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

Involvement of the central nervous system (CNS) is common in patients with advanced disease due to human immunodeficiency virus (HIV). Symptoms range from lethargy and apathy to coma, incoordination and ataxia to hemiparesis, loss of memory to severe dementia, and focal to major motor seizures. Involvement may be closely associated with HIV infection per se, as in the AIDS dementia complex, but is frequently caused by opportunistic pathogens such as Toxoplasma gondii and Cryptococcus neoformans or malignancies such as primary lymphoma of the CNS. The clinical presentations of attendant and direct CNS involvement are remarkably non-specific and overlapping, yet a correct diagnosis is critical to successful intervention. Toxoplasmic encephalitis is one of the most common and most treatable causes of AIDS-associated pathology of the CNS. A great deal has been learned in the last 10 years about its unique presentation in the HIV-infected patient with advanced disease. Drs. Benjamin J. Luft of the State University of New York at Stony Brook and Jack S. Remington of the Stanford University School of Medicine and Palo Alto Medical Foundation's Research Institute have studied T. gondii for many years and are two of the leading experts in the field. This commentary comprises an update of their initial review (J Infect Dis 1988;157:1-6) and a presentation of the current approaches to diagnosing and managing toxoplasmic encephalitis in HIV-infected patients.
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PMID:Toxoplasmic encephalitis in AIDS. 152 Jul 57

Dendritic cells (DC) have a potent antigen-presenting capacity for recruiting resting T cells into immune responses. They also promote expansion of already activated memory T cells. By contrast, macrophages (M phi) are only effective in stimulating memory responses. Infection and depletion of DC occur in human immunodeficiency virus (HIV)-infected individuals and recruitment of T cells into primary responses is blocked. Here comparisons between DC and M phi in stimulating secondary T-cell responses in HIV infection were made. Adherent M phi, and DC isolated by a new method, were separated from peripheral blood of patients in different stages of HIV infection and from uninfected controls and added to allogeneic lymphocytes in mixed leucocyte reactions (MLR). Some were pulsed with influenza virus or tetanus toxoid and used to stimulate autologous T cells. Responses were measured from uptake of [3H]thymidine in 20 microliters hanging drop cultures. DC, but not M phi, from normal individuals stimulated MLR but both populations stimulated secondary responses to recall antigens. DC from all HIV seropositive individuals caused little or no stimulation of any lymphocyte responses. However, M phi from HIV seropositive asymptomatic individuals and those with persistent generalized lymphadenopathy stimulated responses to recall antigens. There was no stimulation using cells from acquired immune deficiency syndrome (AIDS) patients. Blocked DC but not M phi function may underlie progressive immunological non-responsiveness in HIV infection. Without recruitment of resting T cells, loss of memory T cells may be cumulative; failure of secondary activation (e.g. by M phi) would lead to lost T-cell activity. Identification and circumvention of the defect in DC could offer new therapeutic approaches.
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PMID:Antigen-presentation by macrophages but not by dendritic cells in human immunodeficiency virus (HIV) infection. 153 9

The germinal center forms a specialized microenvironment that is thought to play a key role in the induction of antibody synthesis, affinity maturation of B cells, isotype switching, and memory B-cell formation. Moreover, the germinal center may also be involved in the maintenance of T-cell memory. In this paper we focus on the role of adhesion receptors in cellular interactions in the germinal center, and discuss evidence indicating that these molecules play an important role in regulating B-cell activation and differentiation. Furthermore, we discuss two important diseases involving the germinal center, i.e., HIV infection and malignant lymphoma. In HIV infection, destruction of the FDC network may explain the selective loss of memory cells observed in otherwise asymptomatic patients and is likely to represent a major pathway leading to AIDS. In follicular lymphoma, escape from physiological apoptosis in the germinal center by overexpression of Bcl-2 appears be a major pathogenetic pathway.
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PMID:Cellular interactions in the germinal center: role of adhesion receptors and significance for the pathogenesis of AIDS and malignant lymphoma. 159 19

T-lymphocyte activation is accompanied by a loss of CD45RA determinant and gain of CD45RO marker. Previous work suggests that the CD45RO population could represent the T-cell memory pool since it contains most of the cells that can respond to recall soluble antigens. A selective loss of memory T cells was recently found in early stages of human immunodeficiency virus (HIV) infection, which could contribute to the qualitative defects observed in HIV-infected patients. In order to investigate whether HIV infection could induce an alteration in the process of differentiation from naive cells to cells with a memory phenotype, we studied the expression of CD45RA and CD45RO in CD4+ and CD8+ lymphocytes, by flow cytometric analysis, after mitogenic stimulation of mononuclear cells from patients with HIV infection. These preliminary results suggest that after in vitro activation the CD4+ and CD8+ populations from HIV-infected patients lose the CD45RA marker and concomitantly acquire the CD45RO determinant in the same way as shown for the healthy control population studied simultaneously. Thus, it appears that an alteration in the process of conversion of CD45RA into CD45RO does not contribute to the defects observed in the memory T-cell population in HIV infection.
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PMID:Loss of CD45RA and gain of CD45RO after in vitro activation of lymphocytes from HIV-infected patients. 183 25

To investigate the effects of persistant human immunodeficiency virus (HIV) infection on T cell reactivity, functional properties of peripheral blood T cells from HIV-seropositive homosexual men in various stages of infection were studied. T cell activation via CD3 resulting in proliferation and differentiation was measured in a model system independent of accessory cells, using immobilized anti-CD3 monoclonal antibodies (mAb). T cells from HIV-infected asymptomatic men had a decreased proliferative response compared to HIV-negative controls. T cells from AIDS-related complex (ARC) and AIDS patients, compared to T cells from asymptomatic HIV-infected men, had a significantly lower proliferative response to anti-CD3 mAb. This diminished response to anti-CD3 mAb was shown to be due to decreased interleukin (IL) 2 production and could be enhanced by co-stimulation with anti-CD28 mAb or by adding IL 2. Anti-CD3-induced generation of cytotoxic T lymphocytes was fully intact in early infection but was severely decreased in T cells from ARC and AIDS patients. Cytotoxic activity could be restored to near normal levels after co-stimulation with either anti-CD28 mAb or IL 2. Our data demonstrate a differential loss of T cell functions in the course of HIV infection which is predominantly caused by a lack of IL 2 production after stimulation via the CD3/T cell receptor complex. In early HIV infection this seems to be predominantly caused by a specific loss of memory T cells. However, in later stages of infection when both naive and memory T cell subsets are depleted, resulting in a normal naive/memory T cell ratio, T cell functions further deteriorate probably due to intrinsic activation defects. These findings may be of pathogenic relevance since diminished T cell reactivity may facilitate spreading and replication of virulent HIV variants heralding development of ARC and AIDS.
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PMID:Selective loss of T cell functions in different stages of HIV infection. Early loss of anti-CD3-induced T cell proliferation followed by decreased anti-CD3-induced cytotoxic T lymphocyte generation in AIDS-related complex and AIDS. 216 75

The clinical manifestations of AIDS (acquired immune deficiency syndrome) often include neuropsychiatric and neurological deficits, including early memory loss and progressive dementia. HIV (human immunodeficiency virus), the aetiological agent of AIDS, is probably carried by infected macrophages in the central nervous system. The virus enters cells by binding its envelope glycoprotein gp120 to the CD4 antigen present on brain and immune cells. From the data reported in this paper, we now suggest that the neuronal deficits associated with HIV may not be entirely a result of infectivity, but that gp120 shed from HIV could directly produce the neuropathology as a result of its interference with endogenous neurotrophic substances. It is known that an analogue of a sequence contained in vasoactive intestinal peptide (VIP) occurs in all known sequenced gp120 isolates and that VIP is important for neuronal survival in cell culture. Here we show that purified gp120 from two diverse HIV isolates and a recombinant gp120 from a third isolate were all potent in specifically producing significant neuronal cell death in dissociated hippocampal cultures derived from fetal mice, and that this could be reduced by monoclonal antibodies against the murine CD4 antigen and completely antagonized by VIP.
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PMID:Neuronal cell killing by the envelope protein of HIV and its prevention by vasoactive intestinal peptide. 284 76

Eight patients with acquired immune deficiency syndrome (AIDS) presented complications affecting the nervous system. The complaints were headache, seizure, confusion or hallucination. Neurologic manifestations included meningitis, focal deficits, cranial nerve palsy, and dementia. Cerebrospinal fluid exhibited a decrease in the percentage of T helper lymphocytes with an inverted helper-to-suppressor cell ratio. The neurologic manifestations of AIDS may depend on multiple factors, such as HIV infection of the central nervous system, concomitant infections with other agents or meningeal invasion by systemic lymphoma or Kaposi's sarcoma. Many patients develop a diffuse encephalopathy which characteristically begins with impaired concentration and mild memory loss, and progresses to severe global cognitive impairment and dementia. Perivascular infiltrates and scattered microglial nodules, consisting of aggregates of microglia and astrocytes, are the most common findings in these patients.
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PMID:[Neurologic complications accompanying acquired immunodeficiency syndrome (AIDS): study of a group of 8 cases]. 295 8

We have demonstrated that a single intravenous bolus of rat anti-CD4 MoAb caused a small but prolonged increase in apoptosis in murine lymph nodes. We have quantified this process using the novel Highly Optimized Microscope Environment (HOME) interactive images analysis system and shown that the increase in apoptosis was sufficient to account for the observed depletion of the peripheral CD4+ T cell subset. This occurred in the absence of any other exogenous signal. Furthermore, there was no evidence of an inflammatory or necrotic response in the tissues, indicating that this was unlikely to be Fc or complement-mediated antibody killing. The anti-CD4-induced depletion selectively removed CD44- T cells. Using mice previously immunized with yeast-derived HIV-1 p24 recombinant protein there was sparing of memory T cell function after in vivo anti-CD4 treatment, except during a window of less than 24 h duration, when simultaneous exposure to antigen and anti-CD4 antibody resulted in the depletion of specific memory T lymphocyte function. This indicated that a very minor alteration in the frequency of apoptosis had a marked effect on cell number over time, and suggested that opportunistic infection associated with CD4+ T cell depletion may be explained by loss of memory cells when there is antigenic stimulation at the same time as CD4 ligation. These results have implications for the pathology of HIV-associated disease which is associated with ligation of CD4 molecules in vivo.
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PMID:Peripheral T lymphocyte depletion by apoptosis after CD4 ligation in vivo: selective loss of CD44- and 'activating' memory T cells. 750 14

The immunologic and clinical abnormalities associated with pediatric human immunodeficiency virus (HIV) infection are reviewed, the rationale for using intravenous immune globulin (IVIG) to prevent serious bacterial infections is described, and clinical experience with IVIG for this indication is summarized. Immunologic and clinical abnormalities seen in pediatric HIV-infected patients differ from those seen in adult HIV-infected patients. In pediatric patients, impaired B-cell activity is an early and prominent manifestation of HIV infection. Infants infected with HIV do not develop the antigen-specific B- and T-cell clones required for immunologic memory, amplification, and production of specific antibodies. B-cell defects and lack of memory B cells result in a high rate of serious bacterial infections in HIV-infected children compared with adults. Natural killer cell dysfunction may also increase HIV-infected children's susceptibility to secondary infections. IVIG therapy in HIV-infected pediatric patients is based on evidence of impaired antibody function in these patients, although this use remains controversial. Case reports and one unblinded comparative study published during the 1980s suggest that IVIG may decrease morbidity and improve cellular and humoral immune response. One recent large-scale, double-blind, placebo-controlled study showed that IVIG 400 mg/kg every 28 days can decrease the morbidity associated with serious bacterial infections in HIV-infected children with CD4 cell counts of > 200 cells/cu mm. Another study involving HIV-infected children receiving concurrent zidovudine demonstrated that IVIG helped prevent serious bacterial infections in children who were not concurrently receiving trimethoprim-sulfamethoxazole but not in those who were. Although IVIG has not been shown to alter mortality in HIV-infected children, regular use may decrease the morbidity associated with serious bacterial infections.
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PMID:Intravenous immune globulin for prevention of bacterial infections in pediatric AIDS patients. 763 15

The objective of this study was to evaluate the reliability and validity of a brief index to measure symptoms in individuals infected with human immunodeficiency virus (HIV). From an ambulatory clinic that specializes in the care of HIV-infected individuals at a university hospital in northeast Ohio, 148 randomly selected outpatients (predominantly homosexual men) with a broad spectrum of HIV disease were enrolled in a prospective, cohort study. In standard interviews, patients rated the frequency of 36 symptoms related to HIV infection on an ordinal scale from zero (never) to three (daily); these interviews were repeated and outcomes determined every 3 months for one year. Clinical data were abstracted from the medical record with a standard chart review. Using specific criteria, 12 symptoms were selected for the HIV Symptom Index: fatigue, fevers, headache, imbalance, paresthesias, memory loss, cough, nausea, diarrhea, sadness, sleep disturbance, and skin problems. The HIV Symptom score (the sum of frequency ratings for the 12 symptoms) ranged from 0 to 31 with a mean of 9.4 (+/- SD 6.6). The test-retest reliability was high (intraclass correlation coefficient = 0.92) as was the internal consistency (Cronbach's alpha = 0.79). The validity of the index was established with three observations. (1) The HIV Symptom Index makes clinical sense and includes a representative spectrum of symptoms of infection. (2) Symptom Index scores were greater in patients with more advanced disease and in patients who were functionally impaired. (3) The Index was responsive to changes in health as the disease progressed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:An index of symptoms for infection with human immunodeficiency virus: reliability and validity. 773 Aug 79


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