained ADA1 predominantly. Meanwhile, ADA2 was the main component of serum ADA. ADA activity was significantly elevated in the sera from patients with hepatic diseases, hematological malignancies and infectious diseases. Serum concentrations of ADA1 were high in patients with acute leukemias, chronic myeloid blast crisis leukemia and acute liver injury. Serum ADA2 levels were raised in patients with adult T-cell leukemia, multiple myeloma (B-J type), infectious mononucleosis, rubella, acquired immunodeficiency syndrome, chronic hepatic diseases and tuberculosis. It is supposed that ADA1 is derived mainly from injured tissues or cells while ADA2 comes from stimulated T-cells.
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PMID:[Adenosine deaminase]. 760 76

The elevation of ADA in CSF is useful as a diagnostic means for detecting tuberculous meningitis, and in other etiologies such as lymphoma, neurosarcoidosis, fulminant bacterial meningitis, cryptococcal meningitis, neurobrucellosis and AIDS. We report an increase of ADA in CSF in association with SHA. In our case the total activity of ADA was the same as that obtained in serum, which can be interpreted among the false positives of the determination.
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PMID:False positive of ADA determination in cerebrospinal fluid. 770

To insert a new genetic information by gene transfer into haemopoietic stem cells would result in expression of the transgene in progenitors and progeny of cell blood lineages. If successfull, such an approach would open interesting prospectives in the field of experimental research and in the possibility to treat genetic defects affecting blood lineages such as immune deficiencies (ADA, SCID, AIDS) or enzymes defects. Moreover progenitors could be engineered to become more resistant to chemotherapy or oncogenic process. Many parameters and technical problems are still involved in this issue, including identification, isolation and selection of the most primitive progenitors, and search for the most efficient vectors to insert new genes into the target cells. So far retroviral vectors have been shown to be the most effective but search for better vectors are still underway. Peripheral blood stem cells isolated from patients stimulated by cytokines and/or chemotherapy appear interesting target cells for genetic manipulations aimed to correct an acquired or genetic defect.
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PMID:[Gene transfer in human hematopoietic stem cells isolated from peripheral blood]. 888 Dec 70

Recent studies have demonstrated that the beta-chemokines RANTES, MIP-1alpha, and MIP-1beta suppress human immunodeficiency virus type 1 (HIV-1) replication in vitro and may play an important role in protecting exposed but uninfected individuals from HIV-1 infection. However, levels of beta-chemokines in AIDS patients are comparable to and can exceed levels in nonprogressing individuals, indicating that global beta-chemokine production may have little effect on HIV-1 disease progression. We sought to clarify the role of beta-chemokines in nonprogressors and AIDS patients by examination of beta-chemokine production and HIV-1 infection in patient T-lymphocyte clones established by herpesvirus saimiri immortalization. Both CD4+ and CD8+ clones were established, and they resembled primary T cells in their phenotypes and expression of activated T-cell markers. CD4+ T-cell clones from all patients had normal levels of mRNA-encoding CCR5, a coreceptor for non-syncytium-inducing (NSI) HIV-1. CD4+ clones from nonprogressors and CD8+ clones from AIDS patients secreted high levels of RANTES, MIP1alpha, and MIP-1beta. In contrast, CD4+ clones from AIDS patients produced no RANTES and little or no MIP-1alpha or MIP-1beta. The infection of CD4+ clones with the NSI HIV-1 strain ADA revealed an inverse correlation to beta-chemokine production; clones from nonprogressors were poorly susceptible to ADA replication, but clones from AIDS patients were highly infectable. The resistance to ADA infection in CD4+ clones from nonprogressors could be partially reversed by treatment with anti-beta-chemokine antibodies. These results indicate that CD4+ cells can be protected against NSI-HIV-1 infection in culture through endogenously produced factors, including beta-chemokines, and that beta-chemokine production by CD4+, but not CD8+, T cells may constitute one mechanism of disease-free survival for HIV-1-infected individuals.
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PMID:Endogenous production of beta-chemokines by CD4+, but not CD8+, T-cell clones correlates with the clinical state of human immunodeficiency virus type 1 (HIV-1)-infected individuals and may be responsible for blocking infection with non-syncytium-inducing HIV-1 in vitro. 942 Mar 4

We previously demonstrated that completion of reverse transcription in macrophages inoculated with the HIV-1 Ba-L variant was established only in the subpopulation of cells with proliferative capacity. In our present study we further extended this observation with three additional HIV-1 isolates, being the macrophage-tropic ADA strain and two primary macrophage-tropic HIV-1 variants isolated from cerebrospinal fluid and from bronchoalveolar lavage from AIDS patients. On inoculation, irrespective of the virus variant used, elongated reverse transcription products could be demonstrated only in macrophages that had proliferated during inoculation as evidenced by the incorporation of bromodeoxyuridine (BrdU), a thymidine analog. The presence of newly synthesized early products of reverse transcription also in the BrdU-negative fraction indicated that viral entry is not disturbed in nondividing cells. Our data indicate that the process of reverse transcription is dependent on cellular conditions that coincide with cell proliferation, and therefore that HIV-1 replication is restricted to cells with proliferative potential.
AIDS Res Hum Retroviruses 1998 Mar 01
PMID:Proliferation-dependent replication in primary macrophages of macrophage-tropic HIV type 1 variants. 951 95


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