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

In a neuropathological autopsy study of 21 cases of AIDS-associated PML no fundamental morphological differences to non-AIDS PML were found. PML in AIDS often showed very large foci as well as necrotizing lesions. Partial involvement of cerebral cortex and deep gray matter were common findings; infratentorial lesions could be observed in more than three quarters of cases. Perivascular mononuclear infiltrates within PML foci were frequent and obviously not associated with a more benign clinical course. Possible reasons for these peculiarities of PML in AIDS are discussed. In 7 cases evidence of concomitant HIV encephalopathy was found; this may be one relevant factor contributing to severity of PML in AIDS. PML has to be regarded as a common complication of HIV infection, which may show atypical morphological and neuroradiological features.
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PMID:Progressive multifocal leukoencephalopathy (PML) in the acquired immunodeficiency syndrome (AIDS). A neuropathological autopsy study of 21 cases. 832 44

Of the multiple causes of mental disturbance in HIV infection, it is generally safest to consider organic causes first, including opportunistic infections, tumours, medications, and HIV encephalopathy. The psychological stress of the illness will cause different or overlapping presentations that include anxiety and depression. When managing these situations, one should also pay attention to the effects of stress on the social network of the infected person.
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PMID:Mental health aspects of HIV infection. 832 10

In 10 children infected by HIV at birth, who presented early and severe immunodeficiency encephalopathy, the lesions observed in the central nervous system were different from those found in adults. Using standard neuropathological techniques, the main abnormalities were white matter palor and atrophy, pyramidal tract demyelination, moderate perivascular inflammation, numerous calcifications of blood vessels in basal ganglia, white matter and occasional in the cortex, few opportunistic infections including cytomegalovirus ventriculitis, polymorphonuclear microabcessses and aspergillus abscesses; no toxoplasma was detected. An 18-month-old girl presented with an angiocentric lymphoproliferative disorder in central and peripheral nervous system and muscle, with predominance of B cells. In most cases, low levels of HIV replication were detected in brain tissue, as demonstrated by the presence of only few microglial nodules and giant cells, feeble detection of HIV p24 and p17 antigens by immunocytochemistry, in situ hybridization of HIV DNA and RNA and polymerase chain reaction, despite severe clinical encephalopathy. Zidovudine did not improve any patient. In children with severe AIDS encephalopathy, HIV might not be directly implicated in the central nervous system lesions: an intermediate factor such as cytokines or another toxic substance secreted by activated macrophages and/or lymphocytes, could induce severe lesions in the central nervous system and minor pathology of the peripheral nervous system and muscles.
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PMID:[A neuropathological study of 10 HIV-infected children]. 833 60

The pathology of AIDS encephalopathy and its relation to other CNS infections in AIDS was studied in 112 autopsies of AIDS patients and 14 of HIV-positive patients. Special interest was focused on gliomesenchymal nodules (GMNs), a common finding in encephalitis of various etiologies, and on giant cells. GMNs and giant cells were found in 40 patients. These 40 were used for the present study, they were further divided into five groups: I. 21 with AIDS encephalopathy; II. 3 with HIV infection but no AIDS; III. 8 with Toxoplasma encephalitis; IV. 7 with cytomegalovirus encephalitis; and V. 1 with cryptococcus encephalitis. Comparison of the morphological features of GMNs between the five groups revealed parameters which may help distinguish GMNs in HIV infection from opportunistic infections. Small GMN size, low cellular density, ill-defined demarcation from the adjacent brain paraenchyma, minimal tissue rarefaction in the area of GMNs and a strong predilection for the superficial and deep white matter were typical of AIDS encephalopathy. In contrast, opportunistic infections were usually associated with clear demarcation from surrounding brain tissue, high cellular density, strong tissue rarefaction and a predilection for gray matter. Rod cells and macrophages in great numbers were also more commonly found in the AIDS and HIV groups.
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PMID:Cellular composition and distribution of gliomesenchymal nodules in the CNS of AIDS patients. 839 54

The reactivities of intrathecal and serum IgG and IgM, and IgG1-4 subclass antibodies to various HIV-1 proteins were assessed by immunoblotting at various stages of HIV-1 infection. All patients were examined neurologically including CT and/or MRI, and with HIV-1-specific and nonspecific tests of the cerebrospinal fluid (CSF). In early infection, the occurrence of anti-gag antibodies in both CSF and serum was higher than that of anti-pol antibodies among all IgG subclasses (P < 0.05). Also in late infection, anti-gag IgG1 response was most frequent (P < 0.04), while anti-gag IgG3 and IgG4 reactivities predominated over similar anti-pol antibodies (P < 0.05, respectively). Of anti-pol reactivities, in the CSF of subjects at early infection anti-p32 IgG and IgG1 antibodies were more frequent than in patients at late stages (P < 0.015). In late infection, however, the occurrence of anti-p64 IgM and IgG2-4 antibodies of both CSF and serum was higher than at early stages (P = 0.014). Regarding anti-env response, in patients with advanced infection, the CSF and serum IgG subclass reactivity against gp120 was restricted to IgG1. The CSF of individual patients with HIV encephalopathy showed a higher or similar occurrence of polyisotypic anti-gag and anti-pol IgG3 antibodies than corresponding serum. These results indicate association between declining frequency of anti-pol p32 and anti-env gp120 antibodies and severity of HIV-1 disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:HIV-1 specificity of cerebrospinal fluid and serum IgG, IgM, and IgG1-G4 antibodies in relation to clinical disease. 841 46

Survival analysis was performed for AIDS cases diagnosed in Washington state from 1982 through 1989 and reported through October 31, 1991. No difference in survival time among diagnosis years 1987, 1988, and 1989 (p = 0.29) was found. Since September 1987, survival time was longest for cases with human immunodeficiency virus (HIV) wasting syndrome and HIV encephalopathy. Adjusted risk for death was significantly lower for these cases relative to all other cases (relative risk, 0.5; 95% confidence interval, 0.4-0.6). Explanations for the absence of continuing increase in survival time between 1987 and 1989 include changes in the frequency and timing of anti-HIV therapy. Longer survival time among cases diagnosed with HIV wasting or HIV encephalopathy is likely due to diagnosis earlier in the course of HIV disease. These results emphasize how changes over time in the definition of AIDS and evolving therapeutic standards may affect assessment of survival time when using surveillance data.
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PMID:Survival after AIDS diagnosis in Washington State: trends through 1989 and effect of the case definition change of 1987. 841 Jun 72

We analyzed brain tissue from 39 patients for the presence of proviral HIV-1 sequences, using the polymerase chain reaction (PCR) for the amplification of segments of the viral LTR and gag genes. A novel primer extension procedure allowed the detection of a single HIV-1 copy in 1 micrograms DNA. We detected proviral HIV-1 DNA in 16 of 25 brain samples from AIDS patients. Semiquantitative evaluation of the amplified DNAs indicated considerable variation in viral load. Highest levels of proviral DNA were present in brain samples from six patients with clinical evidence of HIV-associated cognitive/motor complex and the histopathologic correlate of HIV leukoencephalopathy or HIV encephalitis. An additional 11 brain samples contained smaller amounts of proviral DNA. In these patients, clinical data were inconclusive regarding the diagnosis of HIV-1 encephalopathy and histopathologically there was no evidence of HIV-1-induced tissue lesions. In nine of 25 seropositive patients with AIDS (36%), brain samples scored negative or did not contain an unequivocal signal indicating the presence of proviral DNA. HIV-1 sequences were not detected in any of 14 control brain samples from HIV-1 seronegative patients. Our data indicate that HIV-1 is present in the central nervous system of the majority (two thirds) of AIDS patients and that the highest levels of proviral DNA in brain tissue are associated with HIV encephalopathy.
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PMID:PCR identification of HIV-1 DNA sequences in brain tissue of patients with AIDS encephalopathy. 841 37

HIV encephalopathy, which is probably primarily caused by human immunodeficiency virus, is the most common neurological disorder in HIV-infected patients and is more frequent than opportunistic diseases of the central nervous system. It is characterized most often by slowly progressing cognitive impairment, psychomotoric slowing and increasing apathy. The syndrome is found almost exclusively in the late stages of HIV infection; its frequency in patients with full-blown AIDS is estimated as being between 40 and 70%. Although numerous studies have demonstrated alterations in the electrophysiological parameters, cerebral perfusion and cerebrospinal fluid in many asymptomatic patients, there are no reliable parameters that can predict the risk of developing HIV encephalopathy. Also, there is no sufficient correlation between the extent of the frequent but mostly subtle neuropathological changes and the clinical degree of the severity of the encephalopathy. The mechanisms causing cerebral injury are poorly understood. Recent studies indicate that the indirect effects of HIV infection of the brain are the most important pathogenetic factors. In particular, certain viral proteins and cytokines produced by infected macrophages or activated microglia seem to induce neuronal dysfunction and finally loss of nerve cells.
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PMID:[HIV encephalopathy--clinical aspects, neuropathology and pathogenesis]. 845 Aug 99

A Japanese child case of subacute progressive encephalopathy was presented. Not only the pathological findings of HIV growth in microglias, astrocytes and macrophages in the central nervous system, but also the pathobiological findings of neuronal apoptosis were shown as etiologies of HIV encephalopathy. Epidemiology, diagnosis, prophylaxis, fetomaternal transmission and embryopathy were discussed briefly.
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PMID:[AIDS virus]. 846 Nov 64

We reviewed the course of 545 human immunodeficiency virus (HIV)-infected patients seen between 1983 and March 30, 1991. A majority were Caucasian homosexual or bisexual men, while parenteral drug abusers represented a smaller proportion than seen nationwide. In the 274 patients with the acquired immunodeficiency syndrome (AIDS), the distribution of AIDS-defining conditions was generally consistent with those reported in studies from elsewhere in the United States. However, toxoplasmosis remained relatively uncommon. There was a slightly higher incidence of disseminated histoplasmosis compared to other studies. HIV encephalopathy (AIDS dementia) was likely underdiagnosed. Although data suggested prolongation of the asymptomatic phase of HIV infection, median survival after AIDS diagnosis remained approximately 12 months.
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PMID:Clinical experience with HIV-infected patients at the University of Oklahoma Health Sciences Center: an update. 848 26


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