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D Scott-Algara

Publications and source records attributed to D Scott-Algara.

At least 19 recordsLinked to original sources

[Cryptococcal meningo-encephalitis in an apparently immunocompetent patient].

INTRODUCTION: Cryptococcal meningo-encephalitis is a rare disease occurring more frequently in immunocompromised hosts. CASE REPORT: We report the case of an apparently immunocompetent patient who developed a recurrent neurological deficit with lymphocytic meningitis. The time from the first symptoms to diagnosis was 8 months. We noted mild CD4+ lymphocytopenia (500 cells/mm3) without HIV infection. CD4+ lymphocytes were not reactive for a panel of antigens. CONCLUSION: This case illustrates the usefulness of cerebrospinal fluid Cryptococcus Neoformans antigen test in patients with an unexplained neurological syndrome with a lymphocytic meningitis together with quantification of circulating lymphocytes clusters and analyse of their function in opportunistic infections.

Amphotericin B↗

Partial restoration of cytokine profile despite reconstitution of cytomegalovirus-specific cell-mediated immunity in human immunodeficiency virus-infected patients during highly active antiretroviral treatment.

We reconstituted cytomegalovirus (CMV)-specific T-cell responses in human immunodeficiency virus-1-positive, CMV-positive patients receiving highly active antiretroviral treatment (HAART). We used several combinations of functionality parameters to determine the degree of T-lymphocyte reconstitution obtained during 1 year of treatment. Untreated patients displayed CMV-specific cytotoxic T-lymphocyte (CTL) activity despite the absence of CMV-specific lymphoproliferative responses (LPRs) and despite the fact that interferon-gamma (IFN-gamma) and interleukin-2 (IL-2) were not secreted. The absence of LPRs, IFN-gamma and IL-2 before antiretroviral treatment suggests that CMV-specific immunity was deregulated despite the high CD4+ T-cell counts presented by our cohort, which are critical to the reactivation of CMV disease. After 6 months of HAART, CTL activity had increased compared with the baseline, as had the levels of secreted IFN-gamma and LPR. However, the levels of specific IL-2 produced did not change during therapy, and no specific IL-2 was detected during the follow-up period. Taken together, our findings suggest that 1 year of HAART led to the recovery of some, but not all, CMV-specific responses in our cohort of patients.

Adult↗

Temporary restoration of immune response against Toxoplasma gondii in HIV-infected individuals after HAART, as studied in the hu-PBMC-SCID mouse model.

We studied immune reconstitution against the parasite T. gondii in HIV-infected patients treated for 1 years with highly active antiretroviral therapy (HAART). We used SCID mice, humanized with peripheral blood mononuclear cells (PBMC) from patients, which were then infected with T. gondii cysts. Mice humanized with PBMC from patients before the start of HAART were highly susceptible to infection. In contrast, mice humanized with PBMC from patients who had received HAART for 6 months displayed higher survival rates, correlating with lower intracerebral parasite loads. However, this resistance was lost during follow up because mice humanized with PBMC from patients treated with HAART for 12 months survived for no longer than mice that had not been humanized. Specific lymphocyte proliferation assays showed that the increase in proliferative response depended on treatment duration and that HAART induced changes in IFN-gamma secretion in the presence of Toxoplasma antigens. Thus, our results indicate partial immune reconstitution against T. gondii in HIV-infected patients following HAART, possibly due to changes in the patterns of specific IFN-gamma production and redistribution of functional memory CD4+ cells.

Animals↗

Frequency and phenotyping of human immunodeficiency virus (HIV)-specific CD8+ T cells in HIV-infected children, using major histocompatibility complex class I peptide tetramers.

HLA-A*02 tetramers complexed to human immunodeficiency virus (HIV) Gag SLYNTVATL and HIV Pol ILKEPVHGV peptides were used to characterize HLA class I-restricted CD8(+) T cells in 41 HIV-infected children. The frequencies and the phenotype of specific circulating CD8(+) T cells were determined in whole-blood samples by means of cytometric analysis. Background staining of 13 HLA-A*02-negative patients showed that the frequency of CD8(+) T cells was <0.01%. Of the 28 HLA-A*02-positive patients, blood samples from 26 stained positive at least once the Gag tetramer (mean CD8(+) T cells, 0.87%; range, 0.1%-3.9%), and blood samples from 21 stained positive for the Pol tetramer (mean CD8(+) T cells, 0.59%; range, 0.1%-5.5%). The tetramer-binding cells were CD28(-), CD45RA(-), CD45RO(+), HLA-DR(+), and CD69(-) T lymphocytes. HIV-specific CD8(+) T cells can be detected easily in peripheral blood of HIV-infected children, using HLA tetramers combined with HIV peptides. These cells are memory activated CD28(-)CD8(+) T lymphocytes.

Adolescent↗

Functional monocyte-derived dendritic cells can be generated in chronic lymphocytic leukaemia.

Chronic lymphocytic leukaemia (CLL) remains an incurable disease. Although modern available treatments are able to induce disease regression, relapse almost inexorably occurs. Therefore, novel therapeutic strategies aimed at reducing the disease relapse rate are very much needed. Among these, the induction of tumour-associated antigen-specific cytotoxic T lymphocytes (CTL), through either DNA vaccines or injection of idiotype pulsed dendritic cells (DCs), has been actively investigated with encouraging preliminary results in B-cell malignancies. As the CLL B lymphocyte characteristically expresses low amounts of surface immunoglobulin (Ig) and T cells from these patients have been reported to display impaired functional activity, there are concerns related to the possibility of generating specific cytotoxic antitumoral T cells in this disease. In addition, no information is presently available regarding the functional ability of CLL-derived DCs. In the present work, freshly purified monocytes from CLL patients and normal donors were induced to differentiate in granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin (IL)-4 serum-free medium and compared for their morphological, phenotypic and functional characteristics. Our results demonstrate that: (1) functional DCs can be generated from CLL patients with similar phenotype and function to those observed from normal donors; (2) in contrast to normal control subjects, monocyte-derived DCs from CLL patients spontaneously secrete endogenous IL-10; and (3) interferon (IFN)-gamma in combination with CD40L plays a major role in priming DCs from CLL patients for IL-12 and IL-15 production. Overall, these results indicate that it is possible to derive functionally competent DCs from circulating monocytes in CLL patients.

Aged↗

CD4 T cell recovery is slower in patients experiencing viral load rebounds during HAART.

To determine whether viral load rebounds during HAART impact on CD4+ T cell recovery and immune reconstitution, we studied a prospective cohort of 355 antiretroviral naive patients enrolled to be randomized in a trial of three strategies of induction/maintenance HAART. The extent of immune reconstitution in blood through 72 weeks of antiretroviral treatment was evaluated. Lymphocyte subset markers (CD4, CD8, CD45RA, CD62L, CD16, CD19), activation markers (HLA-DR, CD38, CD25) were performed by cytometry analysis. Our results showed that plasma HIV-1 RNA was suppressed to below 500 copies per ml through week 72 in 240 patients (group 1) while the remaining 115 patients experienced at least one viral rebound (group 2). At baseline, CD4 cell count was higher and HIV-1 RNA was lower in group 1 than in group 2. Over 72 weeks, mean increase in CD4+ T cell count was 0.32 cell/mm3/day in group 1 and only 0.14 cell/mm3/day in group 2 (P < 0.0001). However, the patterns of changes in CD4+ and CD8+ T cell subsets during therapy were very similar across the two groups with only subtle and very limited differences. We conclude that permanent control of HIV replication could be necessary for faster immune reconstitution.

Adult↗

Short-term bioeffects of an infrared pulsed laser device on burned rat skin monitored by transverse relaxation times (NMR).

BACKGROUND AND OBJECTIVE: The aim of this study was to determine whether the application of an infrared pulsed laser device (IPLD) on the burned skin of rats induced significant changes in the water dynamics of the burned tissues as measured by nuclear magnetic resonance (NMR) at a proton frequency of 90 MHz by using transverse relaxation times (T2, I/T2). STUDY DESIGN/MATERIALS AND METHODS: Seven groups (GI-GVII), each consisting of four albino rats (Sprague-Dawley), of 12-14 weeks of age were used in the experiment. Rats in GI-GVI were anesthetized and burned with a hot tip. GI, GIII, GV were not irradiated. GII, GIV, GVI were irradiated at 0 hours; 0 and 24 hours; and 0, 24, and 48 hours, respectively. Rats in GVII served as controls and were neither burned nor irradiated. Samples from all groups were obtained and monitored by NMR by using transverse relaxation times (T2 and 1/T2). An unpaired Student's t-test and a one-way analysis of variance (ANOVA I) were preformed on the mean values obtained (T2, 1/T2). The statistical design was chosen to give a 95% power of contrast 1-beta (1/T2). The modulated beam of the IPLD used is composed of two superposed waves; a carrier wave (3 MHz), and a drive force wave in the near infrared (904 nm, f = 1014 Hz). A dose of 1.5 x 10(3) J/M2 per session was applied by placing the IPLD directly over the burned tissue by using a top-hat distribution. RESULTS: The results of a t-test on the T2 and 1/T2 values did not show statistically significant differences at 0 and 24 hours between the irradiated groups, the nonirradiated groups, and the nonburned nonirradiated (control) group. Nonetheless, at 48 hours after the burn, we found a statistically significant difference in the 1/T2 values for the irradiated specimens compared with the nonirradiated specimens and the control group. Furthermore, the variance of the 1/T2 values as a function of time showed a tendency to decrease significantly only for the irradiated specimens. CONCLUSION: These findings show possible effects on the water dynamics of burned rat tissue in a short term as a result of the IPLD's application.

Animals↗

Flow cytometric analysis of protein-tyrosine phosphorylation in peripheral T cell subsets. Application to healthy and HIV-seropositive subjects.

This paper describes an improved method for detecting tyrosine phosphorylation levels in T cell subsets by flow cytometry early after CD3 crosslinking stimulation. It consists in introducing gentle paraformaldehyde fixation between CD3 crosslinking in cold conditions and the shift to 37 degrees C, which activates downstream signalling machinery. We used the combined properties of monoclonal antibodies for stimulating cells and for detecting surface markers to analyze protein-tyrosine phosphorylation levels in T cells subsets following stimulations which mimic physiological activation. Overall data obtained in healthy subjects, using two- or three-color immunofluorescence, indicated that: (1) most CD3 positive cells phosphorylate tyrosine substrates following CD3 crosslinking stimulation and (2) helper cells phosphorylate tyrosine to a slightly better extent than cytotoxic cells after CD3 crosslinking. Nevertheless, the two subsets follow similar kinetic patterns and tend to retain a homogeneous profile. Processing of samples from HIV-seropositive patients showed heterogeneous phosphorylation levels in both subsets, when compared to normal donors. This assay should, in the future, lead to easy and rapid exploration of the signal transduction pathway in different subsets of T cells under normal and pathological conditions.

CD3 Complex↗

Neonatal deletion and selective expansion of mouse T cells by exposure to rabies virus nucleocapsid superantigen.

The nucleocapsid (NC) of the rabies virus behaves as an exogenous superantigen (SAg) in humans. In the present report, we analyzed whether it is also a SAg in mice by studying the effect of NC on T cell receptor (TCR) V beta expression in BALB/c mice. Repeated injection of NC in newborn BALB/c mice led to a marked reduction by two- to sixfold of V beta 6 expressing CD4+ T cells in spleen and in peripheral blood. Decrease of V beta 6-expressing CD3+ mature T cells was also observed in thymus. Single NC injection in footpad resulted in a three- to sixfold expansion of V beta 6 CD4+ T cells, but not of CD8+ T cells, in the draining lymph nodes of BALB/c mice. The intensity of the stimulation was dose dependent and was maximal 3 d after the NC injection. The clonal deletion of T cells bearing a particular V beta demonstrates that NC is a SAg in mice. T cells, especially CD4+ T cells, are an essential factor in host resistance to rabies virus and also in the pathophysiology of paralysis; thus, we postulate that a rabies virus component, which stimulates T cells, such as a SAg, may increase virus immunopathogenicity. To evaluate this hypothesis, we compared the course of rabies in adult BALB/c lacking V beta 6, 7, 8.1, and 9 T cells and in normal BALB/c. Immune-related paralysis was decreased in BALB/c missing the NC target V beta T cells. Transfer of V beta 6 but not of V beta 8.1-3 T cells into recipient mice lacking V beta 6, 7, 8.1, and 9 allowed the immune-related paralysis to evolve. Taken together, these results strongly support the hypothesis that T cells expressing rabies SAg-specific V beta 6 T cells, are involved in the genesis of the immunopathology that is characteristic of paralytic rabies.

Animals↗

Viral superantigen-induced hyporesponsiveness of T cells and polyclonal B cell activation in HIV-1 infection.

The mechanisms of CD4 depletion and hyporesponsiveness during human immunodeficiency virus (HIV) infection are still unknown. Given the ability of superantigens to stimulate a higher number of lymphocytes than conventional antigens, they may play a major role in this process. Recently, a novel superantigen, the rabies virus nucleocapsid (NC), was described in humans. In the present work, we tested the responses of peripheral blood lymphocytes from asymptomatic HIV-infected patients to this superantigen. In contrast to its effect in normal controls, NC failed to expand T cells from HIV-infected individuals expressing the V beta 8 family, and induced a strong decrease in the response to CD3 activation. This absence of response was not the consequence of programmed cell death, and was explained by an anergic state induced by the superantigen. NC superantigen was also able to induce polyclonal activation of B cells, as measured by the secretion of anti-HIV antibodies and autoantibodies. Moreover, V beta 8 depletion experiments showed that induction of autoantibody secretion was V beta 8 dependent, whereas secretion of HIV-1 antibody was not. Interleukin secretion studies showed that NC was able to induce high levels of interleukin-4 and interleukin-10. Taken together, our results suggest a role for exogenous viral superantigens such as NC in the induction of T cell hyporesponsiveness and polyclonal B cell activation during HIV infection. The induction of a Th2 response and the role of these superantigens in the immunopathogenesis of acquired immunodeficiency syndrome are discussed.

Acquired Immunodeficiency Syndrome↗

In vitro non-productive infection of purified natural killer cells by the BRU isolate of the human immunodeficiency virus type 1.

Highly purified natural killer (NK) cell lines and clones, displaying the typical phenotype, morphology and function and obtained from healthy blood donors, were infected in vitro with the BRU isolate of human immunodeficiency virus type 1 (HIV-1). There was no significant increase in reverse transcriptase activity and levels of p24 antigen in the supernatants, but positive staining was observed using an immunogold technique with polyclonal anti-HIV-1 antibodies. When infected NK cells were co-cultivated with autologous non-infected CD4+ mitogen-activated cells, significant levels of reverse transcriptase activity and p24 antigen in supernatants were detected. Giant syncytial cells and a high number of mature virion particles were also evident. When NK cell lines or clones from HIV-1-infected patients were studied, neither the presence of p24 antigen nor reverse transcriptase activity was detected in the supernatants after stimulation with mitogens, cytokines or co-culture with allogeneic CD4+ mitogen-activated cells. PCR studies did not detect HIV-1 genes in freshly purified NK cells, cell lines or clones from infected patients. Taken together these results suggest that (i) normal NK cells can be infected in vitro by the HIV-1 BRU isolate in a non-productive fashion, (ii) PCR with NK cell DNA of HIV-1-infected patients indicates that in vivo few of these cells, if any, are infected by HIV-1 and (iii) the mechanisms responsible for the impairment of NK cell function during HIV-1 infection remain to be determined and are probably not related to a direct cytopathic effect of the virus.

Cell Line↗

Differential requirements for HIV-1 replication in naive and memory CD4 T cells from asymptomatic HIV-1 seropositive carriers and AIDS patients.

One of the major routes for modulating HIV-1 expression by infected T cells is through the control of transcription initiation from the HIV-1 long terminal repeat (LTR), which is regulated either by its own viral gene products or by several cellular DNA-binding proteins induced during T cell activation. Previous work reported preferential HIV-1 infection and replication of memory CD4 T cells from infected individuals, which was explained either by a higher viral burden of this subset or by differences between naive and memory cells in the activation of the general transcription machinery involved in HIV-1 replication. In this work, we have studied HIV-1 replication by highly purified naive and memory CD4 T cells from asymptomatic seropositive carriers (ASC) and AIDS patients following different activation signals. Our results demonstrate that viral replication in memory cells from ASC was observed after mitogenic (phytohaemagglutinin (PHA) and/or phorbol myristate acetate (PMA)) recombinant tumour necrosis factor-alpha (rTNF-alpha) and CD3-mediated activation. In contrast, in naive subsets, early viral replication was almost exclusively observed upon CD3-mediated activation. AIDS patients are characterized by similar levels of viral replication in both subsets after PHA and soluble or immobilized anti-CD3 MoAb activation. However, naive subsets from AIDS patients still displayed differential requirements since they failed to replicate HIV-1 after treatment with PMA and rTNF-alpha. Taken together, these results provide evidence that HIV-1 replication in CD4+ T cells from infected individuals is a function of the differentiation stage of the cells, the disease stage of the patient and the activation signal employed.

Acquired Immunodeficiency Syndrome↗

Evidence for a viral superantigen in humans.

Superantigens bind class II major histocompatibility proteins and stimulate powerful proliferative responses of T lymphocytes bearing particular V beta sequences as part of their alpha beta antigen receptor. Exogenous bacterial superantigens are responsible for food poisoning and toxic shock syndrome. Murine virus-encoded self-superantigens induce clonal deletion of T lymphocytes. Although superantigen-like properties have been suggested for human immunodeficiency virus-1, no viral superantigen has been identified in humans. Here we report that the nucleocapsid of the rabies virus is an exogenous superantigen specific for V beta 8 human T lymphocytes which binds to HLA class II alpha-chains.

Antigen-Presenting Cells↗

Nucleocapsid specific T and B cell responses in humans after rabies vaccination.

The importance of the immune response directed to the internal component of the rabies virus, the nucleocapsid (NC), was evaluated in humans after rabies vaccination. T cell activation was measured with a bulk proliferative assay and relative frequencies of circulating NC-specific PBL were calculated with the limiting dilution technique. Vaccinees were classified into two groups: NC responders and NC non-responders. In NC responders, the frequency of NC-specific circulating lymphocytes was up to 6 times higher than the frequency of virus-specific lymphocytes. In non-responders, NC-specific lymphocytes were up to 25 times less common than virus-specific ones. The NC capacity to induce a secondary antibody response was tested in vitro. After a stimulation with complete virus, lymphocytes originating from donors vaccinated with tissue culture vaccine produced a secondary antibody-response composed mainly of glycoprotein-specific neutralizing antibodies, whereas lymphocytes from suckling mouse brain vaccines produced essentially NC-specific antibodies. This result confirmed the serological status of suckling mouse brain vaccinees, who usually developed high titres of NC-specific antibodies. After an in vitro NC stimulation, lymphocytes collected from NC responders produced not only NC-specific antibodies, provided they have NC-specific B cells at the time of blood sampling, but most surprisingly, they also produce glycoprotein-specific neutralizing antibodies. This finding indicates that NC free of glycoprotein is capable, in some individuals, of boosting an heterologous glycoprotein response.

Antibodies, Viral↗

Evaluation of serum levels of tumour necrosis factor-alpha (TNF-alpha) and soluble IL-2 receptor (sIL-2R) and CD4, CD8 and natural killer (NK) populations during infrared pulsed laser device (IPLD) treatment.

The purpose of this study was to evaluate serum levels of TNF-alpha, sIL-2R and distribution of peripheral leucocyte subsets in patients with advanced neoplastic disease undergoing IPLD treatment. Fifteen cancer patients with evidence of persistent disease were further divided in two groups according to outcome at the end of the period of clinical evaluation: group 1 patients were still alive and group 2 patients had died. Our results show: (i) an increase in the initial level of TNF-alpha in both groups; (ii) a decrease in TNF-alpha levels during the follow up of group 1 patients; (iii) a significant increase in serum levels of sIL-2R in patients in group 2 compared with those in group 1; (iv) a progressive and constant increase in TNF-alpha levels in group 2; (v) a decrease in CD4+CD45RA+ subpopulation in both groups; (vi) an increase in CD25+ cells; (vii) an increase in CD4+, CD4+CD45RA+ and CD25+ cells during the follow up of group 2 patients. The data generated here form the basis for further investigations on the use of IPLD as a single agent and in combination with other biological response modifiers in cancer patients.

Antigens, CD↗

Impaired proliferative capacity and abnormal cytokine profile of naive and memory CD4 T cells from HIV-seropositive patients.

Purified naive and memory CD4 T cells from healthy donors, HIV+ asymptomatic carriers and AIDS patients were examined for their proliferative activity and their pattern of cytokine secretion (IL-4, IL-6, interferon-gamma (IFN-gamma) and tumour necrosis factor-alpha (TNF-alpha)) upon stimulation with phytohaemagglutinin (PHA), phorbol myristate acetate (PMA) and cross-linked anti-CD3 MoAb, in the presence of recombinant IL-2 (rIL-2). We found a decrease in the proliferative capacity of naive CD4 T cells following stimulation with PHA and PMA, and a sharp decline in this response upon cross-linked anti-CD3 stimulation in both subsets, although it predominated in the naive subpopulation. In AIDS patients, less pronounced impairment of thymidine uptake by the naive subset was found upon PHA and cross-linked anti-CD3 MoAb stimulation. In addition, an altered secretion pattern of the different cytokines was observed, consisting of abnormal secretion of IL-6 by both naive and memory cells, an abnormal pattern of IFN-gamma secretion and frequent loss of detectable IL-4 production by HIV patients. These abnormalities were even more pronounced in AIDS patients than in the asymptomatic carriers. Overall, our results extend previous reports indicating functional impairment of memory CD4 subsets in HIV+ subjects by showing that this impairment involves naive CD4 T cells.

Acquired Immunodeficiency Syndrome↗

Natural killer (NK) cell activity during HIV infection: a decrease in NK activity is observed at the clonal level and is not restored after in vitro long-term culture of NK cells.

NK cell activity is impaired in HIV-infected patients. The mechanisms behind the altered NK functions are not clear, and conflicting data concerning NK and antibody-dependent cellular cytotoxicity (ADCC) activity have been reported. In order to investigate whether this impairment is also observed at the clonal level and whether it is related to a defect at the target cell binding and/or the post-binding level, we evaluated highly purified NK cell lines and cloned NK cells obtained from 22 HIV-infected patients at different stages of disease and compared them with normal controls for their ability to: (i) kill K-562 and U-937 cell lines using a 51Cr release assay; (ii) bind and kill K-562 and U-937 cells at the single cell binding level; (iii) release NK cytotoxic factor (NKCF), tumour necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma); (iv) kill anti-IgM preincubated Daudi cell line (ADCC activity). This study with cloned NK cells or NK cell lines from HIV-infected individuals showed: (i) a decrease in their lytic capability against target cell lines; (ii) a low ability to form conjugates with K-562 and U-937 cell lines with respect to controls; (iii) a decreased ability to kill bound target cells; (iv) low levels of released NKCF, TNF-alpha and IFN-gamma after incubation with U-937 cells. Taken together, these findings suggest that the impaired NK cell function during HIV infection is also observed at the clonal level and is related to defects both at the target and post-binding levels. However, the precise mechanisms remain to be determined. The inability to restore normal NK activity after long-term culture in the presence of high levels of recombinant IL-2 is in agreement with the hypothesis of a 'general anergic process' during HIV infection.

Acquired Immunodeficiency Syndrome↗

Serum levels of IL-2, IL-1 alpha, TNF-alpha, and soluble receptor of IL-2 in HIV-1-infected patients.

Serum levels of the interleukins (IL-1 alpha, IL-2), tumor necrosis factor-alpha (TNF-alpha), and soluble receptor of IL-2 (sIL-2R) were studied by enzyme-linked immunosorbent assay (ELISA) in 12 normal healthy controls and 52 HIV-1 seropositive patients. Results indicated that: (1) sIL-2R levels were significantly increased in most HIV-1 seropositive patients. This increase appeared to be correlated with low CD4 cell counts and with the presence of detectable levels of p25 antigen. Furthermore, initially high levels of sIL-2R appeared to be correlated with progression of disease. (2) IL-2 levels were found to be increased in about 43% of asymptomatic carriers (ASY) and subjects with lymphoadenopathy-associated syndrome (LAS) compared with 12% in the case of AIDS-related complex (ARC) and AIDS patients. (3) There was a positive correlation between serum levels of TNF-alpha and IL-1 alpha in nearly all patients. Detectable levels of both cytokines were found in 34% of ASY and LAS patients and only rarely were detectable in ARC and AIDS patients. (4) Sixteen patients in whom progression of disease was observed were studied initially and at the moment they upstaged. No significant modification of serum levels of the three cytokines and sIL-2R studied could be evidenced. It was concluded that sIL-2R could be a useful marker of disease activity and progression, though a prospective study is necessary. For IL-2, IL-1 alpha, and TNF-alpha, this study indicated the presence of variable alterations in serum levels in HIV-1-infected patients.

AIDS-Related Complex↗