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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Approximately half of patients with advanced acquired immune deficiency syndrome (AIDS) develop a subcortical dementia. The brains of all autopsies on AIDS patients performed at UCSD between 1982 and 1986 (N = 93) were studied. Neuropathologic changes consistent with a viral encephalitis were present in 54 brains (58%). Human immunodeficiency virus (HIV) antigens were detected in 37 of the brains (40%), most frequently in macrophages, multinucleated giant cells, and endothelial cells. Cytomegalovirus (CMV) was detected in 31 of the brains (33%), 22 of which also contained HIV. Cellular localization of CMV antigens suggests that CMV disseminates to the central nervous system hematogenously where the virus can infect endothelial cells, glia, and neurons. While the temporal course of the appearance of these two viruses within the CNS is not clear, the common simultaneous occurrence of both viruses within the brains of AIDS patients suggests that in vivo interaction between them may play a role in the pathogenesis of AIDS-associated encephalitis. Given the significant neurologic symptoms described in AIDS patients, the paucity of viral antigens suggests a pathogenic mechanism of indirect CNS damage rather than direct viral infection.
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PMID:Role of human immunodeficiency virus and cytomegalovirus in AIDS encephalitis. 284 92

A variety of diseases of the central and peripheral nervous systems evolves during the course of human immunodeficiency virus (HIV) infections. Most are not related to documented opportunistic infections and may be the direct result of HIV infections, as large proportions of healthy and ill HIV-infected persons show evidence of nervous system infection. These diseases occur at different times during the infection and have diverse inflammatory, demyelinating, or degenerative pathological features that suggest different pathogenetic mechanisms. The route and determinants of HIV invasion of the nervous system are unknown. Within the brain, viral antigen and RNA are found predominantly in macrophages, but the reason why profound dementia and cortical atrophy result from this infection remains a mystery. By analogy to other lentivirus infections, particularly visna virus in sheep, neuropathological changes may be mediated by cytokines. Other possible pathogenetic mechanisms include toxicity of viral polypeptides, transactivation of viral or cellular genes, autoimmunity, or other opportunistic infections. Clarification of the pathogenesis of HIV-related diseases is critical to the design of rational therapies.
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PMID:The neurobiology of human immunodeficiency virus infections. 284 95

Clinical neurological involvement at various times throughout the illness was recorded in 52% of 122 patients seen in central London who died from acquired immunodeficiency syndrome (AIDS). Various metabolic encephalopathies, dementias, focal encephalopathies, retinopathies and peripheral nerve pathology were the most frequent manifestations. Seven of 9 patients with a neurological presentation had no other major systemic illness. The median time from diagnosis of AIDS to death was 9 months and from onset of neurological symptoms to death 4 months. Human immunodeficiency virus dementia, central nervous system opportunistic infections, presence of Kaposi sarcoma, neurological presentations and minor symptoms were not associated with major change in survival time.
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PMID:Nature, incidence and prognosis of neurological involvement in the acquired immunodeficiency syndrome in central London. 285 52

Patients with human immunodeficiency virus (HIV) have often progressive dementia. Human T cell lymphotropic virus Type I (HTLV-I) infection has not been reported to cause dementia. We tested antibodies to HTLV-I and HIV in serum and cerebrospinal fluid in 69 Finnish patients referred because of dementia to an outpatient department of neurology. No antibodies to HTLV-I and HIV were detected in patients with the clinical diagnosis of Alzheimer's disease, vascular dementia, secondary dementia due to a specific cause, or in cases of atypical dementia.
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PMID:No antibodies to HTLV-I and HIV in patients with dementia in Finland. 289 Feb 55

The Centers for Disease Control (CDC) revised the surveillance case definition for Acquired immunodeficiency syndrome (AIDS) in August, 1987. To determine the impact of this revision, information was extracted from the medical charts of the 630 patients receiving comprehensive medical care as of 1980 at 6 hemophilia treatment centers, and who were therefore likely to have been infected with human immunodeficiency virus (HIV). 38 (6%) and 47 (7%) met the 1985 and 1987 case definitions, respectively (22% increase). Of the cases added by use of the 1987 case definition, 3 patients had HIV dementia, 3 had Pneumocystis carinii pneumonia (2 of whom were presumptively diagnosed and 1 who had been receiving steroids and immunosuppressives), and 3 had HIV wasting syndrome. These data suggest that the revision of the AIDS case definition will have a substantial impact on future AIDS surveillance trends in persons with hemophilia and perhaps in other risk groups.
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PMID:Potential effect of revising the CDC surveillance case definition for AIDS. 289 28

We identified 13 patients who contracted acquired immunodeficiency syndrome or human immunodeficiency virus-related disease after a cardiothoracic operation. The operations were performed between January 1981 and November 1984, and the diagnosis of human immunodeficiency virus-related disease was established from 26 to 54 months after operation. The survival time from diagnosis ranged from 8 days to 14 months in the 10 patients who have died. A clinical illness developed in three of the patients immediately postoperatively that was consistent with primary human immunodeficiency virus mononucleosis. The clinical features included a wide variety of opportunistic infections, but an abnormally high percentage of the patients first showed symptoms of dementia or neoplastic disease. In many patients, the diagnosis was not suspected for a prolonged period of time. On the basis of the prolonged incubation period, the incidence of this disease is likely to increase for several more years.
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PMID:Acquired immunodeficiency syndrome, a complication of cardiothoracic surgery. 291 Nov 89

Dementia is common in patients with AIDS, but the mechanism by which the human immunodeficiency virus type 1 (HIV-1) causes the neurological impairment is unknown. In this study the possibility that an antigen of HIV-1 suppresses neuronal responses to neurotrophic factors was examined. Both HIV-1 and a related retrovirus, simian immunodeficiency virus (SIV), inhibited the growth of sensory neurons from chick dorsal root ganglia in medium containing neuroleukin (NLK) but not in medium containing nerve growth factor. An unrelated type D retrovirus, simian acquired immunodeficiency syndrome virus, did not affect the growth of neurons in the presence of either neurotrophic factor. The inhibition by HIV-1 of neuron growth in the presence of NLK was found to be due to the gp120 envelope glycoprotein. Regions of sequence homology between gp120 and NLK may account for this inhibitory property of gp120 and functional interactions between gp120 and NLK may be important in the pathogenesis of the AIDS dementia complex.
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PMID:Functional interaction and partial homology between human immunodeficiency virus and neuroleukin. 303 62

Fourteen patients with AIDS were treated for 23 neurologic complications: four episodes of acute meningoencephalitis; eight episodes of subacute encephalopathy; two cases of progressive multifocal leukoencephalopathy; and nine cases of polyneuropathy. Nine patients were treated with 9-(1,3-dihydroxy-2-propoxymethyl)guanine (DHPG), one with 3'-azido-3'-deoxythymidine (AZT), and four initially with DHPG directed against cytomegalovirus (CMV) retinitis or encephalitis and subsequently with AZT against human immunodeficiency virus (HIV) encephalopathy. CMV retinitis was a helpful clinical observation indicating neurologic involvement. DHPG produced improvement in two of three cases of acute meningoencephalitis but was ineffective in cases of subacute encephalopathy or neuropathy. AZT therapy resulted in resolution in both of the two treated cases of acute confusional state and in two of the four treated cases of polyradiculoneuropathy with paraparesis but was ineffective in the late stage of subacute encephalopathy. These results suggest that CMV is important in some cases of acute meningoencephalitis, whereas HIV is a dominant pathogen in subacute dementia and polyneuropathy in patients with AIDS. DHPG may be beneficial in the former, whereas AZT appears to be effective in the latter complications.
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PMID:Responses of neurologic complications of AIDS to 3'-azido-3'-deoxythymidine and 9-(1,3-dihydroxy-2-propoxymethyl) guanine. I. Clinical features. 316 17

HIV disease often leads to neuropsychiatric disturbance, either through direct infection of the brain by the virus or through CNS disease secondary to immunodeficiency. Neuropsychiatric complications of AIDS and AIDS-related disorders may present clinically as acute or chronic organic mental syndromes, or may mimic functional psychiatric illness, in particular depression, anxiety, or psychotic states. Two cases of hypomanic states in homosexual men suffering from AIDS are reported. Neither of the two men had a personal or family history of affective disorder. In one man, hypomanic symptoms were caused by early HIV encephalopathy; he rapidly developed typical HIV dementia with a marked downhill course. In the second case, a clear connection between the hypomanic symptoms and direct HIV brain involvement was not established.
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PMID:Two cases of hypomania in AIDS. 316 73


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