Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chance of opportunistic infections in hospitals is increasing year by year, because of the steady increase in the number of compromised hosts. Opportunistic infections in the nervous system include fungal, protozoal, bacterial and viral infections. Cytomegalovirus and herpes virus (HSV1 and HSV2) cause encephalitis, myelitis and radiculoneuritis. Varicella-zoster virus (VZV) often causes herpes zoster, which sometimes disseminates when immunodeficiency is severe. VZV also causes encephalitis. Progressive multifocal leukoencephalopathy (PML) is caused by JC virus in severely compromised hosts. HIV encephalopathy or AIDS dementia complex is one of late stage complications of HIV infection. Prevalence of PML and HIV encephalopathy among AIDS patients tend to increase as other opportunistic infections became controllable recently. Primary CNS lymphoma in immunocompromised hosts is supposed to be caused by EB virus and/or Kaposi's sarcoma-associated herpes virus (KSHV, HHV8). In this sense, CNS lymphoma and Kaposi's sarcoma can be defined as virus infection-related condition.
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PMID:[Virus-related neurological disorders complicating in compromised hosts]. 910

Progressive multifocal leukoencephalopathy (PML) is a demyelinating disease of the central nervous system caused by infection of oligodendrocytes by JC virus. As patients with HIV survive longer with severe immunodeficiency, the incidence of PML is rising. Diagnosis is not always easy and the gold standard remains histological confirmation of the characteristic lesions of PML which requires a brain biopsy. This is considered too invasive by many clinicians and patients alike and detection of JC virus DNA in the cerebrospinal fluid (CSF) using polymerase chain reaction (PCR) is used as an alternative to biopsy. JC virus subtype detection in brain, CSF and blood leukocytes may offer further diagnostic and prognostic possibilities. The aetiology, clinical features and diagnostic problems of PML are reviewed. At present the outlook for patients with confirmed PML is poor and there is currently no effective treatment. However, novel approaches to treatment are under investigation and show some promise.
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PMID:Progressive multifocal leukoencephalopathy in HIV. 917 44

Progressive multifocal leukoencephalopathy (PML) is a demyelinating disorder of the CNS that usually causes hemiparesis or hemianopsia. Dementia occurs in combination with other neurologic abnormalities. We report a human immunodeficiency virus type 1 (HIV)-infected man whose only manifestation of proven PML was dementia that was clinically indistinguishable from HIV-associated dementia.
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PMID:Progressive multifocal leukoencephalopathy presenting as human immunodeficiency virus type 1 (HIV)-associated dementia. 922 4

Progressive multifocal leukoencephalopathy, a formerly rare disease that chiefly occurred in persons with underlying lymphoma and chronic lymphocytic leukemia, is now seen with increasing frequency in the era of acquired immunodeficiency syndrome. Progressive multifocal leukoencephalopathy is currently estimated to arise in 5% of all human immunodeficiency virus-infected individuals. The clinical features of the disorder in patients with acquired immunodeficiency syndrome do not appear to be significantly different from progressive multifocal leukoencephalopathy occurring in association with other immunosuppressive disorders. Radiographically, the appearance of HIV dementia on magnetic resonance imaging is sometimes confused with that of progressive multifocal leukoencephalopathy. Among the characteristics that are helpful in distinguishing between the two disorders are the presence of focal findings, the rate of disease progression, the specific magnetic resonance imaging attributes, including the location of the lesions, and certain cerebrospinal fluid parameters, including surrogate markers for human immunodeficiency virus dementia and the presence of myelin basic protein. The remarkable increase in the burden of progressive multifocal leukoencephalopathy has provided a vital impetus for its study, particularly with respect to diagnosis and therapy. Establishing an unequivocal diagnosis of progressive multifocal leukoencephalopathy currently requires brain biopsy. The application of polymerase chain reaction for JC virus amplification to cerebrospinal fluid samples suggests that it may provide an alternative means of diagnosis. Recent in vitro studies of cytosine arabinoside and camptothecin suggest that they, or similar agents, may prove useful in the treatment of this illness and well-designed clinical trials are underway.
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PMID:Progressive multifocal leukoencephalopathy: the evolution of a disease once considered rare. 922 38

JC virus (JCV) acts as an opportunistic virus in immunocompromised human immunodeficiency virus type 1 (HIV-1)-infected patients. The role of peripheral blood cells in central nervous system invasion, before the onset of progressive multifocal leukoencephalopathy (PML), remains controversial. In order to clarify JCV latency or reactivation status in peripheral blood, 72 HIV-1-infected patients were studied, together with 7 HIV-1-positive PML patients and 50 blood donors. Blood leukocytes, plasma, and B lymphocytes were investigated by two complementary DNA amplification procedures within the early T and late VP1 JCV genes and two reverse transcription techniques for the detection of corresponding early transcripts and mRNAs. JCV DNA was detected in 40.3% of the HIV-1-infected patients but only 8% of the blood donors (P < 0.001). Leukocytes represented 82.7% of the positive samples, but plasma from 12 patients (41.4%) contained JCV DNA. B lymphocytes seemed to be involved in the natural history of JCV but did not represent the unique cell target. JCV DNA was intermittently found in blood, and JCV mRNAs for VP1 capsid protein were detected exclusively in one PML patient. Such observations demonstrate that JCV, when detected in blood, does not undergo active multiplication. They support the JCV hematogenous spread hypothesis, but do not indicate any direct link between peripheral virus and dissemination in the central nervous system at the time of immunodepression.
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PMID:Latency and reactivation of JC virus in peripheral blood of human immunodeficiency virus type 1-infected patients. 927 4

To measure the effect of the human immunodeficiency virus (HIV) epidemic on mortality from opportunistic infections (OIs) in 1993, national multiple-cause death certificate data were examined using two approaches. First, for each OI, the percentage of deaths with HIV infection reported as the underlying cause was calculated. Second, the age-adjusted rate of death per million population was compared with the rate predicted from a model of rates in 1970-1980 or 1979-1981, as available. The percentage of deaths with HIV as the underlying cause and the ratio of observed to predicted death rates were as follows: toxoplasmosis, 91% and 86 (5.24/0.06); cryptosporidiosis/isosporiasis, 90% and infinite (1.61/0.00); progressive multifocal leukoencephalopathy, 87% and 19 (2.58/0.13); pneumocystosis, 82% and 18 (15.44/0.87); cytomegalovirus disease, 82% and 17 (12.60/0.74); nontuberculous mycobacteriosis, 79% and 18 (15.51/0.84); cryptococcosis, 76% and 4 (5.80/1.35); and histoplasmosis, 68% and 6 (1.36/0.23). Thus, the HIV epidemic has greatly increased mortality from several OIs.
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PMID:Effect of the human immunodeficiency virus epidemic on mortality from opportunistic infections in the United States in 1993. 929 8

We have assessed the diagnostic efficacy of a novel polyclonal rabbit antiserum directed to the recombinant major capsid protein VP1 of JC virus (JCV). Immunohistochemistry for VP1 was compared to non-radioactive JCV DNA in situ hybridization (ISH) in ten cases of progressive multifocal leukoencephalopathy (PML). Tissue sections from postmortem brains were studied from PML patients suffering from immunodeficient conditions of various causes: immunodeficiency syndrome (AIDS, n = 7), severe combined immune deficiency due to adenosine deaminase deficiency (n = 1), sarcoidosis (n = 1) and leukemia (n = 1). VP1 immunohistochemistry demonstrated the presence of JCV in lesional oligodendrocytes of all PML patients, whereas ISH was able to detect JCV in nine out of ten cases. We conclude that VP1 immunohistochemistry is a specific, sensitive and rapid method for confirming the diagnosis of PML.
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PMID:Detection of JC virus by anti-VP1 immunohistochemistry in brains with progressive multifocal leukoencephalopathy. 929 91

Progressive multifocal leukoencephalopathy is a rare viral-induced demyelinating disease associated to immunodeficiency. A 10-year-old boy with AIDS is reported, who developed subacute cerebellar signs and symptoms with multiple cranial nerve involvement and dementia. A computed tomography scan revealed a focal nonenhancing area of low attenuation in the cerebellum. On magnetic resonance imaging high signal lesions in T2 weighted sequences were shown. The biopsy of one of those lesions showed the typical histological findings of progressive multifocal leukoencephalopathy. It seems important to consider this diagnosis in children with AIDS who present with progressive neurological features.
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PMID:Progressive multifocal leukoencephalopathy in a child with acquired immunodeficiency syndrome (AIDS). 933 71

A twenty-six year old, previously healthy nurse presented with new onset of seizures and was given a clinical diagnosis of herpes simplex encephalitis. After treatment with acyclovir there was incomplete resolution of the lesions by MRI scans and within a few months the patient's neurologic symptoms worsened, prompting a stereotactic biopsy. A diagnosis of progressive multifocal leukoencephalopathy (PML) was made using electron microscopy, and in situ hybridization studies. Subsequent to this biopsy, she was shown to be infected with human immunodeficiency virus (HIV) and had a CD4 T-cell count of 63. She had no known risk factors for HIV infections and had been tested as recently as eighteen months previously during her pregnancy. Neither the husband nor the child were positive for HIV. PML as a presenting sign of HIV infection is rare.
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PMID:Case of the month: September 1997--a 26 year old woman with new onset seizures. 945 83

JC virus (JCV) is thought to reach the central nervous system by a vascular route. To determine whether JCV is conveyed in peripheral blood as latent or reactivated virus, blood leukocytes, plasma, and urine from 50 AIDS patients and plasma and B lymphocytes from 60 AIDS patients were investigated. Peripheral blood from 88 human immunodeficiency virus-negative blood donors was studied. Nested polymerase chain reaction assays allowed the identification of JCV T DNA and VP1 mRNAs. The latter indicate viral replication. Blood harbored JCV DNA in 31.8% of AIDS patients (only 2.3% of blood donors; P > .001) and urine in 56%. VP1 mRNAs were detected in blood of 1 AIDS patient. Notably, 38% of DNA-positive urine samples and 10 cerebrospinal fluid samples (CSF) from AIDS patients with progressive multifocal leukoencephalopathy contained JCV mRNAs. Thus, JCV was significantly more frequent in blood from AIDS patients than from controls, but, in most instances, it was latent, whereas active replication was detected in urine and CSF.
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PMID:JC virus remains latent in peripheral blood B lymphocytes but replicates actively in urine from AIDS patients. 960 26


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