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

Neurological disease occurs frequently in patients infected with the human immunodeficiency virus. Disorders may affect either the central or peripheral nervous systems and may be the presenting manifestation of human immunodeficiency virus-related disease. Opportunistic infections and lymphomas are major causes of central nervous system disease. Increasingly, however, human immunodeficiency virus infection of the central nervous system is being recognized and is now associated with a syndrome of progressive dementia in adults, referred to as the acquired immunodeficiency syndrome dementia complex, and an encephalopathy in infants born to human immunodeficiency virus-infected mothers. Whether brain disease related to this virus will respond to antiretroviral drugs will be a major focus of future research. Although less frequent than central nervous system disease, disorders of the peripheral nervous system are increasingly being recognized, including cases that probably have an autoimmune basis.
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PMID:AIDS and neurological disorders: an overview. 283 2

Human immunodeficiency virus antigen (HIV-Ag) was detected in the serum of most adult (13/16) and paediatric (6/6) AIDS patients and rarely in the serum of symptomless seropositive controls (1/13). It was present in the cerebrospinal fluid (CSF) of all 5 children and most (5/9) adults with AIDS-related encephalopathy, but not in the CSF of 13 symptomless seropositive controls, of whom 8 had antibody in the CSF. A longitudinal study of 1 of the controls with antibody in the CSF showed that HIV-Ag in CSF was present transiently before the occurrence of antibody in the CSF. In serial samples of serum from 35 men who seroconverted HIV-Ag was detected in 11 persons--in 5 before seroconversion and in 6 after. 3 of the 6 who became antigenaemic after seroconversion remained so for the rest of the follow-up. AIDS was diagnosed in 1 patient, 3 months after HIV-Ag was first detected in serum and 6 months after seroconversion. The findings suggest that HIV-Ag appears early and transiently in primary HIV infection. Antibody production follows, after which HIV-Ag may disappear. Its persistence or reappearance seems to correlate with clinical, immunological, and neurological deterioration.
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PMID:Expression of human immunodeficiency virus antigen (HIV-Ag) in serum and cerebrospinal fluid during acute and chronic infection. 287 36

Human immunodeficiency virus type-1 (HIV-1) antigen was assayed in paired serum/cerebrospinal fluid (CSF) specimen from 85 adults and 58 children with acquired immunodeficiency syndrome and was compared with clinical neurological status. A quantitative comparison of HIV-1 antigen levels in matched serum and CSF specimens indicated that HIV-1 antigen expression in these compartments is independent and is correlated with acquired immunodeficiency syndrome dementia complex in adults and progressive encephalopathy in children. In a longitudinal study (n = 47), 16 patients tested positive for HIV-1 antigen in the CSF before (n = 2) or coincident (n = 14) with neurological deterioration. Six patients who tested positive for HIV-1 antigen in the CSF remained neurologically normal for a median duration of follow-up of 11 months. Six of 25 patients who tested negative for HIV-1 antigen in the CSF, subsequently showed neurological deterioration. These data indicate that HIV-1 antigen expression in the CSF is not useful in predicting neurological deterioration.
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PMID:Human immunodeficiency virus type 1 antigen in cerebrospinal fluid. Correlation with clinical neurologic status. 291 78

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

HIV infection of the newborn is now known to result mostly from mother-to-foetus transmission. The risk of transmission is at least 40 p. 100. However, the circumstances of passage are little known, and there is no maternal virological parameter capable of evaluating individual risks. The disease is more severe in children than in adults. Rare are the children who remain asymptomatic for more than 15 months; one out of three of them develop severe acquired immunodeficiency syndrome and die within the first 2 or 3 years of life. A specific encephalopathy is observed in about 30 p. 100 of the infected children. Kaposi's sarcoma is exceptional. Since there is no contagion between children, those who are in fairly good clinical condition should have a family and school life as normal as possible.
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PMID:[Infection of the newborn infant by the human immunodeficiency virus]. 296 60

This paper describes the few case reports of neurological effects of acute (primary) HIV infection. Following a typical primary illness (fever, sore throat, headache, rash, lymphadenopathy, superficial oral ulcers, conjunctivitis, leukopenia and thrombocytopenia) aseptic meningitis, myelopathy, spinal myoclonus, peripheral or cranial neuropathy, neuralgia and ganglioneuronitis may occur, usually within 3 weeks. Encephalopathy with spontaneous recovery also occurs, usually without other features of acute HIV infection. Diagnosis depends on demonstration of seroconversion which may be delayed by weeks. No therapy is yet available.
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PMID:The neurological features of acute HIV infection. 304 55

The HIV epidemic probably arose in Africa at about the same time as in the West, and there is a significant seroprevalence of HIV in the central African region. However, the epidemiology and clinical course of AIDS are different in Africa and in the West. In Africa males are infected as often as females, and the commonest means of transmission is heterosexual intercourse. Many HIV-infected people are symptomless, but many others present with or progress to generalized lymphadenopathy, pruritus, herpes zoster, herpes simplex, cellulitis, and oral candidiasis. The World Health Organization developed a clinical case-definition of AIDS in Africa, which was found to have a specificity of 90% and a sensitivity of 59% when tested in Zaire. The Kaposi's sarcoma seen in African AIDS patients is more aggressive than that seen in the West and is often visceral. Gastrointestinal AIDS (the "slim" disease) with weight loss and diarrhea is common in Africa, as are oral and esophageal candidiasis. In Africa Pneumocystis carinii pneumonia is rare, but pulmonary tuberculosis is common. Neurological manifestations include cerebral toxoplasmosis, cytomegalovirus infection, headache, and terminal encephalopathy. About 60% of infants born to seropositive women are infected and die within the 1st year of life. Lack of drugs and diagnostic facilities make both diagnosis and treatment of opportunistic infections difficult.
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PMID:Clinical aspects of HIV infection in developing countries. 305 40

Human immunodeficiency virus type I (HIV-1) is associated with a spectrum of neurological disorders. At the time of primary HIV-1 infection, an acute aseptic meningitis or encephalitis indicates central nervous system invasion. Evidence of HIV-1 infection is found in the CSF of most asymptomatic seropositive individuals, suggesting viral persistence in the nervous system. After a long incubation period, viral activation is signaled by expression of HIV-1 antigen in the CSF, which correlates with a profound dementia in adults or with an analogous progressive encephalopathy in children. The neuropathological substrate of this dementing process consists of multinucleated giant cells and diffuse white matter pallor. Immunocytochemical and in situ hybridization studies demonstrate that antigen presenting cells, including blood derived macrophages and resident brain microglia, are directly infected by HIV-1, and participate in the formation of the syncytial giant cells. Astrocytes and endothelial cells may also be infected, but evidence for infection of oligodendroglia and neurons is lacking. Studies of lentiviral encephalitides in ungulates and non-human primates emphasize the importance of specific viral antigenic stimulation and the role of inflammatory cells as direct or indirect mediators of tissue damage. The disorders of the peripheral nervous system described in patients with HIV-1 infection have not been convincingly linked to direct viral infection. At least two of the neuromuscular complications, the inflammatory motor neuropathy and polymyositis are likely to have an autoimmune pathogenesis.
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PMID:Human immunodeficiency virus type 1 (HIV-1) infection of the nervous system: a review. 307 11

The AIDS Surveillance System in Japan was set up in 1984 and by 1987, 29 AIDS patients had been reported. 10 were homosexuals, 16 were hemophiliacs and 3 were heterosexuals. 9 out of 16 hemophiliacs with AIDS had A-type hemophilia. 2 females were also reported as victims of AIDS. 19 patients have died 5 male homosexuals (4.4%) out of 113 (93 Japanese and 20 Foreigners) individuals were anti-HIV-positive. In 1984 sera from 65 hemophiliacs, 85 hemodialysis patients and 304 healthy volunteer blood donors were examined and 10 (15.4%) of the hemophiliacs proved to be anti-HIV positive. On the other hand, in Tokyo and Nagasaki 50-60% were positive, but in Tottori and Osaka only 25-28% were positive. The enzyme-linked immunosorbent assay (ELISA) test is widely used to detect antibodies, however, the test often gives false-positive reactions, and the blood must be reexamined by means of the Western-blot test or IF method. Therefore, a simple particle agglutination (FA) assay was developed by the authors using gelatin beads as the artificial antigen carrier. This assay is extremely sensitive as compared to IF and ELISA. Among HTLV-1/ATLV-carrying T-cell lines, all except one (TCL-As) were susceptible to HIV infection and showed cytopathic effect (CPE). HIV has quite a broad host range in vivo and in vitro. HIV was detected in brain macrophages from AIDS patients with encephalopathy. HIV may also infect nerve cells or glial cells. The MT-4 cell line was found to be most prone to HIV infection. In order to evaluate the virus-induced CPE of infected MT-4 cells, the H-thymidine incorporation method (cell proliferation assay) was developed that involved that involves measuring the survival of the cells. Inhibition of DNA synthesis in infected MT-4 cells was detected by this assay when the CPE was observed microscopically. This assay system is also useful for measuring the amount of infectious virus. Many chemicophysical agents such as suramin, antimoniotungstate (HFA-23), phosophonoformic acid, ribavirin, 3-azido-3-deoxythymidine (AZT) have suppressive effects on the replication of HIV in vitro. Glycyrrhizin administration was responsible 1 or improvement of immune function in 6 of 7 asymptomatic HIV carriers. Prostaglandin E2 (PGE2) and 12-0-tetradecanoylphorbol-13- acetate (TPA) were found to enhance the production of HIV significantly in infected MT-4 cells. The cell proliferation assay is used for the mass screening of neutralizing antibodies whose presence in the sera from 21 patients with AIDS, 10 individuals with ARC, 20 healthy male homosexuals and 10 healthy males was examined. The assay was sensitive enough to detect neutralizing antibodies up to a dilution of 1:10 thousand. The system using MT-4 cells seems to be suited for this purpose.
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PMID:AIDS studies in Japan. 311 53

Adherent human embryo brain cells have been infected with HIV. Cells replicating HIV were maintained in culture for seven sequential passes over 7 months and continued to produce HIV during that time. Human embryo brain cells displayed glial-cell morphology and expressed glial fibrillary acidic protein. Electron microscopy showed clusters of virus particles around these cells as well as budding virus. Extracted, infected glial cells revealed bands for three major gag proteins, p18, p24 and p55, in Western blotting. It was not possible to detect CD4 antigen on the surface of these cells by indirect immunofluorescence or alkaline phosphatase staining with CD4 monoclonal antibodies. The results of these experiments indicate that HIV replicates in non-malignant brain cells. This observation strengthens the postulated aetiological link between HIV and the encephalopathy, dementia and other neurological symptoms observed in HIV-infected patients.
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PMID:HIV replicates in cultured human brain cells. 312 70


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