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Live attenuated, multiply deleted simian immunodeficiency virus causes AIDS in infant and adult macaques.

A substantial risk in using live attenuated, multiply deleted viruses as vaccines against AIDS is their potential to induce AIDS. A mutant of the simian immunodeficiency virus (SIV) with large deletions in nef and vpr and in the negative regulatory element induced AIDS in six of eight infant macaques vaccinated orally or intravenously. Early signs of immune dysfunction were seen in the remaining two offspring. Prolonged follow-up of sixteen vaccinated adult macaques also showed resurgence of chronic viremia in four animals: two of these developed early signs of disease and one died of AIDS. We conclude that this multiply deleted SIV is pathogenic and that human AIDS vaccines built on similar prototypes may cause AIDS.

Aging↗

Acute effects of 3,4-methylenedioxymethamphetamine alone and in combination with ethanol on the immune system in humans.

Cell-mediated immune response and release of cytokines after the administration of 3,4-methylenedioxymethamphetamine (MDMA, "ecstasy") alone and in combination with ethanol were assessed in a double blind, randomized, crossover, controlled clinical trial. Six healthy male recreational users of MDMA participated in four different experimental sessions, with a washout interval between sessions of 1 week, in which single oral doses of MDMA (100 mg), ethanol (0.8 g/kg), the combination of both drugs, and placebo were tested. Acute MDMA administration produced a time-dependent immune dysfunction in association with serum concentrations of the drug as well as cortisol stimulation kinetics. Although total leukocyte count remained unchanged, there was a decrease in the CD4 T/CD8 T-cell ratio due to a decrease in both the percentage and absolute number of CD4 T-helper cells and simultaneous increase in natural killer (NK) cells. Ethanol consumption produced a decrease in T-helper cells and B lymphocytes. The combination of MDMA and ethanol caused the highest suppressive effect on CD4 T cells and increasing effect in NK cells. Drugs treatment produced a high increase of immunosuppressive cytokines (transforming growth factor-beta and interleukin-10) and a switch from Th1-type cytokines (interleukin-2 and interferon-gamma) to Th2-type cytokines (interleukin-4 and interleukin-10). Disregulation in the production of pro- and anti-inflammatory cytokines with an unbalance toward anti-inflammatory response was also observed. The immune function shows a trend toward baseline levels at 24 h after MDMA kinetics. This transient defect in immunological homeostasis, if temporarily repeated, might alter the immune response with a risk for the general health status.

Adult↗

Long-term study of cell-mediated responses to Borrelia burgdorferi in the laboratory mouse.

Borrelia burgdorferi infection of disease-susceptible (C3H) and -resistant (BALB) mice resulted in impaired proliferation to both T- and B-cell mitogens up to 30 days after inoculation. Interleukin-2 and -4 production was also impaired, paralleling the T-cell response to concanavalin A. Impaired lymphocyte proliferation could not be attributed to diminished numbers of T or B cells and was found to depend on the lymphoid organ (spleen or lymph node) examined. Prostaglandin production accounted for part of this immune dysfunction. Attempts to assess antigen-specific proliferation to B. burgdorferi were inconsistent, and delayed-type hypersensitivity responses were not detected. Adoptive transfer of T-enriched cells from chronically infected donors failed to prevent infection and disease development in recipient C3H mice. The current study emphasizes caution in the study of B. burgdorferi antigen-specific assays and argues against the role of a vigorous T-cell response in Lyme borreliosis in infected laboratory mice.

Animals↗

Immunostimulatory probiotic Lactobacillus rhamnosus HN001 and Bifidobacterium lactis HN019 do not induce pathological inflammation in mouse model of experimental autoimmune thyroiditis.

The possibility that intestinal microflora contribute to the pathogenesis of autoimmune diseases has raised issues regarding the safety of probiotic organisms, especially those with immunostimulating properties, in individuals with such immune dysfunctions. In this study, the effect of consumption of probiotic lactic acid bacteria (LAB) strains Lactobacillus rhamnosus HN001(HN001) and Bifidobacterium lactis HN019 (HN019) on the induction and progression of experimental autoimmune thyroiditis (EAT) was investigated in CBA/CaH (H-2k) mice. HN001 or HN019 in skim milk were fed to mice daily (1-1.5 x 10(8) cfu/mouse/day) for 5 to 9 weeks. A mild form of EAT was induced by subcutaneous injection of mouse thyroglobulin (MTg) with either Freund's adjuvant (complete and incomplete, CFA and IFA) or lipopolysaccharide (LPS). The proliferative responses of spleen lymphocyte to MTg stimulation in vitro and the presence (and degree) of mononuclear cell infiltration in thyroid gland tissues were examined to assess the development and severity of EAT. The levels of serum anti-MTg antibodies (IgG1 and IgG2a) and spleen weight index were determined to detect the presence of autoimmune responses of mice receiving MTg. Results showed that 8 weeks after immunization, 16.67-50% of the mice developed mild EAT with lymphocyte infiltration in the thyroid glands. Probiotic feeding did not induce full-blown EAT. There were no differences in spleen weight index or the proliferative spleenocytes in response to PMA between mice that received MTg alone and mice that received MTg and probiotic LAB strains.

Animals↗

Effects of RRR-alpha-tocopheryl succinate on IL-1 and PGE2 production by macrophages.

Vitamin E is thought to enhance immunity by increasing interleukin-1 (IL-1) production and by downregulating prostaglandin E2 (PGE2) synthesis. In an effort to understand the mechanism(s) whereby the form of vitamin E known as RRR-alpha-tocopheryl succinate [also called vitamin E succinate (VES)] ameliorates retrovirus-induced immune dysfunctions, peritoneal exudate cells (PECs) derived from normal chickens and avian and murine macrophage cell lines were used as in vitro model systems to test the effects of VES treatments on PGE2 and IL-1 production. Supernatants from PECs that were exposed to avian erythroblastosis virus (AEV) for 45 minutes exhibited a 256% increase in PGE2 levels compared with supernatants from replica cultures of PECs not exposed to AEV. Pretreatment of PECs with VES before exposure to AEV maintained PGE2 levels at normal control levels. VES treatment enhanced IL-1 production by avian (HD11) and murine (P388D1) macrophage cells, respectively. Supernatants from VES-treated HD11- and P388D1-stimulated cells contained IL-1 activity 196% and 385%, respectively, greater than that observed with supernatants from untreated control cells. On the basis of these studies, downregulation of retrovirus-induced PGE2 production and/or upregulation of IL-1 production by VES are potential mechanisms for VES amelioration of retrovirus-induced immune suppression.

Animals↗

Aggressive non-Hodgkin's lymphomas in immunocompromised homosexual males.

During the period from 1981 through 1984, 14 immunocompromised homosexual males with intermediate or high-grade non-Hodgkin's lymphoma were seen at University of Texas M.D. Anderson Hospital and Tumor Institute. Six patients had diffuse large-cell lymphoma, seven had diffuse undifferentiated lymphoma, and one had unclassifiable lymphoma that suggested large-cell lymphoma. Eight patients had the acquired immunodeficiency syndrome (AIDS) and five had the AIDS-related complex. Kaposi's sarcoma was initially present in four patients and developed later in two others. The patients with diffuse large-cell lymphoma were characterized by more severely altered immune parameters, multicentric brain mass lesions, pretherapy opportunistic infections, lower performance status, poor response to therapy, and death in all within six months. The undifferentiated lymphoma group had preceding generalized reactive lymphadenopathy, less severe immune dysfunction, and excellent response to combination chemotherapy, with survival time greater than 19 months in three patients. Twelve of the patients had extranodal sites of lymphoma at presentation. There is a definite trend for the development of aggressive non-Hodgkin's lymphomas with unusual sites of extranodal involvement in immunocompromised homosexual males, with the potential for good tolerance to combination chemotherapy and improved survival in the subgroup without severe concomitant opportunistic infections.

Abscess↗

Adenovector-mediated expression of human thrombopoietin cDNA in immune-compromised mice: insights into the pathophysiology of osteomyelofibrosis.

Thrombopoietin (TPO) cDNA can be effectively delivered in vivo by adenovectors. Immune normal mice (BALB/c) and syngeneic mice with variable degrees of immune dysfunction nu, SCID, and NOD-SCID) were treated with an adenovirus vector expressing the human TPO cDNA (AdTPO). Platelet peaks were significantly higher in SCID and NOD-SCID mice compared with BALB/c and nu mice. Human plasma TPO concentration correlated with the platelet counts. SCID and NOD-SCID mice exhibited also granulocytosis and increased numbers of hemopoietic progenitors in bone marrow. Following platelet peak, BALB/c mice developed autoantibodies against murine TPO leading to thrombocytopenia and depletion of megakaryocytes and hemopoietic progenitors in bone marrow. AdTPO-treated SCID mice developed osteomyelofibrosis and extramedullary/extrasplenal hemopoiesis. In contrast, NOD-SCID mice with a similar magnitude of TPO overexpression did not show fibrotic changes in bone marrow. We conclude, first, that a chronic high level of TPO overexpression stimulates megakaryocytopoiesis and myelopoiesis leading to thrombocytosis and granulocytosis. Second, increased megakaryocytopoiesis is not sufficient for development of secondary osteomyelofibrosis. The functionally deficient monocytes and macrophages of NOD-SCID mice probably prevented fibrotic marrow changes. Third, immune deficiency enhances expression of adenovirally mediated transgenes, and fourth, xenogeneic transgene delivered by adenovector to a host with normal immune functions may induce loss of immune tolerance and autoimmune phenomenon.

Adenoviruses, Human↗

Immunodeficiency-related lymphoproliferative disorders: prospective data from the United Kingdom Children's Cancer Study Group Registry.

Clinical data and biological samples were prospectively collected in 42 children with lymphoproliferative disease (LPD) secondary to organ/bone marrow transplant-related immunosuppression (30: 11 liver, 10 heart/lung, 8 kidney and 1 bone marrow), other drug-induced immunosuppression (2), congenital immunodeficiency (8) or human immunodeficiency virus (HIV)-related immune dysfunction (2). Ages ranged from 10 months to 17 years and there were 15 girls. Pathology was centrally reviewed and showed polymorphic features in 5 cases, monomorphic in 23, mixed pattern in 5 patients and 9 other types. Using the Revised European-American Classification of Lymphoid Neoplasms, 5 were B lymphoblastoid, 24 were high-grade B and 14 were other subtypes. Using the Pittsburgh classification, 9 were lymphadenopathic, 10 were systemic, 25 were lymphomatous and, with the Murphy grouping for non-Hodgkin's lymphoma (NHL), 10 were localized and 32 non-localized. Twenty-four out of 38 evaluable cases were Epstein-Barr virus positive. Thirty-five patients were evaluable for clonality; 24 were monoclonal and 11 were polyclonal. Reduced immunosuppression in solid organ transplant patients resulted in resolution of disease in 14/24, which was sustained in 11. Nineteen patients received chemotherapy, 14/18 evaluable responded, which was sustained in 8 cases. Seven out of 29 solid organ transplant and 10/13 other immune-deficient patients died. In the largest group of patients, solid organ transplants, no significant clinical or biological characteristics that predicted outcome were identified. In the transplant group close monitoring of response during reduction in immunosuppression is essential and the early use of B NHL chemotherapy may be effective.

Adolescent↗

Mechanical ventilation exacerbates alveolar macrophage dysfunction in the lungs of ethanol-fed rats.

BACKGROUND: Patients with alcohol abuse have a two- to three-fold increased risk of acute lung injury and respiratory failure after sepsis or trauma but are also at increased risk of nosocomial pneumonia. Mechanical ventilation exacerbates lung injury during critical illnesses. In this study we tested whether mechanical ventilation of the alcoholic lung promotes on balance a proinflammatory phenotype favoring ventilator-induced lung injury or an immunosuppressive phenotype favoring ventilator-associated pneumonia. METHODS: Lungs from rats fed an isocaloric diet with or without ethanol (six weeks) were isolated and ventilated ex vivo with a low-volume (protective) or high-volume (injurious) strategy for two hours with or without prior endotoxemia (two hours). In other experiments, rats were subjected to high-volume ventilation in vivo. Airway levels of the proinflammatory cytokines tumor necrosis factor-alpha, macrophage inflammatory protein-2, and interleukin-1beta were determined after mechanical ventilation ex vivo and compared with edematous lung injury after high-volume ventilation in vivo. In parallel, alveolar macrophage phagocytosis of bacteria and secretion of interleukin-12 during ventilation ex vivo and endotoxin-stimulated alveolar macrophage phagocytosis and tumor necrosis factor-alpha secretion in vitro were determined. RESULTS: Ethanol ingestion suppressed the proinflammatory response to injurious mechanical ventilation and did not increase experimental ventilator-induced lung injury. In parallel, ethanol ingestion blunted the innate immune response of alveolar macrophages during injurious ventilation ex vivo and after endotoxin stimulation in vitro. CONCLUSIONS: Ethanol ingestion dampens ventilator-induced inflammation but exacerbates macrophage immune dysfunction. These findings could explain at least in part why alcoholic patients are at increased risk of ventilator-associated pneumonia.

Alcoholism↗

Cell proliferation and apoptosis in the immune system in the elderly.

Loss of the cell proliferative capability and involution of tissues and organs are among the most important phenomena that characterize the aging process. Some of the aged-linked immune dysfunctions could be partly due to a dysregulation of apoptotic processes and to a lower responsiveness of aged lymphoid cells to activation and proliferation signals. The main changes in proliferative activity and cell death during aging and their impact on the process of immunosenescence are discussed. In fact, a very important function that has been suggested to deteriorate with age and to play a major role in the aging process is the capability of cells from aged subjects to respond to mitogenic stimuli and, consequently, to undergo cell proliferation. However, the cellular activation processes are very complex and the proliferative responses can follow different interconnected signal transduction pathways, and only some of them appear to be modified during age. Moreover, cell growth, immunosenescence, and longevity are strictly interconnected and deeply related to programmed cell death or apoptosis. The cellular equilibrium between cell survival and proliferation, on the one hand, and programmed cell death, on the other hand, seems to be unbalanced with advancing age, although in each type of immune cell it could be differentially modulated, resulting in a variety of clinicopathological consequences. Thus, cell proliferation and cell death are two physiologically active phenomena closely linked and regulated and a failure of these mechanisms determines profound dysregulations of cell homeostasis with major consequences in immune functioning and the onset of autoimmune diseases and cancer, whose incidence appears to be increased in the elderly.

Aging↗

Measurement of CD69 induction in the assessment of immune function in asymptomatic HIV-infected individuals.

Peripheral blood mononuclear cells from many asymptomatic HIV-infected patients exhibit defects in cytokine production and impaired proliferative responses in vitro but the mechanisms underlying this subclinical immune deficiency are controversial. To determine whether abnormalities in the earliest events following receptor engagement may help to explain the in vitro immune dysfunction, we measured the inducibility of the early activation marker CD69 in T cells from asymptomatic HIV-infected individuals in response to stimulation with anti-CD2 or anti-CD3 mAb. In a whole blood assay, we found that induction of CD69 was markedly impaired in CD4+ T cells from later-stage HIV-infected patients (CD4 counts 200-400/mm3) compared to uninfected controls. Among early stage patients (CD4 > 400/mm3), a subset (29%) had impaired CD69 induction. CD69 responses were equally depressed after stimulation through the CD3 or CD2 receptor pathways. Survey of a panel of immunophenotypic markers and propensity for apoptosis demonstrated a significant association between depressed induction of CD69 and decreased percentages of CD4+CD26+ and CD4+CD95+ cells but no association with the level of apoptosis. These data indicate that defects in T lymphocyte activation through CD3 and CD2 can be measured within hours of receptor stimulation in asymptomatic HIV-infected individuals and might be useful to monitor as an indicator of immune function in these patients.

Antigens, CD↗

Thymic hypoplasia and T-cell deficiency in ectodermal dysplasia: case report and review of the literature.

Ectodermal dysplasia is a heterogeneous disorder that includes a constellation of congenital malformations occasionally associated with mild to moderate immune dysfunction. In this report, we describe a female infant with ectodermal dysplasia who was found to have thymic hypoplasia but no other phenotypic features of the DiGeorge anomalad. She experienced Candida parapsilosis sepsis at 1 week of age and a skin infection with Mycobacterium chelonii at 6 months. The numbers of blood B cells were normal and serum immunoglobulins normal to slightly reduced, but serum antibody responses of all immunoglobulin isotypes to protein immunogens were absent. Blood T cells were profoundly reduced and proliferative responses of T cells to mitogens were blunted. In contrast, there was an increased number of natural killer (NK) cells and increased NK activity in the blood. Over the first year of life, some of the immunodeficiencies resolved. Although the numbers of blood T cells (17% of total lymphocytes) remained low, proliferative responses to mitogens normalized and specific antibody responses improved. It seems likely that the thymic hypoplasia in this case was due to a paucity of ectodermal elements in the developing thymus, and that the immune defects were largely secondary to that event. In that respect, this human model of ectodermal dysplasia and thymic hypoplasia resembled the ectodermal/thymic defects found in the nude mouse.

Cell Line↗

Adenosine- and deoxyadenosine-mediated altered pyrimidine metabolism in human adeosine deaminase-deficient lymphoblasts.

To evaluate the importance of altered pyrimidine synthesis in the relationship between immune dysfunction and deficiency of ADA, this pathway has been evaluated in normal and ADA-deficient human lymphoblasts. Adenosine and deoxyadenosine effect comparable reductions of radiolabeled bicarbonate incorporation in uridine nucleosides of both normal and deficient cells, with this effect being more prolonged in deficient cells. In ADA-deficient lymphoblasts this altered pyrimidine metabolism is accompanied by reduced intracellular concentrations of PP-ribose-P with adenosine but not deoxyadenosine. The altered PP-ribose-P levels are accompanied by orotic acid accumulation, but this block does not fully account for the net reduction in uridine nucleotide synthesis. This suggests interference of the pyrimidine pathway at another locus, possibly by altered carbamyl phosphate synthetase activity. The mechanism for deoxyadenosine-mediated inhibition is obscure. Despite the demonstrable adenosine- and deoxyadenosine-mediated alterations of pyrimidine metabolism, these changes are not accompanied by marked interference of cell growth for both normal and ADA-deficient lymphoblasts. These data support the hypothesis that altered pyrimidine metabolism is not the basis for the immune disorder in patients with deficiency of ADA.

Adenosine↗

Alcohol (ethanol) inhibits IL-8 and TNF: role of the p38 pathway.

Acute ethanol (EtOH) intoxication has been identified as a risk factor for infectious complications in trauma and burn victims. However, the mechanism of this immune dysfunction has yet to be elucidated. The monocyte/macrophage production of cytokines, in particular IL-8 and TNF-alpha, is critical in the regulation of the acute inflammatory response to infectious challenge. IL-8 is a potent chemoattractant and activator of neutrophils. TNF-alpha, a proinflammatory cytokine, initiates expression of endothelial cell surface adhesion molecules and neutrophil migration. p38, a member of the mitogen-activated protein kinases, plays an important role in mediating intracellular signal transduction in endotoxin-induced inflammatory responses. We examined the effects of LPS and ethanol on p38 activation and the corresponding IL-8 and TNF-alpha production in human mononuclear cells. LPS-induced IL-8 and TNF-alpha production was inhibited in a similar pattern by pretreatment with either EtOH or SB202190 (1 microM), a specific inhibitor of p38 kinase. Western blot analysis, using a dual phospho-specific p38 mitogen-activated protein kinase Ab, demonstrated that EtOH pretreatment inhibited LPS-induced p38 activation. These results demonstrate that alcohol suppresses the normal host immune inflammatory response to LPS. This dysregulation appears to be mediated in part via inhibition of p38 activation. Inhibition of IL-8 and TNF-alpha production by acute EtOH intoxication may inhibit inflammatory focused neutrophil migration and activation and may be a mechanism explaining the increased risk of trauma- and burn-related infections.

Adult↗

Ethanol-induced expression of cytokines in a first-trimester trophoblast cell line.

OBJECTIVES: Altered cytokine expression at the fetoplacental interface may be a potential mechanism for the development of fetal immune dysfunction in children with fetal alcohol syndrome. This study was conducted to determine whether first-trimester trophoblasts respond to ethanol exposure by the induction of specific cytokines. STUDY DESIGN: HTR-8/SVneo trophoblast cells were cultured in vitro in the presence of either ethanol (0.5% [vol/vol]), lipopolysaccharide (1 microg/mL), or ethanol and lipopolysaccharide. Expression of granulocyte colony-stimulating factor, regulated on activation normal T cell expressed and secreted, and interleukin-6 was examined by Northern analysis and enzyme-linked immunosorbent assay. RESULTS: Culture in the presence of ethanol, lipopolysaccharide, or lipopolysaccharide and ethanol resulted in the increased transcription and secretion of granulocyte colony-stimulating factor, regulated on activation normal T cell expressed and secreted, and interleukin-6 at significantly greater levels (P < .01) than control cultures. CONCLUSIONS: Human first-trimester trophoblasts express high levels of cytokines when cultured in the presence of ethanol. Trophoblasts may therefore be an important exogenous source of cytokines for the fetus, and altered cytokine levels during early gestation may have an adverse effect on the development of the fetal immune system.

Cell Line↗

Protease inhibitors protect macrophages from lipopolysaccharide-induced cytotoxicity: possible role for NF-kappaB.

Recent studies suggest lipopolysaccharide (LPS) mediated cell death as underlying mechanism of hyporesponsiveness and dysfunction of macrophages in the late phase of septic shock. In the present study LPS (0.001 - 30 microg/ml) caused a concentration-dependent toxicity in the macrophage cell line (J774.1A) within 24 h. The toxicity induced by LPS (1 microg/ml) was completely inhibited by the serine protease inhibitors, N-alpha-tosyl-L-phenylalanine chloromethyl ketone (TPCK) and N-alpha-tosyl-L-lysine chloromethyl ketone (TLCK) as measured by the mitochondrial-dependent oxidation of 3-(4,5-dimethyl-thiazol-2-yl)-2,5-diphenyltetrazolium bromid (MTT) to formazan. These inhibitors antagonize the activation of nuclear transcription factor-kappaB (NF-kappaB) indirectly by inhibiting I kappaB alpha-protease. SN50, a direct inhibitor of NF-kappaB translocation into the nucleus also protected macrophages from LPS-mediated toxicity. We conclude from these data that the early phase signal transduction pathway leading to LPS-mediated cytotoxicity in macrophages involves the activation of NF-kappaB. Thus, I kappaB alpha-protease inhibitors might serve as therapeutical agents to maintain macrophage viability during sepsis and to prevent sepsis-induced immune dysfunction.

Amino Acid Sequence↗

Delayed cutaneous hypersensitivity and lymphocyte transformation: dissociation in atopic dermatitis.

Studies of cell mediated immunity (CMI) in atopic dermatitis have demonstrated various defects and frequently contradictory results. The true nature of immune dysfunction remains uncertain. We approached this question by concurrently examining two aspects of CMI: delayed cutaneous hypersensitivity and in vitro lymphocyte transformation. Responses were tested using the antigens Candida albicans and streptokinase-streptodornase (SKSD). Mean lymphocyte transformation was equal in atopic patients and controls, although a subgroup of severely dermatitic patients showed depressed responses. Cutaneous anergy was the rule in atopic patients (96% to candidin and 84% to SKSD). Although normal subjects showed good correlation between in vitro and cutaneous responses, atopic patients showed a significant lack of correlation. Many patients manifested cutaneous anergy in the face of normal lymphocyte transformation re sponses.

Adolescent↗

Relationship of CD4 counts to neurophysiological function in HIV-1--infected homosexual men.

OBJECTIVE: To explore the relationship of immune dysfunction to neurophysiological measures of brain-stem conduction time. DESIGN: Three-year longitudinal prospective cohort study; results of time 1 analyses reported. SETTING: San Francisco (California) General Hospital, Departments of Psychiatry and Epidemiology. PATIENTS: Volunteer sample of 55 human immunodeficiency virus (HIV)-positive and 37 HIV-negative homosexual men recruited from a larger cohort of homosexual men followed up since 1983 at San Francisco General Hospital as part of an ongoing study of the natural history and course of HIV type 1 infection. INTERVENTION: None. MAIN OUTCOME MEASURES: Auditory brain-stem responses and somatosensory evoked potentials for subjects stratified separately on HIV serostatus, Centers for Disease Control and Prevention symptom groupings, and absolute CD4 counts. RESULTS: The HIV-positive subjects had an increased wave III-V interpeak latency of the right ear auditory brain-stem response compared with the HIV-negative subjects (t test, P < .05). There were no significant differences among the three Centers for Disease Control and Prevention groupings on any evoked potential measure. When HIV-positive subjects were stratified on a measure of immune functioning, ie, CD4 counts, individuals with greater immune suppression were more impaired on speed of auditory brain-stem conduction time (Mann-Whitney U test, P < .05). Furthermore, 85% of subjects impaired on this evoked potential measure had CD4 counts of less than 0.40 x 10(9)/L (400/microL), whereas only 15% of those impaired on this measure had CD4 counts of greater than 0.40 x 10(9)/L. CONCLUSIONS: Asymptomatic HIV-positive subjects who do not have evidence of immune suppression do not appear to be at greater risk for neurophysiological impairment than HIV-negative subjects. The HIV-positive individuals who are immune suppressed (even while asymptomatic) appear to have an increased likelihood of central conduction time slowing as measured by evoked potential procedures.

Adolescent↗