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

We report the case of 43-year-old homosexual patient with HIV infection and a history of travel to the Far East in whom visceral leishmaniasis was the first infectious complication. Symptoms were fever, malaise, weight loss, hepatosplenomegaly, generalized lymphadenopathy, and oral thrush. Laboratory abnormalities included a slight elevation of liver enzymes, impairment of liver function tests, leukocytopenia, anemia, hypergammaglobulinemia, and markedly depressed CD4(+)-cell counts. Despite initially successful treatment with pentavalent antimony, a relapse of leishmaniasis occurred after 7 months. Eradication of the infection was not achieved. Treatment was continued as a palliative chronic suppressive treatment with fortnightly pentamidine infusions. The clinical course was complicated by legionella pneumonia and the development of rapidly progressing Kaposi's sarcoma. The case is presented in detail, and the influence of HIV infection on the course of leishmaniasis is discussed.
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PMID:Visceral leishmaniasis in an HIV-infected patient: clinical features and response to treatment. 166 24

To examine whether polyclonal activation of B lymphocytes as measured by hypergammaglobulinemia contributes to lymphadenopathy in human immunodeficiency virus (HIV) infection, correlates of adenopathy were examined in 240 homosexual men. Lymph node size was measured in 12 sites semiannually over 4 years. Both adenopathy and hyperglobulinemia developed within 1 year after seroconversion and persisted at high levels. Adenopathy declined near diagnosis of AIDS whereas serum IgG decreased 8-16 months after diagnosis. Adenopathy attributable to HIV occurred in all palpable node groups. By logistic regression, HIV-positive men were best discriminated from HIV-negative men by size of posterior cervical nodes and the number of sites with enlarged nodes. In a repeated measures model of covariance, adenopathy in HIV-positive men was associated with more CD4+ cells (P less than .002), elevated serum globulins (P less than .01), and lower platelet counts (P less than .05). Adenopathy declined over time (P less than .001) and with diagnosis of AIDS or AIDS-related complex (P less than .03). Thus, adenopathy and hypergammaglobulinemia are correlated and follow a similar course through various stages of HIV infection, suggesting that both are caused by polyclonal B cell activation.
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PMID:The evolution of lymphadenopathy and hypergammaglobulinemia are evidence for early and sustained polyclonal B lymphocyte activation during human immunodeficiency virus infection. 167 Oct 53

Eleven (nine CD4+ and two CD8+) protein purified derivative-specific and eight tetanus toxoid-specific T cell clones (TCC), established from the peripheral blood of healthy persons, were cocultured in vitro with irradiated mononuclear cells from patients infected by HIV in the presence of PHA and polybrene. Two weeks post-HIV exposure, all 17 CD4+, but neither of the two CD8+, TCC exhibited integration of HIV in their genoma, as detected by polymerase chain reaction analysis, and released HIV into their supernatants, as detected by measuring both reverse transcriptase activity and p24 Ag. When co-cultured with either autologous or allogeneic B cells, all CD4+ HIV-infected TCC induced the synthesis of extraordinarily high amounts of IgM, IgG, and IgA. In contrast, their noninfected counterparts could provide helper function for Ig synthesis by autologous B cells only in the presence of the specific Ag (or anti-CD3 antibody), and induced allogeneic B cells to synthesize Ig only upon stimulation with anti-CD3 antibody. The supernatants of HIV-infected TCC failed to stimulate Ig synthesis in B cells. More importantly, when HIV-infected clonal T blasts and B cells were cultured in different chambers separated by a millipore membrane, permeable to molecules but not to cells, Ig synthesis did not occur. The Ig synthesis induced by HIV-infected TCC was also markedly inhibited by the addition in culture of either anti-CD4 or anti-LFA-1 antibody. In contrast, HIV-infected TCC maintained their ability to provide helper function for Ig synthesis in the absence of any stimulus, even after fixation with p-formaldehyde. These data demonstrate that in vitro infection with HIV enables human T cells to stimulate Ig synthesis by B cells by an Ag-nonspecific, MHC-unrestricted, contact-dependent mechanism. This may explain, at least in part, the hypergammaglobulinemia and other phenomena related to polyclonal B cell activation frequently seen in HIV-infected persons.
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PMID:In vitro infection with HIV enables human CD4+ T cell clones to induce noncognate contact-dependent polyclonal B cell activation. 167 84

From November 1985 to January 1990 we examined 156 children born to 154 HIV-1 seropositive mothers every 3 months. Eighty-seven infants were over 18 months by January 1990. Six of them met the CDC criteria of HIV-1 infection or died from AIDS; a transmission rate of 7%. Six of the children aged less than 18 months also met the CDC criteria of HIV-1 infection. These 12 infected children were compared with the 81 presumably unifected children. The perinatal findings were similar in both groups. Most of the HIV-1 infected babies showed early abnormalities in humoral and cellular immunity, hypergammaglobulinemia, low percentage of CD4 circulating lymphocytes and increased spontaneous in vitro immunoglobulin production. These changes were persistent in the HIV-1 infected children, but sporadic in those uninfected. Immunological abnormalities were frequently found before clinical symptoms appeared. We conclude that repeated immunological abnormalities in babies born to HIV-1 seropositive mothers are suggestive of HIV-1 infection.
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PMID:Immunological follow-up in children born to HIV-1 infected mothers. 168 33

We have used the polymerase chain reaction (PCR) to detect HIV proviral sequences in minute amounts of peripheral blood collected onto newborn screening blotters. Forty-three newborns, infants, and children of HIV-infected mothers were serially studied: dried blood spot (DBS) specimens were processed for PCR; serum was assayed for HIV antibodies, p24 antigen, and immunoglobulins; mononuclear cells were cultured and CD4 cells were quantitated by immunofluorescence. There was excellent agreement between the results of blood spot PCR, viral culture, and clinical and immunological indicators of HIV infection. Eighteen of 19 infected children tested positive by both PCR and culture, including six asymptomatic infants who were less than 10 weeks of age. As expected, p24 antigen capture assays were insensitive, detecting only 13 of the 19 infected children. One infected infant tested positive by PCR, but negative by culture and antigen. This infant was seropositive at 27 months and had pronounced hypergammaglobulinemia in association with non-specific symptoms. Twenty-four of the 43 infants were asymptomatic with normal immune profiles, declining antibody levels and no evidence of infection. These children tested repeatedly negative by PCR, culture, and p24 antigen assays. Our results indicate that DBS PCR is a sensitive, specific, and cost-effective alternative to viral culture for the early diagnosis (or exclusion) of perinatal HIV infection. DBS sampling opens the way for large-scale prospective studies to determine the exact rates of vertical HIV transmission in industrialized, as well as, nonindustrialized countries.
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PMID:Diagnosis of vertical HIV-1 transmission using the polymerase chain reaction and dried blood spot specimens. 173 2

Hypergammaglobulinemia is one of the most consistent, and usually the first observable abnormality in infants vertically infected with HIV. We have analyzed serum interleukin (IL)-4, IL-6, tumor necrosis factor (TNF)-alpha, and immunoglobulin (Ig) concentrations in 23 HIV-infected and 21 uninfected children. IL-6 and TNF-alpha concentrations in HIV-infected children were significantly higher than those in uninfected children, and mutually correlated. No differences in serum IL-4 levels between infected and uninfected children were observed. There was a correlation between serum IL-6 and IgG and between IL-6 and IgA concentrations. Furthermore, during follow-up changes in IL-6 levels were usually accompanied by corresponding changes in IgG levels. Our data indicate an association between HIV, IL-6, TNF-alpha and hypergammaglobulinemia. Regardless of the source and initial stimulus, continued production of IL-6 and TNF-alpha may result in augmentation in an auto-feedback manner, accompanied by increases in Ig synthesis and, more importantly, HIV replication. Thus, elucidation of the mechanisms responsible for overproduction of these two cytokines in HIV-infected patients is not only interesting from a biologic point of view, but is likely to have important clinical implications as well.
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PMID:Serum interleukin-6 concentrations are elevated and associated with elevated tumor necrosis factor-alpha and immunoglobulin G and A concentrations in children with HIV infection. 176 80

The prevalence, clinical manifestations and serological markers of hepatitis B virus (HBV) and human immunodeficiency (HIV) infections were studied in 117 Israeli hemophiliacs. Positive serological markers for HBV infection (HB surface antigen, antibody to HB surface antigen or antibody to HB core antigen) were more common in patients treated with non heat-treated F-VIII concentrates (NHTC) than with cryoprecipitate (48/49 vs. 23/29, P less than 0.05), and in patients treated with greater than 10,000 factor units/year (90% vs. 62%, P less than 0.05). Of the 117 patients, 55% were HIV negative, 29% had asymptomatic HIV seropositivity and 16% had symptomatic HIV infection (lymphadenopathy syndrome, AIDS-related complex or AIDS). HIVB seropositivity was more common in patients treated with NHTC than in those treated with cryoprecipitate (83% vs. 11%, P less than 0.001), and in patients treated with greater than 100,000 compared to less than 10,000 F-VIII units/year (70% vs. 15%, P less than 0.001). Hypergammaglobulinemia correlated with HIV seropositivity, alanine aminotransferase levels and type and amount of concentrate therapy. Of 50 HIV-seropositive patients, 40 (98%) had serological markers of HBV infection compared with only 40 of 52 HIV-negative patients (77%) (P less than 0.01). Symptomatic HIV infection was more common in patients with a positive history of jaundice, 7 of 18 (38%) compared with 12 of 99 (12%) (P less than 0.005). These findings suggest that HBV and HIV infections are less prevalent in cryoprecipitate-treated patients, and that HBV seropositivity is a predictor of HIV seropositivity in hemophiliacs.
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PMID:The prevalence and interaction of human immunodeficiency virus and hepatitis B virus infections in Israeli hemophiliacs. 195 12

Blood mononuclear cells from 47 cats experimentally infected with feline immunodeficiency virus (FIV) were examined by using monoclonal antibodies directed against feline CD4 and CD8 homologs, a pan-T-cell antigen, and cell surface immunoglobulin. Significant inversion of the CD4+/CD8+ T-cell ratio was observed only in cats that were infected for 18 months or more. This inversion was associated with a decrease in the absolute numbers of CD4+ T cells and a concomitant increase in CD8+ cells. However, the total numbers of circulating T and B cells were not significantly reduced. Cats infected with FIV for 24 to 28 months also had significantly elevated levels of serum immunoglobulin G (IgG), but normal levels of IgA and IgM. The long-term decline in CD4+ T cells and hypergammaglobulinemia observed in FIV-infected cats resemble the abnormalities occurring in humans after human immunodeficiency virus infection.
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PMID:Immunologic abnormalities in pathogen-free cats experimentally infected with feline immunodeficiency virus. 197 26

Freshly isolated B lymphocytes from patients infected with human immunodeficiency virus (HIV), in contrast to B cells from normal controls, were shown to induce viral expression in two cell lines: ACH-2, a T cell line, and U1, a promonocytic cell line, which are chronically infected with HIV, as well as in autologous T cells. In 10 out of 10 HIV-infected individuals with hypergammaglobulinemia, spontaneous HIV-inductive capacity was found with highly purified peripheral blood B cells, whereas peripheral blood or tonsillar B cells from six healthy, HIV-negative donors did not induce HIV expression unless the cells were stimulated in vitro. The induction of HIV expression was observed in direct coculture experiments of B lymphocytes and HIV-infected cells, and could also be mediated by supernatants from cultures of B cells. Significantly higher amounts of interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-alpha) were detected in the B cell culture supernatants from HIV-infected patients with hypergammaglobulinemia (IL-6: mean = 536 pg/ml; TNF-alpha: mean = 493 pg/ml), as compared with normal uninfected controls (IL-6: mean = 18 pg/ml; TNF-alpha: mean = 23 pg/ml). Antibodies against these cytokines abolished the HIV-inductive capacity of B cells. We conclude that in vivo activated B cells in HIV-infected individuals can upregulate the expression of virus in infected cells by secreting cytokines such as TNF-alpha and IL-6, and, therefore, may play a role in the progression of HIV infection.
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PMID:Activated B lymphocytes from human immunodeficiency virus-infected individuals induce virus expression in infected T cells and a promonocytic cell line, U1. 198 16

Infection with the human immunodeficiency virus (HIV) results in a progressive immune deficiency involving many components of the immune system. The major target cells for infection are CD-4 antigen-bearing cells which include predominantly, but not exclusively, the helper T-cell subset and the monocyte/macrophage cell system. Defective cell-mediated immunity occurs in association with hypergammaglobulinemia, which is a common and early feature of HIV infection. Ability to mount specific antibody responses is often impaired and the in vitro B-cell differentiation responses to T-dependent and T-independent stimuli are depressed. Our investigations with HIV envelope proteins suggest that the viral proteins can exert both stimulatory and suppressive influences on B and T lymphocytes. In addition to the opportunistic infections, children with HIV disease frequently develop serious bacterial infections. Among the currently available immunotherapeutic strategies, iv immunoglobulin therapy has received the most attention as a means to provide antibody replacement in children with recurrent bacterial infections. This modality is likely to be most valuable as adjunctive therapy in treatment protocols directed at HIV and its disease complications.
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PMID:Immune defects in pediatric AIDS, their pathogenesis, and role of immunotherapy. 215 3


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