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

A literature search of coinfection with HIV and leprosy retrieved 4 case reports, 4 epidemiologic studies, 2 primate studies, and an editorial The 1st case was a 43-year old male with borderline tuberculoid leprosy who was successfully treated with dapsone and clofazimine, but later developed Kaposi's sarcoma and pulmonary tuberculosis. The 2nd case was a 28-year old male from Martinique who had been treated with triple therapy (dapsone, rifampin, and clofazimine) for lepromatous disease with erythema nodosum leprosum for 9 years, but later developed reactive polyarthritis and 1+ bacterial index along with generalized lymphadenopathy with his HIV. A 3rd case was a 27-year old male who had been treated for cutaneous leprosy for 4 years. 5 years later he had polyneuropathy and palpable nerve trunks suggestive of a reversal reaction, and candida esophagitis with a CD4/CD8 ratio of 0.3. The 4th case was a 35-year old woman with BT-BB leprosy on clinical grounds, but apparent BL leprosy by histology. It was also noted that her granulomas had a high CD4+ lymphocyte count, while her circulating CD4/CD8 ratio was 0.6 with a low CD4 count of 300. The 4 epidemiologic series were from Zambia, Haiti, Ethiopia, and a large series of cases from Ivory Coast, Congo, Senegal, and Yemen. Some preliminary conclusions from these data were that HIV infection does not affect the clinical classification of leprosy, that HIV infection may confer anergy to lepromin, that HIV infection may cause relapse of leprosy, and that leprosy may accelerate the progression of HIV. There were 2 cases where leprosy grading reaction reversed or downgraded in coinfected patients. In the primate model, coinfection with SIV and M. leprae increases susceptibility of monkeys to leprosy.
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PMID:Leprosy and AIDS: a review of the literature and speculations on the impact of CD4+ lymphocyte depletion on immunity to Mycobacterium leprae. 168 45

250 determinations of lymphocyte T subsets in 130 HIV infected patients (79 asymptomatic carriers or with lymphadenopathy, 31 ARC- and 20 AIDS-patients) were analyzed as to the percentage, number, and ratio of T4 (helper) and T8 (cytotoxic/suppressor) lymphocytes in sequential clinical stages of HIV infection. Asymptomatic HIV carriers or patients with lymphadenopathy were found to have statistically significant higher counts of erythrocytes, platelets, total lymphocytes, percentage and number of T4 lymphocytes and T4/T8 lymphocyte ratio than the ARC-patients. Persons with ARC in comparison with AIDS-patients were found to have significantly higher values of erythrocytes, platelets, leucocytes, total lymphocytes, T4 lymphocytes, percentage and count of T8 lymphocytes and T4/T8 lymphocyte ratio. In AIDS patients a statistically significant correlation was seen between number of T4 lymphocyte and number of erythrocytes, platelets, total number of lymphocytes and value of T4/T8 lymphocyte ratio.
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PMID:[T4 lymphocytes (helper cells) and T8 lymphocytes (cytotoxic and suppressor cells) in patients with asymptomatic and symptomatic HIV infection]. 168 8

A double-blind, randomized, placebo-controlled trial comparing two daily doses of oral ribavirin (600 and 800 mg) and a placebo was performed at four medical centers geographically distributed throughout the USA. One hundred and sixty-four HIV-infected adult men with lymphadenopathy were enrolled over a 2-month period and received active treatment for 24 weeks followed by a 4-week interval during which they did not receive the study drug. A marked interlaboratory variation in HIV isolation from peripheral blood mononuclear cells was observed, underscoring the critical role of quality assurance in similar multicenter trials. Nevertheless, the combined data indicate that ribavirin did not significantly suppress HIV activity (on measurement of reverse transcriptase activity) after week 6 or reduce serum p24 antigenemia.
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PMID:A multicenter clinical trial of oral ribavirin in HIV-infected people with lymphadenopathy: virologic observations. Ribavirin-LAS Collaborative Group. 169 May 51

We and others have shown that several T cell responses induced by the mitogen phytohaemagglutinin (PHA), including T cell colony formation, IL-2 receptor (IL-2R) expression, and IL-2 production are impaired in patients with AIDS and lymphadenopathy syndrome (LAS). We investigated whether phorbol myristate acetate (PMA) could act in synergy with PHA (as it does in healthy subjects) to enhance in vitro T cell responses of patients at all stages of infection by HIV. In AIDS patients with opportunistic infections (AIDS/OI), PHA + IL-2 + PMA led to a total disappearance of T cell colonies in 10/11 patients, among whom six already displayed very low numbers of colonies induced by PHA + IL-2 (less than 50 colonies/5 x 10(4) cells). In contrast, T cell colony formation induced by PHA + IL-2 + PMA was maintained or increased, compared with that induced by PHA + IL-2, in five out of six AIDS patients with Kaposi's sarcoma (AIDS/KS), 10/14 LAS and six out of seven HIV-seropositive asymptomatic (HIV+/AS) homosexuals. In these three groups of patients, a low percentage of colony cells induced by PHA + IL-2 + PMA expressed CD3 and CD4 molecules, but 50-89% of cells were IL-2R (Tac) positive, as in healthy controls. Studies on T cell activation and IL-2 production were performed on a selected group of 12 HIV-infected patients for whom sufficient numbers of lymphocytes could be obtained. PMA induced CD4 down-modulation in controls and in HIV-infected patients. However, CD3 down-modulation and induction of the Tac chain of IL-2R by PMA were significantly impaired in patients, compared with controls, and these two parameters were correlated. Although PHA alone induced virtually normal levels of Tac antigen on patients' cells, Tac induction by PHA + PMA was significantly decreased in patients versus controls. Cells from five out of 10 patients tested failed to produce detectable amounts of IL-2 after PHA stimulation, whereas IL-2 production increased significantly in all patients tested (n = 9) after PHA + PMA, with a level of IL-2 activity significantly higher than in controls. No correlation was found in this group of patients between the effects of PMA + PHA on T cell colony formation, Tac expression, or IL-2 production, as compared with PHA alone. Taken together, our results indicate that in vitro T cell functional studies with PMA may be useful to evaluate better the defects of T cell activation in HIV-infected patients.
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PMID:Effect of phorbol myristate acetate on T cell colony formation, interleukin-2 (IL-2) receptor expression and IL-2 production by cells from patients at all stages of HIV infection. 169 61

On July 27, 1989, the International Conference on Molecular Aspects of Immune Response and Infectious Diseases devoted a symposium to the subject of the use of intravenous gamma globulin (IVIG) in acquired immunodeficiency syndrome (AIDS). The information presented confirmed that IVIG benefits human immunodeficiency virus (HIV)-infected children with recurrent infections and that much remains to be learned about the influence of IVIG in adult AIDS. The symposium participants recognized the urgent need to develop randomized clinical trials using a control group to assess the efficacy of a treatment with IVIG in PGL (persistent generalized lymphadenopathy), ARC (AIDS-related complex), and AIDS. To prepare this report, a committee was established, including individuals with expertise in immunology, immunopharmacology, microbiology, virology, infectious diseases, general medicine, and pediatrics and representing research experience in academia and hospitals. After an introduction to the report with a summary of immunotherapeutic agents under evaluation to treat HIV infection, section 1 lays out the present understanding of the disease pathogenesis. Section 2 then outlines the treatment of HIV-seropositive individuals, discussing the uncertainties that any treatment entails. Section 3 discusses the rationale for treating HIV-infected individuals with IVIG, and Section 4 examines the major differences between IVIG and hyperimmunoglobulins for the treatment of HIV infection. Section 5 looks at IVIG as a mean to delay the emergence of opportunistic infections and restore immunocompetence in AIDS and related illnesses, and Sections 6 and 7 suggest a pilot protocol on the use of IVIG in association with low-dose or standard-dose zidovudine (AZT).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Report of the symposium on the use of intravenous gammaglobulin in adults infected with the human immunodeficiency virus. 169 38

B cell subpopulations, as defined by double-labelling techniques with CD5 and CD19 monoclonal antibodies (MoAbs), were serially studied in 335 HIV-1 seropositive patients. At the time of the first consultation, no important modifications in either CD5+ or CD5- subpopulations were observed, whatever the stage of the disease. However, in 18 out of the 335 patients (5.37%), a sharp increase in B cells exceeding 20% and 300/mm3 was observed. This increase in B cells was mainly accounted for CD5-CD19+ B cell subpopulations and was associated with: (i) evolution of the disease, since only four patients presented it at their first consultation (one lymphadenopathy-associated syndrome (LAS) and three AIDS); (ii) advanced stages of disease since, at the time of B cell augmentation, two patients were staged as LAS, four as ARC and 12 as AIDS; (iii) a high incidence of non-Hodgkin's lymphomas (NHL) since three out of the 18 patients presented a histologically confirmed NHL and three others a clinical pattern compatible with this diagnosis. However, in three patients with B hyperlymphocytosis, polymerase chain reaction (PCR) studies of immunoglobulin gene rearrangement revealed the existence of a polyclonal expansion of B cells. These results justify inclusion of a pan-B cell marker in routine phenotypic studies of HIV-infected individuals, as well as the search for NHL among patients presenting this abnormality.
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PMID:Serial study of CD5+ and CD5- B cell subpopulations in 335 HIV seropositive patients. 171 42

Currently discussed models of AIDS pathogenesis attribute a pivotal role to HIV-variants developing in T cells during the course of the disease resulting in an increasingly rapid depletion of the infected T cells. Such models do not however explain the morphological findings observed in AIDS lymphadenopathy. To clarify the significance of the hyperplasia and subsequent destruction of the lymphoid follicles in HIV-related lymphadenopathy, we used in situ hybridization in combination with immunohistological labelling techniques to identify the phenotype of HIV-infected cells in lymph nodes. In addition to few T helper cells, mainly in germinal centres, large amounts of HIV-RNA were found in CD4-negative follicular dendritic cells (FDC) rather than in macrophages or other cells. This finding is well in accordance with the recent observations made by other authors suggesting that purified FDC can be infected with HIV in vitro. Furthermore, TNF alpha expression is localized mainly in centroblasts (activated B cells) of germinal centres. TNF alpha, released by antigen-activated B cells in vitro, has been shown to induce HIV replication in latently infected T cells. On the basis of these observations we propose that latently infected CD4+ T cells, having entered germinal centres, start HIV replication under the influence of cytokines present in this microcompartment of all lymphoreticular tissues. Here the T cells infect FDC which, in turn, pass on the virus to new healthy T helper cells. This model may explain both peculiarities of the lymphadenopathy syndrome as well as the long latency period of HIV-infection, ultimately leading to AIDS.
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PMID:[Lymphoid tissues and AIDS: role of lymphocytes and follicular dendritic cells (FDC)]. 172 49

At the IV International Conference on AIDS in Stockholm, a Symposium on the pathology of HIV-related diseases was organized. During this Symposium the "European Study Group on HIV-Pathology" presented a histological classification of lymph node alterations seen in HIV-associated lymphadenopathy. The goal of the Study group was to offer a common terminology for histologic changes previously described with different terms by different authors. In the present review the most important histological criteria used in the proposed classification are summarized. Since the classification is based on the conspicuous changes of the follicles, a brief review of the possible pathogenic mechanisms leading to disintegration of the germinal centers will also be given.
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PMID:[Histologic classification of HIV-1 induced lymphadenopathy. Current results on the pathogenesis of germinal center changes]. 172 55

The constitutively expressed IL-2R beta (p70) chain participates in the formation of high-affinity (h.a.) IL-2R and transduces IL-2-mediated signals to normal cells. Its expression on HIV-infected patients' PBMC was evaluated and was found to be decreased in both nonstimulated CD4+ and CD8+ cells. Mitogenic cell stimulation induced IL-2R beta chain expression on both CD4+ and CD8+ cells from asymptomatic and persistent generalized lymphadenopathy patients but not on those from AIDS patients. Comparison of mean fluorescence intensity of IL-2R beta positively stained cells from normals and patients did not reveal significant differences. Cross-linking of 125I-rIL-2 on patients' PHA-blasts revealed decreased signals corresponding to both IL-2-binding chains and, in some cases, neither IL-2R alpha nor IL-2R beta chains could be detected. Decreased expression of IL-2R beta polypeptide was associated with impaired accumulation of the corresponding mRNA transcripts. Binding experiments with 125I-rIL-2 under h.a. conditions showed a decreased number of IL-2-binding sites/cell which was more pronounced in patients with AIDS than in patients with less advanced clinical stages. In vitro HIV infection of normal PHA-blasts also resulted in a decreased number of h.a. IL-2R/cell. High concentrations of rIL-2 in the absence of other mitogenic stimuli induced a decreased cell proliferation and expression of the IL-2R alpha chain and did not enhance the constitutive NK and the generation of LAK activity in several patients, suggesting an impaired IL-2R beta chain-mediated cell activation.
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PMID:Abnormal expression of IL-2R beta (p70)-binding polypeptide on HIV-infected patients' cells. 173 5

Serum concentrations of trypsin and elastase I were determined in 109 HIV Ab-positive patients (52 asymptomatic HIV-infected patients, 25 with lymphadenopathy syndrome, and 32 with acquired immunodeficiency syndrome) to assess the prevalence of possible pancreatic damage in these patients. Serum trypsin was abnormally elevated in 46 of the 109 patients (42.2%): 19 of the 52 asymptomatic HIV-infected patients (36.6%), 9 of the 25 with lymphadenopathy syndrome (36%), and 18 of the 32 with acquired immunodeficiency syndrome (56.3%). Serum elastase 1 was elevated in 14 of the 109 HIV Ab-positive patients (12.8%): 3 of the 52 asymptomatic HIV-infected patients (5.8%), 3 of the 25 with lymphadenopathy syndrome (12%), and 8 of the 32 with acquired immunodeficiency syndrome (25%). None of the patients with abnormally high serum pancreatic enzyme concentrations had clinically evident pancreatic disease. There was no statistically significant difference in serum levels of trypsin and elastase I between drug addicts and nonaddicts, between alcoholics and nonalcoholics, or between those with cytomegalovirus infection and those without. A significant inverse relationship was found between serum enzyme concentrations and the number of CD4+ lymphocytes. The results of this study show that high levels of serum trypsin and elastase are present in an elevated percentage of patients with acquired immunodeficiency syndrome, suggesting that the pancreas is frequently damaged in this disease. The finding of abnormally high serum enzyme concentrations not only in patients with AIDS, but also in asymptomatic carriers and in patients with lymphadenopathy syndrome suggests an association between HIV infection and the development of pancreatic lesions.
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PMID:Serum pancreatic enzymes in HIV-seropositive patients. 173 48


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