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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study analyzes the correlation of basic laboratory test results with clinical outcome in 94 children with perinatally acquired human immunodeficiency virus 1 infection who did not receive zidovudine during the study period of 1983 to 1988. Two life-threatening conditions highly correlated with survival, opportunistic infection and severe encephalopathy, were the end points of the study. At a median age of 25 months 30 (32%) of the 94 children had developed such conditions (Group I), and their survival at 3 years of age was 48% (95% confidence interval, 24 to 72%), contrasting with the 97% survival rate (95% confidence interval, 94 to 100%) of the remaining 64 (68%) children who had not developed such conditions by age 25 months. (Group II). Compared with children in Group II, children with life-threatening complications were more likely at the onset of symptoms to be younger and have a lower CD4 count, an impaired in vitro lymphocytic proliferation and a lack of p18 or p25 antibodies in the Western blot profile and, during the progression of the disease, a negative slope of the subsequent CD4 counts. These results highlight the need for an early diagnosis of the human immunodeficiency virus 1 infection in children and demonstrate that it is possible to determine the prognosis of their disease as early as in the first year of life.
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PMID:Natural history of human immunodeficiency virus type 1 infection in children: prognostic value of laboratory tests on the bimodal progression of the disease. 152 73

To better define the clinical and biological evolution of infants after vertical human immunodeficiency virus type 1 infection, we analyzed 94 consecutive infected patients followed up after their first clinical symptoms. The expression of clinical symptoms and biological abnormalities followed a bimodal distribution, some patients having an early and severe disease and the others having a slowly progressive one. One third of our patients suffered from early onset of opportunistic infection (OI). These patients had a significantly higher incidence of severe encephalopathy compared with patients without OI. The rate of survival at 3 years was 48% +/- 24%. In contrast, the patients without early OI or severe encephalopathy had a probability of survival at 3 years of 97% +/- 3%. This probability was not modified by the occurrence of bacterial infection or lymphoid interstitial pneumonitis. Lymphoid interstitial pneumonitis occurred at a mean age of 29 months, significantly later than OI or severe encephalopathy. Laboratory results at initial examination were correlated with clinical symptoms. Thus, when the number of CD4 lymphocytes was less than 500/mm3, children suffered more frequently from life-threatening symptoms (OI and severe encephalopathy): 15 of 22 vs 14 of 69. The same was true when the lymphocytes did not proliferate after antigenic stimulation, when anti-p18 and/or anti-p25 antibodies were absent in the serum, and when p24 antigen was detected in serum. Finally, severe encephalopathy was associated with low anti-human immunodeficiency virus cerebrospinal fluid antibody titer, whereas 88% of patients with moderate or no encephalopathy had signs of intrathecal anti-human immunodeficiency virus antibody synthesis. In conclusion, a subgroup of patients expressed very early signs of severe immunodeficiency and encephalopathy, whereas the majority of patients had a longer survival and less severe clinical symptoms during their first years of life than previously thought.
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PMID:Longitudinal study of 94 symptomatic infants with perinatally acquired human immunodeficiency virus infection. Evidence for a bimodal expression of clinical and biological symptoms. 166 56

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

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