Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019693 (HIV)
170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cytomegalovirus polyradiculopathy, a late complication of HIV infection, is characterized by lower extremity weakness, urinary retention, and sacral dysesthesias. We describe four patients (mean CD4 T-cell count = 25 cells/mm3) who developed this "infectious cauda equina syndrome." The characteristic cerebrospinal fluid (CSF) findings, notably atypical for a viral infection, included polymorphonuclear leukocytosis (mean white blood cell count = 1512 cells/mm3, 72% polymorphonuclear leukocytes), elevated protein level (mean = 370 mg/dl), and hypoglycorrhacia (mean = 28 mg/dl). Physicians who treat patients with HIV should be familiar with this syndrome because early intervention, prior to microbiologic confirmation, provides the best hope for improving neurologic function.
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PMID:Cytomegalovirus polyradiculopathy in HIV-infected patients. 890 13

Knowledge of the polyprotein cleavage sites by HIV protease will refine our understanding of its specificity and the information thus acquired is useful for designing specific and efficient HIV protease inhibitors. The pace in searching for the proper inhibitors of HIV protease will be greatly expedited if one can find an accurate and rapid method for predicting the cleavage sites in proteins by HIV protease. Various prediction models or algorithms have been developed during the past 5 years. This Review is devoted to addressing the following problems: (1) Why is it important to predict the cleavability of a peptide by HIV protease? (2) What progresses have been made in developing the prediction methods, and what merits and weakness does each of these methods carry? The attention is focused on the state-of-the-art, which is featured by a discriminant function algorithm developed very recently as well as an improved database (the program and database are available upon request) established according to new experimental results.
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PMID:Prediction of human immunodeficiency virus protease cleavage sites in proteins. 878 41

Zidovudine (ZDV), a nucleoside analogue which inhibits viral replication, is currently used in the treatment of type 1 human immunodeficiency virus (HIV-1) infection. It has been considered to be the cause of an acquired form of myopathy associated with a depletion of mitochondrial DNA (mtDNA) in muscle fibres, although the fact that the patients previously studied were clearly symptomatic, and the theoretical difficulty in differentiating on HIV-related myopathy from the effects of ZDV, led to a controversy on the possible deleterious effect of ZDV on muscle fibres. We studied the muscle biopsy taken from 42 HIV-1 infected patients, regardless of their medical complaints, and two series of controls: 12 HIV-negative patients suffering from diverse neuromuscular diseases and 10 normal patients who underwent orthopaedic surgery. Whole DNA was extracted following standard procedures and analysed by means of Southern blotting and polymerase chain reaction (PCR). We found that mtDNA was only depleted in HIV-1 infected patients treated with ZDV, but not in controls or patients untreated with this antiretroviral drug. Moreover, the depletion was more marked in patients who either presented weakness, myalgia, raised serum creatine kinase (CK), or ragged-red fibres. Mitochondrial DNA deletions were found in low proportion in all groups of patients, regardless of their HIV infection or ZDV status, but not in normal controls. We conclude that ZDV treatment in HIV-1 positive patients produces depletion of muscle mtDNA. The depletion can be demonstrated even in asymptotic patients, but is more marked in patients with clinical symptoms or abnormalities in their muscle biopsies. Other mtDNA abnormalities such as deletions seemed to be more related to other circumstances concurring in HIV-1 infected patients than to the effects of ZDV.
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PMID:The effect of zidovudine on skeletal muscle mtDNA in HIV-1 infected patients with mild or no muscle dysfunction. 881 97

We present a case report of a young asiatic women presenting Kikuchi's lymphadenitis, a suprahyoidea mass, pharyngitis, fever, weakness and lack of appetite. The clinical picture quickly improved after biopsy until complete remission within two months. Sierologic studies showed significant antibody titres revealing a previous EBV infection; they were also negative for Toxotest, HbsAg, HIV and serogroup 3 and 9 Yersinia Enterocolitica. Histological findings showed necrotic changes and large foci of infiltration in the cortex and/or paracortex. They consisted of variable numbers of small lymphocytes, immunoblasts, macrophages and so-called plasmacytoid monocytes, neutrophils were absent. Immunohistochemistry revealed within the lesion T-Lymphocytes displaying a phenotype CD4+ while T-Lymphocytes CD8+ were observed in the paracortex and in the peripheral region of the lesion.
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PMID:Histiocytic necrotizing lymphadenitis (Kikuchi's disease). 891 44

Sporadic inclusion body myositis (IBM) is the most common inflammatory myopathy affecting patients over the age of 50 years. Dysimmune and degenerative aetiologies have been postulated, but viral infections have not been associated with the disease. Two HIV-I (human immunodeficiency virus type 1) infected men and one woman infected with HTLV-1 (human T cell leukaemia virus type 1) developed progressive proximal muscle weakness unrelated to antiretroviral therapy. Their muscle biopsies were studied by light and electron microscopy, by immunocytochemistry to determine the expression of major histocompatibility complex (MHC) molecules and identify the type of infiltrating cells and T cell receptor (TCR) subunits, and by reverse transcription-polymerase chain reaction (RT-PCR) and single or double immunocytochemistry to search for retrovirally infected endomysial cells. The clinical features were consistent with sporadic IBM. The muscle biopsies showed primary endomysial inflammation, red-rimmed vacuoles, amyloid deposits, eosinophilic inclusions, and small round fibres in groups, all diagnostic of IBM. The muscle fibres expressed MHC class-1 antigens and were invaded primarily by CD8+ T-lymphocytes preferentially bearing TCR V beta 5.1 and V beta 13 chains. The HIV-1 or HTLV-1 antigens were detected only on endomysial macrophages on or around muscle fibres, but not within the muscle fibres. We conclude that IBM occurs in HIV-1 and HTLV-1 infected individuals and has a clinical, histological and immunological pattern identical to sporadic IBM in the non-retrovirally infected patients. Retroviruses do not directly infect the muscle, but persistent retroviral infections may provide superantigenic stimulation and trigger an endomysial inflammatory response identical to that occurring in sporadic IBM.
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PMID:Inclusion body myositis in HIV-1 and HTLV-1 infected patients. 900 95

The third case in the literature is reported of an infection produced by Pleistophora. The clinical detail of the three cases are discussed. Two of the patients-including the reported one-were infected by HIV. All patients suffered from myositis with fever, resting and at palpation myalgia, and progressive weakness. Blood tests showed anaemia and high levels of muscle enzymes. Necrotic muscle fibrosis induced disabling contractures. Diagnosis was obtained by detecting the protozoon in a muscle biopsy. The spores may be detectable by means of different staining methods at light microscopy although electron microscopy remains the most reliable technique. Since this is such a rare condition there is no known treatment. Whether the albendazole could be as useful as occurs in patients infected by other genera of microsporidia in still uncertain.
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PMID:[Myositis caused by Pleistophora in a patient with AIDS]. 901 6

The purpose of this study was to determine the criteria by which the diagnosis of HIV dementia was made by providers in a public HIV outpatient clinic and hospital, and to evaluate the extent to which the providers' diagnosis confirmed or denied the presence of HIV dementia according to CDC recommendations. Retrospective chart analysis was conducted detailing symptomology, laboratory findings, and social characteristics of 103 HIV-infected patients from Nov 1, 1990 to Dec 31, 1993. Seventy-eight patients were evaluated by providers and given a preliminary HIV dementia diagnosis; 25 patients received no preliminary diagnosis. On follow-up, 39 were confirmed diagnosis while 64 patients received no follow-up (confirmatory) diagnosis. Inability to pay attention or remember details, memory deficit, motor weakness, and mild disorientation were all found to be significantly associated with being evaluated by a provider. Substance use was prevalent. Inconsistent manner in which HIV-demented patients were identified highlights the need for a standardized evaluation of signs and symptoms known to be associated with HIV dementia.
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PMID:Diagnosing HIV dementia: a retrospective analysis. 902 36

Although skeletal muscle abnormalities have been described in association with human immunodeficiency virus (HIV), the effects of HIV infection on respiratory muscle function have not been well characterized. We hypothesized that HIV+ individuals may develop respiratory muscle weakness and that respiratory muscle dysfunction may contribute to the unexplained dyspnea that occurs in the setting of HIV. To test this hypothesis we studied maximal inspiratory pressure (MIP), maximal expiratory pressure (MEP), inspiratory muscle endurance, and respiratory symptoms in 23 HIV+ male outpatients who had no history of acquired immune deficiency syndrome (AIDS)-related pulmonary complications, with a CD4+ T-lymphocyte count of 331.6 +/- 62.1 (mean +/- SEM). Respiratory muscle endurance was measured with an incremental threshold loading (ITL) protocol. We compared these results to those for 14 HIV- males matched for age and weight. Compared with the controls, HIV+ subjects had a significantly lower mean MIP (98.7 +/- 7.4 versus 121.4 +/- 9.3 cm H2O, p < 0.05) and MEP (115.0 +/- 9.3 versus 152.1 +/- 14.8 cm H2O, p < 0.05). Furthermore, during ITL, the mean load at task failure in the HIV+ group was 295.7 +/- 36.2 g, versus 405.8 +/- 52.2 g in the control group (p < 0.05). In the HIV+ subjects there was no relationship between muscle performance and CD4+ count or azidothymidine (AZT) use. There was, however, a highly significant relationship between respiratory muscle dysfunction and symptoms of dyspnea. We conclude that HIV seropositivity is associated with a decline in respiratory muscle performance. This impairment in respiratory muscle function may contribute to the feeling of breathlessness that has been well described in this patient population.
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PMID:Respiratory muscle dysfunction associated with human immunodeficiency virus infection. 911 90

Endpoints are a continuing source of controversy in clinical trials of antiretroviral (specifically, anti-HIV) treatments. The most visible disagreement is about the respective roles of morbidity and mortality as endpoints, and laboratory measurements as endpoints. Laboratory measurements have been intensely examined as possible surrogates for clinical outcomes, but the definition of the usual clinical outcome-first occurrence or recurrence of an AIDS-defining condition or death-has received little critical scrutiny. First disease progression has serious weakness as an endpoint, and one should consider alternatives. In this paper, we suggest using rule-based schemes to rank patients' post-randomization histories and then using the ranks as an outcome measure, an extension of the work by Follmann et al. on heart disease. We evaluated six rule-based ranking schemes for antiretroviral trials by applying them to 60 participants in CPCRA 002 and comparing the results to subjective rankings given by five experts. The expert's rankings were in good agreement with each other, and the six rule-based schemes were clearly differentiated by their degree of agreement with the expert's rankings. The ranking scheme most in accord with the experts ranked patients first by seriousness of their most serious AIDS-defining disease, second by the timing of that disease, and the third by the total number of AIDS-defining diseases they experienced. Finally, we used this rule-based rankings to re-analyse CPCRA 002.
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PMID:Rule-based ranking schemes for antiretroviral trials. 917 82

An interesting aspect of HIV disease is the immunoendocrine dialogue, via the hypothalamo-pituitary-adrenal axis, between glucocorticoids and cytokines and its potential role in HIV disease progression. This study reports recent data on the interaction between glucocorticoids and the immune system in AIDS patients with an acquired form of glucocorticoid resistance. Clinically, glucocorticoid-resistant AIDS patients (AIDS-GR; about 12% in our series of patients) present Addisonian symptoms (weakness, weight loss, hypotension, hyponatremia and intense mucocutaneous melanosis) in spite of elevated values of plasma cortisol and urinary free cortisol. Monocytes from these patients have a significantly lower receptor affinity (higher Kd) for glucocorticoids and a higher receptor density than other patients and controls. Such receptor alteration is associated with higher values of plasma interferon alpha (IFN alpha). In AIDS-GR there is a significant correlation between the values of receptor Kd and of plasma IFN alpha (r = 0.77). After poly(I):poly(C) stimulation, monocytes from AIDS-GR produce much more IFN alpha than other AIDS patients. While in patients with no resistance and in control patients, monocyte production of IFN alpha is inhibited by dexamethasone (the effect being reversed by RU-486), a very slight inhibition of dexamethasone on IFN alpha production is observed in monocytes from AIDS-GR. In conclusion, these data demonstrate that the immunosuppressive mechanisms acting in AIDS may be reversed, as shown by the increased stimulus on IFN alpha production found in cortisol-resistant patients. These data also suggest that antiglucocorticoid drugs may be helpful in HIV disease as they antagonize the excessive immunosuppression induced by the increased production of glucocorticoids found at every stage of HIV disease.
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PMID:Glucocorticoids and the immune system in AIDS. 926 43


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