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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The three known groups of nonhuman primate retroviruses (simian immunodeficiency virus, simian T cell lymphotropic/leukemic virus type I, and simian foamy virus) are thought to have equivalent human counterparts. This is clearly the case with human immunodeficiency virus types 1 and 2, the causative agents of acquired immunodeficiency syndrome, and with human T cell lymphotropic/leukemia virus type I (HTLV-I), which causes T cell leukemia and a progressive form of myelopathy (tropical spastic paraparesis/HTLV-I-associated myelopathy), and HTLV-II. However, the presence of spumaviruses (foamy viruses) in humans remains uncertain. Data accumulated in the last 5 years suggest the possibility that the human retroviruses are indeed the result of transmission of simian retroviruses to humans. In this article we attempt to parallel the genetic features of the simian retroviridae with their human counterparts and argue for the possibility of horizontal transmission of these viruses from monkeys to humans.
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PMID:Phylogenesis and genetic complexity of the nonhuman primate retroviridae. 782 92

A 27-year-old man positive for human immunodeficiency virus (HIV) presented with severe depressive stupor, peripheral neuropathy, and myelopathy. The onset of psychiatric symptoms, closely followed by neurological symptoms, without other possible somatic etiology suggests that HIV itself might precipitate psychosis. The patient was treated successfully with electroconvulsive therapy. The advantages and risks are discussed.
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PMID:HIV-induced stupor treated with ECT. 783 62

Neurological lesions are frequent complications of human immunodeficiency virus (HIV) infections. Organs involved include the brain, peripheral nerves and muscles. Since the widespread use of immunodepressive agents, spinal cord complications have also appeared although poorly documented in the literature. We observed six cases of spinal cord involvement which help indicate the modalities of practical management. In the first case, a 45-year old HIV1 + male presented dysesthesia evolving progressively over the T10 to L2 zones leading to the diagnosis of spinal cord toxoplasmosis. A gait disorder was the first sign in the second case, a 60-year old HIV1 + male. Neurological involvement progressed and the patient developed paraparesia, decreased muscular force with hypoesthesia and impaired proprioception of the lower limbs. Further complications led to coma and death and on autopsy, the patient was found to have cytomegalovirus myeloencephalitis. A 21 HIV1 + haemophiliac was our third case. Here paraplegia resulted from epidural compression due to Burkitt malignant lymphocytosis. The aggravation of paresthesia of the lower limbs, complicated by painful dysesthesia and proximal motor deficiency led to the suspected diagnosis of HIV-related myelitis in a particularly complicated case in a 52-year old seropositive male. In the fifth case, HIV infection led to major demelinization of the cervical and dorsal spinal cord due to toxoplasmosis and vacuolar myelopathy. In the sixth case, acute myelitis in an HIV2 positive male regressed spontaneously in 15 days. In clinical practice, spinal cord complications would appear to be frequent but less so than brain involvement. In the future, a better understanding of these complications should lead to specific identification of spinal cord signs in the neurological symptomatology of patients with HIV infection and allow adapted specific management.
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PMID:[Lesions of the spinal cord in HIV infection]. 789 90

Human retroviral infections result in significant neoplastic disease. Human T cell lymphotropic virus I (HTLV-I), the first human retrovirus to be discovered, is associated with the development of acute T cell leukemia with characteristic hypercalcemia and skin lesions after many years of chronic infection of CD4+ cells. HTLV-I also produces myelopathy. A minor T cell immunodeficiency occurs in HTLV-I acute T cell leukemia with associated strongyloidiasis and Pneumocystis carinii pneumonia. Human T cell lymphotropic virus II (HTLV-II) is found to be endemic in Amerindians and intravenous drug users (IVDUs) and has been linked to some cases of hairy-cell leukemia. HTLV-II infects the CD8+ population, with significant cell-associated viremia. Clinical neurological disease is rare, with one patient with myelopathy having been described. Immunodeficiency does not seem to occur. Human immunodeficiency virus 1 (HIV-1) produces aggressive large cell and Burkitt's lymphoma in as many as 10% of HIV-1-infected patients. More than 20% of homosexual men infected with HIV-1 develop Kaposi's sarcoma (KS). The pathogenesis of KS is better understood through studying KS-like cell lines that induce angiogenic factors. In some patients HIV-1 and HTLV-I or HTLV-II infections occur concomitantly. HIV-1 accelerates the tumorigenesis of HTLV-I and produces unusual skin diseases when combined with HTLV-II. Immunodeficiency occurs in all HIV-1-infected patients.
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PMID:Human retroviruses and neoplastic disease. 790 70

The dementia associated with human immunodeficiency virus (HIV) is poorly understood. Dementia is accompanied by infection and activation of macrophage lineage cells in the brain and production of toxic products by these cells has been postulated to play a role in the pathogenesis of dementia. Eicosanoids are potential products of activated macrophages that can mediate cell injury. We measured the levels of prostaglandin E2 in the cerebrospinal fluid of HIV-positive individuals with dementia and/or myelopathy and compared these levels with those of HIV-negative patients with other neurological diseases and HIV-positive patients without dementia. Cerebrospinal fluid prostaglandin E2 levels were increased in dementia. This increase was associated with severity of dementia and correlated with cerebrospinal fluid levels of neopterin and beta 2-microglobulin. Prostaglandins F2 alpha and thromboxane B2, additional products of the cyclooxygenase pathway of arachidonic acid metabolism, were also elevated in dementia, but leukotriene C4, a product of the lipoxygenase pathway was not. Since synthesis of prostaglandins is regulated in part by the levels of inducible forms of cyclooxygenase, we measured the levels of cyclooxygenase-1 and 2 mRNAs in the brains of HIV-positive individuals with and without dementia by reverse transcriptase polymerase chain reaction. Levels of intact cyclooxygenase-1 mRNA were higher in the brains of demented individuals, but this did not reach statistical significance. These data demonstrate that prostaglandins are increased in the central nervous system in HIV-associated dementia and may play a role in the development of neurological dysfunction.
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PMID:Elevated central nervous system prostaglandins in human immunodeficiency virus-associated dementia. 791 4

We evaluated 49 paired cerebrospinal fluid (CSF) and serum samples of 35 patients infected with the human immunodeficiency virus type 1 (HIV-1) for laboratory evidence of cytomegalovirus (CMV) infection. The patients were grouped according to clinical criteria as probable CMV encephalitis/polyradiculomyelitis, CMV retinitis, cerebral toxoplasmosis, progressive multifocal leukoencephalopathy, HIV-1-related cognitive/motor complex, HIV-1-associated myelopathy, and other neurological diseases. Paired CSF and serum samples were analysed for CMV deoxyribonucleic acid (DNA) by polymerase chain reaction (PCR), quantitative intrathecal synthesis of immunoglobulin G (IgG) antibodies specific for recombinant phosphoprotein 150 (pp150) of CMV and CMV-specific serum IgM. Intrathecal synthesis of pp150-specific IgG was detected in 26% of patients (9/35), serum IgM was found in 23% of patients (8/35), and PCR of CSF was positive in 11% of patients (4/35). Detection of CMV-specific DNA in CSF preceded the intrathecal antibody synthesis in three patients for whom serial samples were available. PCR results of the CSF became negative in one patient with CMV polyradiculomyelitis after successful therapy with 9-[2-hydroxy-1-(hydroxymethyl) ethoxymethyl] guanine (DHPG). PCR has a higher diagnostic specificity in the acute phase of CMV infection than intrathecal antibody synthesis. The serum IgM response to CMV cannot be used to monitor a compartmentalized immune response in the central nervous system while an intrathecal immune response seems to be associated with recovery either spontaneously or as a result of treatment.
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PMID:Comparative analysis of intrathecal antibody synthesis and DNA amplification for the diagnosis of cytomegalovirus infection of the central nervous system in AIDS patients. 793 40

Human immunodeficiency virus (HIV) affects all organ systems. Infection of the heart can manifest with evidence of myocarditis, pericarditis, or cardiomyopathy. The most common gastrointestinal symptom is diarrhea, which can result from infection with a variety of bacterial, fungal, or protozoal organisms. In about 15% of cases, no pathogen is recognized and the diarrhea syndrome is termed AIDS enteropathy. Any portion of the alimentary tract can be affected as well as the liver, gallbladder, and pancreas. Cryptosporidium, a previously infrequent cause of human illness, has emerged as an important pathogen in the HIV-infected patient and is responsible for chronic diarrhea, cholecystitis, and biliary tract obstruction. Evidence of neurologic involvement is present in more than 80% of patients at the time of autopsy. Cryptococcal meningitis, toxoplasma encephalitis, and neurosyphilis are the most often encountered central nervous system infections. While all three are responsive to therapy, treatment must be prolonged or persist for the duration of the patient's life to avoid recurrence. Peripheral nervous system manifestations include myelopathy, myopathy, and a variety of peripheral neuropathies. Retinal infection with cytomegalovirus (CMV) and toxoplasma can lead to irreversible loss of vision. Cotton wool spots are a common benign physical finding that must be differentiated from the early signs of CMV or toxoplasma infection. Management of the HIV-infected patient, while most often conducted by specialists in Internal Medicine or Infectious Diseases, is often an issue for the emergency physician. Many of the commonly afforded therapies are reviewed. Part 1 of this two-part series discussed the pathophysiology and clinical expression, epidemiology, laboratory testing, and the general clinical manifestations of AIDS, as well as dermatologic, pulmonary, and cardiac symptoms. Part 2 discusses the gastrointestinal, neurologic, and ocular symptoms, as well as the treatment and management of the AIDS patient.
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PMID:The acquired immune deficiency syndrome: an overview for the emergency physician, Part 2. 796 96

Infectious agents have been postulated as causes of multiple sclerosis for over a century. The possible role of a virus or viruses is supported by data that (1) a childhood exposure is involved and "viral" infections may precipitate exacerbations of disease, (2) experimental infections in animals and natural infections in humans can cause diseases with long incubation periods, remitting and relapsing courses, and demyelination, and (3) patients with multiple sclerosis have abnormal immune responses to viruses. The pathogenesis of three human demyelinating diseases of known viral etiology is discussed. In progressive multifocal leukoencephalopathy, a papovavirus selectively infects oligodendrocytes and causes focal areas of demyelination. In postmeasles encephalomyelitis, the virus is lymphotrophic and disrupts immune regulation that can result in an autoimmune perivenular demyelinating illness without evidence of infection of the central nervous system. In human immunodeficiency virus-encephalopathy and myelopathy virus is present in macrophages and microglia and the myelin abnormalities apparently are caused by soluble factors such as viral proteins, cytokines, or neurotoxins. These findings may have implications on how, when, and where to seek viruses in multiple sclerosis.
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PMID:The virology of demyelinating diseases. 801 89

Studies of lentiviral infections of various animals and man have shown that all may invade the CNS and induce pathological lesions. This is well established in infections with VV, CAEV, SIV, HIV-1, and FIV. Although VV and CAEV do not cause an overt immunodeficiency, they share several features pertinent for the establishment of neuropathologic lesions with those that induce immunodeficiency. This holds especially true for the initial steps and early CNS lesions. 1) Infection of the CNS is from the blood stream. Although a definite proof of how the different viruses cross the blood-brain barrier remains to be brought forward there are indications that it may occur through migration of infected monocytes and/or lymphocytes into the brain. Furthermore free virus may enter the CNS, either directly or through infection of endothelial cells. 2) The lesion pattern at least in initial stages is similar; that is, it consists of meningitis, perivascular infiltrations especially of the deep white matter, and inflammation of the choroid plexus. In visna a local amplification of the inflammatory response is frequently observed in choroid plexus often with formation of active lymphoid follicles. Multinucleated giant cells are prominent in HIV-1 and SIV infections, but rare in VV, and practically nonexistent in infections with FIV and CAEV, possibly a reflection of differences in virus replication. Myelin breakdown is a feature of various lentiviral infections but its mechanisms and morphological expression may vary. Sharply demarcated plaques of primary demyelination seem to be unique for VV infection and vacuolar myelopathy for infection with HIV-1. 3) The main target cells in the brain are cells of the monocyte/macrophage/microglial lineage. In visna infected monocytes are found but evidence for infection of the enigmatic resident microglial cells is still lacking. Infection, especially productive, of neuroectodermal cells is rare, but may, however be important for viral persistence. Infection of endothelial cells occurs in the various lentiviral infections and may play a part in viral entry into the CNS and contribute to tissue damage. 4) The discrepancy between the frequency of productively infected cells and cell types infected and extent and character of pathological lesions, indicates that a mechanism other than the direct effect of the virus contributes to the evolution of CNS lesions. In HIV-1 infection evidence, mainly obtained by in vitro studies, indicates that lesions are mediated by cytokines and other toxic factors secreted by inflammatory or glial cells.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Neuropathologic aspects of lentiviral infections. 803 Sep 77

The nervous system is frequently involved in patients with AIDS. The lesions can be due to the human immunodeficiency virus (HIV), to opportunistic agents, to the development of tumours, and to occasional nonspecific factors, such as circulatory, metabolic and degenerative changes. The changes directly related to the presence of the HIV include the HIV encephalitis and leucoencephalopathy, the diffuse polydystrophy and the vacuolar myelopathy. The pathogenesis of these lesions is not yet completely clear. Macrophages are the main cells infected by the HIV, and it seems that the cytotoxic effects on the nervous tissue are indirect, may be due to the release of substances by infected macrophages. Among the opportunistic infections, the most frequent is toxoplasmosis followed by cryptococcosis and cytomegalovirus infection, with some differences in series from various countries. Many other agents have been observed in the brain of patients with AIDS. B-cell lymphoma is the most frequent tumour found in the brain and it is not uncommon the association of infections and/or tumours.
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PMID:[The neuropathology of the acquired immunodeficiency syndrome (AIDS)]. 812 70


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