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

This report describes the neurologic manifestations of 36 children with human immunodeficiency virus (HIV) infection. In this cohort, in 16 of 21 children with acquired immunodeficiency syndrome (AIDS), three of 12 children with AIDS-related complex, and one of three asymptomatic seropositive children, a progressive encephalopathy developed. Neurologic signs were often detected early but tended to worsen coincident with progression of the immunodeficiency. The presence of progressive encephalopathy correlated with the absence of serum neutralizing antibodies to HIV and with a poor, usually fatal, outcome. The incubation period from initial HIV infection in the perinatal period to the onset of progressive encephalopathy varied from 2 months to 5 years. Intrablood-brain barrier synthesis of HIV-specific antibodies was demonstrated in eight of 14 children with AIDS and AIDS-related complex, indicating active brain infection with HIV. In three cases this was unassociated with progressive neurologic signs. Unique neuropathologic findings in children who died with HIV infection further suggest that the progressive encephalopathy is the result of primary and persistent infection of the brain with this retrovirus. These findings broaden the spectrum of HIV infection in children and have important implications for the development of antiviral therapy.
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PMID:Neurologic manifestations of human immunodeficiency virus infection in children. 242 48

The immunohistochemical reactivity of four monoclonal antibodies (MAbs): CVK, 49-5, 49-6 and 63-FH2, raised against the p18 protein of HIV-1 was assessed in tissues obtained from HIV-infected and uninfected individuals. As already reported, all the MAbs specifically labelled follicular dendritic cells (FDC) in lymph nodes from HIV-infected patients with lymphadenopathy, and cells of microglial nodules in the brain from patients with AIDS-related encephalopathy. However, cross-reactivity with normal uninfected tissues was also observed: epithelial cells of the skin, the thymus and tonsils with CVK, and astrocytes in the brain of 49-6 and 63-FH2. Such cross-reactivities suggest that 'molecular mimicry' could exist between p18 of HIV and normal constituents of human cells. This phenomenon could be relevant for the diagnostic use of anti-p18 MAbs on pathological specimens, and it could be of importance in the pathophysiology of HIV infection.
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PMID:Monoclonal antibodies to the human immunodeficiency virus p18 protein cross-react with normal human tissues. 245 86

Severe thrombocytopenia has been diagnosed in HIV seropositive patients independently of the clinical stage of disease. In view of its immunologic origin, attempts have been made to treat this condition with drugs which have proved effective in the treatment of autoimmune thrombocytopenia, though with little or no beneficial effect to these patients. This communication deals with the observation (5-22 months) of 5 HIV seropositive patients with severe thrombocytopenia who were resistant to steroids, high dose i.v. immunoglobulin and Danazol. They all responded well to splenectomy, with only one patient relapsing after 4 months. However, 2 patients showed deterioration of the immunodeficient state: in one patient the number of CD4 lymphocytes decreased and the other died of multifocal leuko-encephalopathy 4 months after splenectomy. Based on this small series, splenectomy seems to be effective in the treatment of thrombocytopenic HIV seropositive patients. However, long-term hazards still have to be assessed.
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PMID:[Thrombocytopenia and HIV: the role of splenectomy]. 246 72

The natural course of HIV infection in 205 intravenous drug users (IVDU) presenting at 11 centers in Italy was followed since 1983. Criteria for entering the study were spontaneous attendance at the clinic from January 1983-April 1988; history of IVDU; dated negative HIV test and a positive test not over 18 months later. 13 of the 205 subjects developed AIDS by 30 April 1988, a total of 447.25 person-years, for an overall incidence of AIDS of 2.9% person-years. The clinical presentation was opportunistic infections in 7, wasting syndrome in 5, and encephalopathy in 1. No Kaposi's sarcoma was seen. The incidence of AIDS was 1.5% in the 1st year; 2.9% after 2 years; 9.9% after 3 years and 17.9% after 42-48 months. The risk of AIDS increased significantly 24 months after seroconversion. 11 others developed AIDS-related complex (ARC) in the 4-year period, an incidence of 3.4% person-years. The minor opportunistic infections seen were zona (4 cases), oral candidiasis (2), and hairy leukoplakia (1). 2 subjects had myelopathy. 87 others developed persistent generalized lymphadenopathy (PGL). 45.8% of the group remained asymptomatic. The subjects mean age was 26, and the sex ratio was 4:1 overall, but 12:1 among the AIDS group. The natural history of AIDS in this series closely resembled other reports on male homosexuals.
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PMID:The natural history of HIV infection in intravenous drug users: risk of disease progression in a cohort of seroconverters. 249 24

Brains of AIDS patients do often display characters of HIV specificity, in the presence or not of opportunistic lesions. Mesodermal nodules with giant cells, and a peculiar primary demyelination, the progressive diffuse leukoencephalopathy of Kleihues et al., which can be found only in brains with giant cells, have been pointed out as typical. In 100 intra venous drug user patients, younger than 32 years (mean age: 26) the HIV specificity described was observed on 49 occasions. All these patients presented with Seitelberger's glio-neuronal poliodystrophy (GP), quite similar to that encountered in several kinds of encephalopathies. Nevertheless, in 35 of the patients with HIV typical findings, there was in the cortex and some other grey matter regions, an amount of diffuse mesodermal elements uncommon in encephalopathies, and so relevant as to contradict the notion itself of this kind of cerebral lesion, where "inflammatory" events ought not to appear. This aspect of HIV encephalopathy was indicated by us as "GP plus". An optic microscopy examination of the cortex allowed us to establish how in GP plus the neuronal changes are more severe and apparently older than in the other patients considered. The fact that the astrocytes did not behave differently in the two aspects of encephalopathy lead us to conclude that GP plus sets in through processes distinct from those in encephalopathy tout-court, and to put forward that it is a further character of HIV specificity.
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PMID:[Cerebral cortex and HIV lesion specificity. A neuropathological study of the brain of 100 drug addicts]. 253 92

Neuropathological changes were studied in a consecutive autopsy series of 135 cases, comprising 73% of all patients who died of AIDS in Switzerland between April 1981 and December 1987. Central nervous system involvement was found in 119 patients (88%), 19 of which had multiple concomitant intracerebral lesions. Among the non-viral opportunistic infections, encephalitis due to Toxoplasma gondii was most frequent and occurred in 35 patients (26%), followed by central nervous system infection with Cryptococcus neoformans, which was found in five patients (4%). Cytomegalovirus (CMV) encephalitis was present in 14 patients (10%). Disseminated microglial nodules without morphological or immunocytochemical evidence of CMV was encountered in 18 patients (13%). However, in all but two of these patients there was evidence of extracerebral CMV infection, suggesting that CMV was responsible for these nodular encephalitides. Nine patients (7%) had progressive multifocal leukoencephalopathy (PML); in five of these, demyelination was associated with extensive tissue destruction and cyst formation. HIV-associated encephalopathy was observed in 21 patients (16%) and showed two characteristic morphological patterns: progressive diffuse leukoencephalopathy (PDL) and multifocal giant cell encephalitis (MGCE). PDL was observed in 13 cases and characterized by diffuse pallor and gliosis of the cerebral and cerebellar white matter with scattered multinucleated giant cells, but without significant inflammatory response. MGCE was found in eight patients and characterized by clusters of numerous multinucleated giant cells, rod cells, macrophages, lymphocytic infiltrates and occasional necroses. In our view, PDL and MGCE represent the two opposite variants of HIV-induced encephalopathies, with overlapping intermediate manifestations.
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PMID:Neuropathology of the acquired immune deficiency syndrome (AIDS): a report of 135 consecutive autopsy cases from Switzerland. 254 Jun 10

Animal models of AIDS are essential for understanding the pathogenesis of retrovirus-induced immune deficiency and encephalopathy and for development and testing of new therapies and vaccines. AIDS and related disorders are etiologically linked to members of the lentivirus subfamily of retroviruses; these lymphocytopathic lentiviruses are designated human immuno-deficiency virus type 1 (HIV-1) and human immuno-deficiency virus type 2 (HIV-2). The only animals susceptible to experimental HIV-1 infection are the chimpanzee, gibbon ape, and rabbit but AIDS-like disease has not yet been reported in these species. Macaques can be persistently infected with some strains of HIV-2 but no AIDS-like disease has resulted. It is not yet clear how suitable HIV-infected SCID-hu mice will be as a model for AIDS. Several subfamilies of naturally occurring cytopathic retroviruses cause immune suppression, including fatal immunodeficiency syndromes in chickens, mice, cats, and monkeys. Domestic cats suffer immunosuppression from both an onco-virus, feline leukemia virus, and a member of the lentivirus subfamily, feline immunodeficiency virus (FIV). Asian macaques are susceptible to fatal simian AIDS from a type D retrovirus, indigenous in macaques, and from a lentivirus, simian immunodeficiency virus (SIV), which is indigenous to healthy African monkeys. SIV is the animal lentivirus most closely related to HIV. Of these animal models, the lentivirus infections of cats (FIV) and macaques (SIV) appear to bear the closest similarity in their pathogenesis to HIV infection and AIDS. This review will summarize these various animal model systems for AIDS and illustrate their usefulness for antiviral therapy and vaccinology.
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PMID:Animal models of AIDS. 255 12

We describe our experience at Jackson Memorial Hospital in Miami, Florida, with 172 children who were given diagnoses of perinatally acquired infection with human immunodeficiency virus type 1 (HIV-1). The 146 mothers of the children acquired HIV-1 through heterosexual contact (69 percent), intravenous drug use (30 percent), or blood transfusion (1 percent). The children presented with symptomatic disease at a median age of eight months; only 21 percent presented after the age of two years. The most common first manifestations of disease were lymphoid interstitial pneumonia (in 17 percent), encephalopathy (in 12 percent), recurrent bacterial infections (in 10 percent), and candida esophagitis (in 8 percent), for which the median survival times from diagnosis were 72, 11, 50, and 12 months, respectively. Nine percent of the children had Pneumocystis carinii pneumonia at a median age of five months and had a median survival of only one month. The median survival for all 172 children was 38 months from the time of diagnosis. Mortality was highest in the first year of life (17 percent), and by proportional-hazard analysis the probability of long-term survival is low. In multivariate analyses, early age at diagnosis and the first identifiable pattern of clinical disease were found to be independently related to survival. We conclude that children with perinatally acquired HIV-1 infection have a very poor prognosis and that most become symptomatic before one year of age. Early diagnosis is important, since there is only a short interval in which to initiate prophylactic or antiviral treatment before progressive disease begins.
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PMID:Survival in children with perinatally acquired human immunodeficiency virus type 1 infection. 259 38

Patients treated with chronic dialysis have a high risk of acquiring viral infections and blood transfusions are commonly considered to be the vehicle of transmission. In Brazil this source is implicated in infection of 15 percent of patients developing acquired immunodeficiency syndrome (AIDS). So, we evaluated the relative risk of our patients in dialysis becoming infected with human immunodeficiency virus (HIV), the virus associated with the AIDS. An enzyme immunoassay showed 6 of 104 patients on dialysis to have antibodies to HIV. In five infection with HIV was confirmed by Western blot tests. Investigation of other risk factors for AIDS showed that blood transfusion was the most likely cause of contamination. There was no correlation between HIV and HBV infections. Only one patient had leucopenia and low OKT4/T8 ratio and she died 90 days after sorologic diagnosis of HIV infection; the cause of death was encephalopathy and sepsis. Two patients died after 4 and 16 months victims of cardiocirculatory problems (non-AIDS related causes). Three patients remain asymptomatic on chronic hemodialysis 20, 36 and 37 months after diagnosis of HIV infection.
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PMID:[Prevalence of anti-HIV antibodies in dialysis patients]. 261 90

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


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