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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous studies have demonstrated that the expression of CD25 can distinguish CD25- latently infected cells from CD25+ cells actively producing virus. Our studies were designed to characterize the nature and stability of the viral genome in CD25- quiescent HIV-1-infected cells and to determine whether these cells could be infected de novo with HIV-1. Our results show that: (i) When unfractionated peripheral blood mononuclear cells are first infected with HIV-1 and the CD25- cells then isolated, the latter contain only incomplete DNA transcripts and no full-length DNA or 2-LTR circles. Phytohemagglutinin activation of these CD25- cells results in the generation of full-length viral DNA and p24 production. (ii) When CD25- CD4+ cells are first purified from peripheral blood mononuclear cells and then incubated with HIV-1, viral DNA cannot be detected, suggesting that these purified cells cannot be infected. Furthermore, CD25-adherent cells do not facilitate the infection of CD4+ CD25- T cells when they were present at the time of incubation with HIV-1. Taken together, these studies suggest either that (i) the CD25- cells containing incomplete DNA transcripts are derived from infected-activated CD25+ cells, which subsequently become CD25- or (ii) the presence of CD25+ cells is required for the infection of CD25- cells in vitro.
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PMID:Highly purified CD25- resting T cells cannot be infected de novo with HIV-1. 903 58

Our study investigated the presence of IL-8 in pleural exudates from tuberculosis patients (TBP) (n = 13), and evaluated whether it was related with the profile of major immunocompetent cells present in their pleural and peripheral compartments. To allow comparisons, an additional group of patients with parapneumonic pleural effusions (PNE) (n = 7) was included. Blood peripheral immunophenotypic studies were also carried out in 12 age-matched healthy controls (Co), and 39 tuberculosis patients classified, according to the extent of pulmonary involvement, into mild (n = 9), and advanced (n = 30) cases. Patients were recruited before starting therapy, had HIV negative serology, and showed no age differences among groups (mean +/- SD., 40.7 +/- 14.7 years). IL-8 concentrations were measured by an ELISA method while immunophenotypic analysis was performed by using FITC-conjugated monoclonal antibodies reacting against the following cell surface molecules: CD3, CD4, CD8, CD25 (IL-2R+ cells), CD19, and CD68. IL-8 was detected in all pleural exudates though levels in the TB patients, 384 +/- 110 pg/ml, appeared significantly higher than the PNE group, 185 +/- 110 pg/mg, (P < 0.015, mean +/- S.D.). In turn, the former group presented values of pleural CD3+, CD4+, and CD25, which were found increased in comparison with PNE patients (P < 0.01). Unlike the pleural compartment, patients with TBP showed a marked and significant decrease in their circulating levels of cells bearing the CD3, CD4, CD19, CD25, and CD68 phenotypes not only when comparing with Co but also with PNE and mild patients. Differences between the levels of pleural and peripheral T-cells from TBP patients may be the reflection of an important influx of T-lymphocytes from the circulatory system to the pleural cavity, probably linked to the presence of chemotactic factors within the pleural fluid like IL-8.
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PMID:Levels of interleukin-8 in tuberculous pleurisy and the profile of immunocompetent cells in pleural and peripheral compartments. 909 79

Replication of human immunodeficiency virus type 1 (HIV-1) is regulated by virus-encoded regulatory proteins, as well as by a variety of cellular factors. Productive infection of human T lymphocytes by HIV-1 is dependent upon the activation status of the target cells. In general, short-term mitogenic stimulation of CD4 T cells is used to enhance infection of peripheral blood mononuclear cells (PBMC) in vitro. Recently, we demonstrated that adoptive transfer of human PBMC into lethally irradiated BALB/c mice, radioprotected with severe combined immunodeficiency (SCID) mouse bone marrow, leads to marked T-cell activation and proliferation. In the present study, we investigated the effect of such xenoactivation of human T cells on their susceptibility to HIV-1 infection. Human cells that were recovered from human/Balb radiation chimeras supported efficient replication of laboratory strains of HIV-1, as well as of HIV-1 clinical isolates. The multiplicity of infection required to attain effective virus replication in the recovered xenoactivated human cells was 10- to 100-fold lower than that needed for infection of short- or long-term phytohemagglutinin (PHA)-stimulated blasts or of various T-cell lines. Analysis of human cell surface activation markers has indicated that xenoactivation in the mouse, in contrast to in vitro stimulation with PHA, is associated with a marked downregulation of CD25 (interleukin 2 receptor). Our results demonstrate that human cells recovered from human/Balb radiation chimeras, which are hypersensitive to HIV-1 infection, differ from in vitro-stimulated cells in their activation status. Therefore, this system could be used to study host factors that participate in HIV-1 infection and replication in vitro and in vivo.
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PMID:Human T cells recovered from human/Balb radiation chimeras are hypersensitive to human immunodeficiency virus type 1 infection. 915 41

Like T cells from healthy subjects, those of HIV-1-infected patients are capable of expressing activation antigens on their surface after antigenic or mitogenic stimulation, but their proliferative activity is strongly reduced or even absent, especially in patients with advanced stages of the disease. The characteristic of expressing activation antigens in response to different stimuli in the absence of cell proliferation is shared by CD4+ and CD8+ T-cell subsets from HIV-1-infected patients. The number of T cells capable of expressing CD25 and CD71 in response to HIV-1-related antigens but not of proliferating increased significantly with the progression of the disease, but the number of T cells capable of expressing the two activation antigens in response to the classic tetanus toxoid recall antigen decreased. The higher numbers of T cells capable of responding to HIV-1-related antigens in conjunction with a reduction in the number of T cells responding to recall antigens may explain the occurrence of different infections, including opportunistic microorganisms, during the more advanced stages of HIV-1 infection. Because the increase in the number of HIV-1 antigen-responding T cells (defined by CD25 and CD71 activation antigen expression) is a characteristic of symptomatic HIV-1-infected patients, expression (by flow cytometry) of these activation antigens on T cells in response to HIV-1 antigens could be used as a new marker of disease progression.
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PMID:T cells from individuals in advanced stages of HIV-1 infection do not proliferate but express activation antigens in response to HIV-1-specific antigens. 921 56

Results of quantitative determinations of peripheral blood lymphocytes presenting CD4 or simultaneously CD4 and CD8 antigens as well as HLA-DR and CD25 antigens in patients with different clinical stages of CD4+ and CD4+CD8+ cells were observed. The fall of CD4+CD8+ lymphocytes percentage was slight in the initial stages of infection but more sharp during the full-blown AIDS. The percentage of HLA-DR positive cells was higher in seropositive patients in comparison with controls and increased with the progression of HIV infection into AIDS. The CD25 expression was also higher in HIV-infected patients, however, it decreased in patients with late stages of AIDS. The observed disturbances could be caused by the direct destruction by replicating HIV or by severe abnormalities of immune system function.
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PMID:[Coexpression of CD4 and CD8 antigens and the appearance of HLA-DR and CD25 receptors on lymphocytes as markers of immune activation in patients with HIV infection]. 927 7

Live-attenuated simian immunodeficiency virus (SIV) protects macaques against challenge with pathogenic SIV. To evaluate the safety of such vaccines, an investigation of whether or not nef-deleted SIV could be reactivated in vivo by immune activation of the host was conducted. In addition, monkeys infected with apathogenic SIV/HIV-1 chimeric viruses, and two control monkeys that had suppressed replication of pathogenic SIV were examined. During the infection virus became undetectable or persisted at a low level of replication in all monkeys. At this time-point 11 monkeys were immune-activated by a vaccinia virus (VV) superinfection. After VV infection up to 80% of their lymphocytes showed expression of the activation markers CD25 and CD69 over 2 weeks. However, only the two non-progressing monkeys infected with pathogenic SIV showed a noticeable but transient enhancement of SIV replication and increased SIV antibody titres. By contrast, in monkeys infected with apathogenic immunodeficiency viruses no change in virus load was observed. Therefore, attenuated immunodeficiency viruses cannot be reactivated in vivo by a VV-induced immune activation.
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PMID:No reactivation of attenuated immunodeficiency viruses in rhesus macaques after vaccinia virus-induced immune activation. 934 73

Apoptosis is a major mechanism whereby HIV-1 depletes uninfected CD4+ and CD8+ T cells. We previously showed that resting peripheral blood T cells derived from healthy donors were killed by an apoptotic mechanism after adsorption to gp120-containing, protease-defective HIV-1 (L-2) particles, more effectively than parental wild-type LAI adsorption or rgp 120-mediated CD4 cross-linking, followed by mitogenic stimulation. Here, we present evidence that the L-2 particle-based apoptosis was induced both in CD4+ and CD8+ cells by generation of effector cells which were mainly derived from a resting memory CD4+CD38- subset. This subset enhanced the CD25 expression on the surface and secreted IFN-gamma in the culture supernatant after L-2 particle exposure. Significant elevation of Fas ligand mRNA was found in the subset by L-2 particle exposure, while expression of Fas antigen on uninfected T cells was induced by exposure to IFN-gamma. These results indicate that L-2 particles can shift the CD4+CD38- subpopulation from a resting to an activated state, and this activation leads to killing of bystander CD4+ and CD8+ T cells by a Fas-mediated mechanism. In fact, purified CD4+CD38- cells exposed to L-2 particles were converted into effector cells that were able to kill autologous as well as allogenic target T cells pretreated with IFN-gamma. Further, we found that the observation of apoptosis due to L-2 particles was a more general phenomenon, that also occurred with Thai primary HIV-1 isolates. These results suggest that such specific types of HIV-1 particles may play a major role in the induction of apoptosis for both bystander CD4+ and CD8+ T cells, through inappropriate activation of CD4+CD38- cells.
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PMID:Exposure of resting peripheral blood T cells to HIV-1 particles generates CD25+ killer cells in a small subset, leading to induction of apoptosis in bystander cells. 935 50

Peripheral blood mononuclear cells were prepared from human immunodeficiency virus-positive (HIV+) individuals (n = 46) to investigate the expression of both chains of the interleukin-2 receptor. Both qualitative and quantitative changes in expression were observed. Total lymphocyte expression of the IL-2 alpha chain (CD25) was decreased compared with HIV-negative (HIV-) controls. This was due to the decrease in the CD4+ population, which favored expression of this receptor, rather than a decrease in expression, per se. CD8+ lymphocytes expressed the beta chain (CD122) in the absence of the alpha chain. However, a significant increase in the number of peripheral blood CD8+ lymphocytes expressing mainly the beta subunit was observed in HIV+ patients (P = 0.02). This was observed to a similar extent in asymptomatic and symptomatic patients and characterized a subpopulation of T lymphocytes expressing high levels of CD8. Lymphocytes from patients with advanced HIV disease failed to up-regulate both alpha and beta chains in response to mitogenic concentrations of phytohaemagglutanin. However, those cells that were able to up-regulate both of the IL-2 receptors were capable of effective signal transduction through the receptor, increasing the proliferative response to stimulation.
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PMID:Dysregulation of the interleukin-2 receptor alpha- and beta-chain expression in CD4 and CD8 T cells in HIV infection. 944 Aug 20

Many enveloped viruses incorporate host membrane proteins, some of which remain functionally active and significantly affect viral phenotype. We investigated whether human retroviruses can transfer host membrane proteins to target cells. Following incubation with HTLV-I, HLA-DR and CD25 were detected on up to 70% of HPB-ALL cells. Similarly, HLA-DR and CD25 were also detected on cells following incubation with HIV-1. Cyclohexamide or azidothymidine (AZT) had no effect on detection, indicating that binding of virus or infection did not induce expression of these proteins. Detection of host proteins on target cells depended on binding as well as fusion of virus to the cell membrane, indicating that these proteins were inserted into target cell membranes. Virions also transferred host proteins to peripheral blood mononuclear cells (PBMCs). This aberrant transfer of T-cell activation proteins by HIV or HTLV may alter the state of activation or proliferation of target cells and contribute to the immunodeficiencies associated with infection by these viruses.
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PMID:Transfer of host T-cell membrane HLA-DR and CD25 to target cells by human retroviruses. 949 17

Dysregulation of T-cell receptor (TCR) alphabeta bearing lymphocytes and an increase in Vdelta1+ gammadelta T cells are typical features of HIV-1 infection. However, the role of gammadelta T cells remains unclear. Therefore, peripheral blood mononuclear cells (PBMC) of 103 HIV-1-infected patients were investigated with respect to expression of Vdelta1. These results were compared to the Vdelta1 expression of bone marrow mononuclear cells (BMMC). In contrast to healthy controls, Vdelta1+ cells dominated among both PBMC and BMMC in HIV-1-infected patients. Analysis of the coexpression of CD25, CD8, HLA-DR and CD45RO revealed a high prevalence of Vdelta1/CD45RO and Vdelta1/HLA-DR double-positive PBMC only in HIV-1-infected patients but not in healthy donors. Furthermore, analysis of the gammadelta TCR repertoire in patients infected with hepatitis B virus, hepatitis C virus, herpes simplex virus (HSV)-1 and HSV-2 showed that the selective enhancement of Vdelta1+ cells was restricted to HIV infection and not observed in other virus diseases. Our data provide further support for the involvement of gammadelta T cells in immunosuppression and progression of HIV infection.
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PMID:Increase in Vdelta1+ gammadelta T cells in the peripheral blood and bone marrow as a selective feature of HIV-1 but not other virus infections. 953 41


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