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

Two cases of combined HIV-CMV encephalitis are described. One presented with a sixth nerve palsy and a tetraparesis, the other with an internuclear ophthalmoplegia. Pathologically brain stem involvement was predominantly due to CMV.
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PMID:Combined HIV-CMV encephalitis presenting with brainstem signs. 255 24

Data of the literature about frequency and specificity of giant cells during AIDS encephalitis are conflicting. These discrepancies could be explained by several factors. Envelope glycoprotein Gp 120, when free, induces the formation of giant cells through the fusion of cerebral monocytes. The concentration of this protein depends on the level of its production, function of the quantity and of the maturation of the HIV, and on the rapidity of its catabolism, due to anti-Gp 120 antibodies. On the other hand, the tropism of the virus for monocytes and lymphocytes could vary; this would lead to the formation of giant cells with a different life span. The fusion capability of HIV-2 might be lower on account of the smaller size of its Gp 120. The frequency of mutations in HIV lentivirus leading to the synchronous development of several different clones of HIV-1 in the same patient and the associated infectious diseases, due to risk factors common to the diseased population, current endemic or opportunistic agents, could explain the variability of the density of giant cells according to the country where the patients live.
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PMID:[Hypothesis: multinucleated giant cells in AIDS neuropathology]. 255 73

The containment of Toxoplasma gondii infection is largely dependent of T cell mediated immunity. In this study, in vitro lymphocyte responsiveness to T. gondii antigen was examined in 59 HIV1 infected individuals and in 58 HIV non-infected controls. Of the 45 patients with serological evidence of past Toxoplasma infection, a significant proliferative response was found in only 18, whereas responses were present in 48 out of 51 controls with anti-Toxoplasma antibodies. In the 27 non-responder patients, the lack of proliferative response to T. gondii antigen was correlated with the loss of CD4+ cells, and the impairment of proliferative responses to other microbial antigens, whereas responsiveness to phytohaemagglutinin and concanavalin A were not significantly diminished. Results are consistent with impairment of cell mediated immunity to T. gondii in patients at risk for reactivation of chronic Toxoplasma infection. Of note, in the one year clinical following, 2 of the 27 non-responder patients developed toxoplasmic encephalitis compared to 0 of 18 with a Toxoplasma specific proliferative response.
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PMID:Impaired in vitro lymphocyte response to toxoplasma antigen in HIV1 infected patients. 262 79

Neurological manifestations of unknown cause occurring in patients who become or are HIV antibody positive with presumed normal immune function have been described recently. This report adds a further six cases, all of whom had normal CD4+ cell counts either throughout the period of observation or after the episode of seroconversion. Three had an acute presentation, two in the context of documented seroconversion consisting of one of the following: an encephalitis, an ataxia, and confusion with neuralgic amyotrophy. Three had a subacute disorder occurring at a later phase of HIV infection but before opportunistic infections or neoplasms, and marked by a static mild cognitive deficit. This report extends the range of abnormalities that may be seen at seroconversion and documents the presence of a non-progressive cognitive deficit occurring in the latent phase of HIV infection.
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PMID:The neurological features of early and 'latent' human immunodeficiency virus infection. 222 59

Neuropathology of acquired immunodeficiency syndrome. The Central Nervous System (CNS) has been examined at autopsy in 60 patients who died of AIDS in a 6-year period in our hospital. Most of the patients were intravenous drug abusers, the mean age was of 34 years, with a high prevalence of males. Neurologic symptoms were present in 62% of patients, while histologic lesions have been observed in 51 cases (85%). Opportunistic infections were found in 27 patients, the commonest being T. gondii (12) and Cytomegalovirus (7); Progressive Multifocal Leukoencephalopathy was observed in 2 cases. HIV-associated lesions included 21 cases of Multifocal Giant Cell Encephalitis (MGCE), 15 of Progressive Diffuse Leukoencephalopathy (PDL) and 7 cases of Vacuolar Myelopathy. Primary CNS lymphoma was noted in 8 patients and secondary deposits were observed in 3 cases. Simultaneous CNS lesions by more than one pathogen were frequently encountered. The main pathogenetic mechanisms for characterization of all the lesions and their relationship with clinical features of the disease are discussed. It is supposed that MGCE and PDL represent two different patterns of HIV-encephalopathy.
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PMID:[Neuropathology of the acquired immunodeficiency syndrome]. 264 Nov 50

Acquired immunodeficiency syndrome (AIDS), first described in 1981, is produced by infection with a retrovirus of the lentivirus family, now called human immunodeficiency virus (HIV). While, initially, the disease was almost exclusively seen in homosexual men, it has become apparent that numerous other categories of people are at risk, i.e., drug addicts who share dirty needles, hemophiliacs and haitians. In addition, epidemiological data from the industrialized nations clearly indicate that heterosexual contact is becoming an important source of viral transmission, as it has been known to occur in several african nations for many years. Initially, studies on patients with AIDS mainly focused on the immunosuppressive effects of the virus and on the various opportunistic infections and neoplastic complications that followed. Not much attention was given to a possible direct HIV infection of the nervous system. Consequently, patients who presented with neurological findings were simply considered to harbor in the CNS the same complications that occurred in other organs. While this was true in many cases, it has become also apparent that important changes in the central and peripheral nervous systems are due to direct viral involvement of these tissues. The first important step in the understanding of nervous system involvement in AIDS was the demonstration, in 1985, of HIV in the CSF and cerebral tissues of patients with neurological symptoms (47). Further studies have shown that, while opportunistic infections and neoplastic complications certainly contribute to the neurological morbidity of AIDS, the most important neuropathological changes, particularly in the brain, are due to direct HIV infection. The aim of this paper is to review the pathology of HIV-induced encephalitis and to discuss pathogenetic hypotheses regarding mechanisms of HIV-mediated tissue injury and the clinical manifestations that follow, particularly the syndrome now known as AIDS-Dementia-Complex (ADC). First, however, it may be appropriate to quickly review some basic notions on the biology of the virus.
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PMID:AIDS-dementia-complex: pathology, pathogenesis and future directions. 267 Aug 16

Central nervous system (CNS) involvement is very frequently observed in pediatric AIDS. Clinical manifestations include encephalopathy, cognitive deficits, acquired microcephaly, neurological signs, myelopathy, and peripheral neuropathy. Neurological complications can be related to opportunistic viral infections such as encephalitis, atypical aseptic meningitis, progressive multifocal leukoencephalopathy, and myelitis. Nonviral syndromes include: toxoplasmosis, cryptococcal meningitis, candidiasis, Mycobacterium tuberculosis meningitis, and Mycobacterium avium subacute encephalitis. Bacterial infections, tumors, cerebrovascular complications, and peripheral neuropathies are not frequently observed in pediatric AIDS. The most severe complications of HIV infection is encephalopathy resulting from HIV infection of brain tissue. Direct HIV invasion of the CNS has been demonstrated. Clinical features of HIV encephalopathy are classified into three categories: (1) normal neurological findings; (2) static encephalopathy; and (3) progressive encephalopathy. AIDS dementia complex can be differentiated from the predominance of behavioral and cognitive disabilities.
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PMID:Acquired immune deficiency syndrome in childhood. Neurological aspects. 268 79

The neuropathologic findings of brains and spinal cords removed at autopsy from 26 infants and children with AIDS is described; in two cases, only the spinal cords were available. The most common finding in the brains was dystrophic calcification of blood vessels of all calibers in the basal ganglia and deep cerebral white matter (21 og 24 cases). The next most frequent finding was subacute encephalitis (SE) (15 of 24 cases) with microglial nodules and multinulceated giant cells. Immunocytochemical and in situ hybridization studies showed HIV antigen or genetic sequences only in the brains of cases with SE. Multinucleated giants cells (MGC) were the most frequent cells with reaction products. MGC were labeled with ricinus lectin (RCA), but not with leukocyte common antigen (LCA) or glial fibrillary acidic protein. Many cells in microglial nodules were labeled with RCA, but not LCA; cells in the perivascular compartment were labeled with LCA, but not RCA. Corticospinal tract degeneration was noted in 15 of 20 spinal cords. In six cases tract degeneration was consistent with delayed myelination, and the remaining cases had axonal injury consistent with Wallerian degeneration. Opportunistic infections were rare (three cases). Central nervous system lymphoma occurred in three children and was the most common mass lesion. In two cases lymphoma occurred in the setting of a systemic polyclonal immunoproliferation possibly related to Epstein-Barr virus infection. Cerebrovascular accidents were noted in seven cases. Two cases had hemorrhage associated with immune thrombocytopenia; one hemorrhage was catastrophic. Two children had large vessel arteriopathy with multiple encephalomalacias. Two children had a necrotizing encephalopathy with encephalomalacia and vascular changes suggestive of a mitochondrial cytopathy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Central nervous system pathology in pediatric AIDS: an autopsy study. 273 40

Cerebrospinal fluid (CSP) glucose values were measured in 37 HIV-positive patients with neurologic symptoms and in 35 HIV-negative controls affected by bacterial or viral meningo-encephalitis (ME). Low CSF glucose values were found more frequently in HIV+ patients (49% of cases) than in ME patients (14%). CSF/serum ratios for glucose were also significantly lower in HIV +. Mean serum glucose did not differ between the two groups. Since HIV is a strongly neurotropic and infects early the endothelial cells of the brain capillaris, where glucose is actively carried from plasma to CSP, it is hypothesized that low CSF glucose in HIV-infected patients with neurological symptoms might be an early sign of CNS invasion by the virus.
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PMID:[Hypoglycorrhachia as an early sign of central nervous system infection caused by HIV]. 273 28

A 22-year-old Haitian man had a 15-month course of progressive meningitis accompanied by multiple cerebral infarcts. Multiple areas of stenosis and occlusion in all branches of the circle of Willis, and hypertrophy of collateral perforating vessels at the base of the brain in a "puff of smoke" appearance typical of moyamoya disease were seen on cerebral angiogram 5 months before the patient died. At autopsy, the patient had meningovascular syphilis and a necrotizing encephalitis with massive treponemal invasion of the brain, the pathology of late-stage degenerative, "quaternary", neurosyphilis. The patient was also infected with human immunodeficiency virus (HIV). Retrovirus-like particles 100 nm in diameter with dense cores were seen by electron microscopy. Nucleic acid obtained from the patient's brain contained sequences homologous to HIV DNA as determined by dot blot hybridization. The moyamoya-like radiologic appearance of neurosyphilis has not been previously described. The autopsy finding of quaternary neurosyphilis in a patient with HIV infection supports the hypothesis that retrovirus may alter the natural history of syphilitic infection.
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PMID:Quaternary neurosyphilis in a Haitian man with human immunodeficiency virus infection. 274 54


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