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

Human immunodeficiency virus type 1 (HIV-1) has been clearly associated with a variety of new illnesses, including profound immunodeficiency (acquired immune deficiency syndrome [AIDS]), wasting syndromes (formerly termed AIDS-related complex [ARC]) and neurologic syndromes, including neuropathy, myelopathy and encephalopathy (often termed subacute encephalitis or AIDS dementia complex). HIV-1 preferentially infects T lymphocytes by binding to a membrane receptor protein, CD4, associated with helper function. The virus can also attack macrophages and, possibly, other cells such as neuronal cells, colonic epithelial cells and B lymphocytes. Infection of macrophages or monocytes may be involved in neurologic disease. Knowledge about HIV-1 has rapidly increased, and investigators have characterized its structure, ways in which it infects cells, replicates and is cytopathic for certain cells, and how the immune system responds to it. The ideal vaccine would prevent adsorption of the virus into the cell, but it is difficult to develop stable resistance because the virus has many antigenic patterns and mutates frequently. The results of vaccine trials in animals have not been promising, but work is being done with monoclonal antibodies. Antiviral therapies being investigated include those to prevent virus binding and entry, to inhibit reverse transcription, to inhibit the virus's life cycle and to restore immune competence in immunocompromised patients.
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PMID:Vaccine and antiviral strategies against infections caused by human immunodeficiency virus. 328 28

Cytomegalovirus (CMV) infection of the nervous system is frequent in acquired immunodeficiency syndrome (AIDS) and can be responsible for encephalitis, encephalomyelitis, meningoradiculitis or polyradiculo-neuropathy. Encephalitis is characterized at microscopy by its periventricular and cerebellar location, and by the presence of cytomegalic cells, containing intranuclear and/or intracytoplasmic inclusions, microglial nodules and necrotic foci. The virus can infect almost all types of cells. Coexistence of CMV and HIV has been observed in giant cells of macrophagic origin. It has been suggested that the two viruses could act in synergy. The nervous system is seldom infected by the varicella-zoster virus (VZV) in AIDS. The infection can be responsible for multifocal leukoencephalitis, ventriculitis, vascular lesions associated or not with cerebral infarction, or with meningomyeloradiculitis. In almost all cell types Cowdry's type A intranuclear inclusions have been found. The virus can be demonstrated by immunohistochemistry or in situ hybridization. VZV antigens have been reported in the walls of vessels damaged by a non inflammatory obliterating vasculopathy or by a granulomatous angiitis. Coexistence of VZV and HIV has been observed in giant cells of macrophagic origin, and synergy between those two viruses has been suspected.
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PMID:[Pathologic anatomy of cytomegalovirus encephalomyelitis and varicella-zona virus encephalomyelitis]. 747 34

Following earlier observations on the snout (SR) and palmomental(PMR) reflexes in AIDS in Tanzania, a series of 1127 adults, 649 HIV-positive and 478 HIV-negative, from 4 groups at different risk of HIV infection were examined neurologically between 1987 and 1992. The prevalence of SR and PMR was calculated according to HIV status, HIV stage, demographic factors and neurologic findings. In the total series of HIV positives the prevalence ranged from SR 39.3% and PMR 22.6% in asymptomatic HIV disease to SR 87% and PMR 69% in terminal AIDS. In HIV negatives the prevalence of SR was 19.2% and PMR 15.3%, and increased with age. There was no relationship with age in the HIV positives and no gender differences. SR and PMR were also associated with neuropathy, myelopathy and AIDS dementia complex independent of HIV stage. This study shows a strong association between SR and PMR and HIV disease in Africa. The prevalence increased with HIV stage and related neurological disorders.
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PMID:The snout and palmomental reflexes in HIV disease in Tanzania. 757 42

The HIV-1 infection of central nervous system, with attendant neuropathy and dementia, poses a unique challenge for antiviral therapy. For practical considerations, it is important to define carefully the precise therapeutic objectives. (1) Is it necessary to inhibit spreading HIV-1 infection in the central nervous system? (2) What is the role of inflammatory responses in central nervous system disease during HIV-1 infection? (3) Is there a correlation between pathology and dementia? (4) Are virions or virus gene products toxic in the central nervous system? (5) Is there a role for immune suppression and opportunistic pathogens in AIDS dementia? The development of therapeutic agents for HIV-1 infection is guided by our knowledge of virus structure, the function of viral proteins, the interactions with host components, and detailed features of the virus life cycle. In each case, unique features of the virus can be identified and established as targets for unique antiviral compounds. Drugs acting as inhibitors of virus enzymatic functions are plagued by the rapid development in vivo of drug-resistant virus variants, although combination or alternating chemotherapeutic regimens may obviate some of these concerns. Novel approaches to inhibiting virus are flourishing. In vitro studies show the value of agents as diverse as molecular decoys for tat activity to efforts to mutagenize integrated proviruses by modified oligonucleotides that form triple helices with chromosomal genes. As each particular clinical situation is better defined, the design and application of these agents can be refined to inhibit HIV-1 replication and reduce the associated morbidity.
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PMID:Therapeutic approaches to HIV infection based on virus structure and the host pathogen interaction. 758 59

Peripheral nerve disorders are among the most common neurological complications of HIV disease. Distal sensory polyneuropathy (DSP) is the most common form of neuropathy in patients with AIDS and can be caused by diverse mechanisms, including infectious, metabolic, inflammatory, nutritional, and toxic factors. Antiretroviral agents may cause or contribute to HIV-related DSP. Recognition of peripheral neuropathy has become increasingly important as more patients receive nucleoside analogue agents for the treatment of HIV disease. It is crucial to correctly distinguish between the neuropathies caused by toxic effects of nucleoside analogues and those that are primarily related to underlying HIV disease, because timely diagnosis and proper treatment of peripheral neuropathies may allow the continuation of antiretroviral therapy as well as improve the quality of life. The identification and treatment of peripheral neuropathies associated with use of the nucleoside drugs zalcitabine (ddC), didanosine (ddI), and stavudine (d4T) are reviewed.
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PMID:Nucleoside analogue-associated peripheral neuropathy in human immunodeficiency virus infection. 774 92

Advances in the development of antiviral drugs have been rapid and dramatic. Since the recognition of HIV-1 as the cause of AIDS in 1984, and improved understanding of retroviral replication and pathogenesis, three antiviral drugs, Zidovudine, Didanosine, and Zalcitabine, have been developed to the point of routine use in humans. There is substantial experience with the former two in children. Despite being unable to cure HIV-1 infection, the benefits of antiretroviral therapy, including extended survival and reductions in opportunistic infections in adults, and improved weight gain and well-being in children, are strong arguments for routine treatment of symptomatic disease. Because these agents may also interfere with human cellular processes and have toxicities including anemia, neutropenia, pancreatitis, and neuropathy, their routine use for the treatment of asymptomatic children requires further controlled study. There are multiple candidate agents being developed for entry into clinical trials. An additional potentially effective strategy is the use of combinations of drugs at the same time or in sequence to maximize the viral targets being attacked, while minimizing toxicity, and to prevent the emergence of a drug-resistant virus.
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PMID:Antiretroviral therapy for children. 783 65

In a randomized, double-blind, large, simple trial, the safety and efficacy of two weight-adjusted dose levels of stavudine were evaluated in patients with advanced human immunodeficiency virus (HIV) infection. All patients were refractory to or intolerant of both zidovudine and didanosine. Patients weighing > or = 60 kg received 20 or 40 mg of stavudine twice daily. The dose was reduced to 15 or 30 mg for patients weighing 40-59 kg and to 10 or 20 mg for those weighing < 40 kg. The primary efficacy end points were survival and time to clinical progression of HIV disease. The primary safety end point was time to dose-limiting neuropathy. A total of 8127 patients were enrolled as of 31 July 1993. Although many patients who might have benefitted from stavudine were reached by the parallel-track program, a review of demographic data revealed disproportionate representation by white men from large metropolitan areas on both coasts.
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PMID:Design and implementation of the stavudine parallel-track program. 786 Oct 16

Value of the bulbocavernosus reflex latency versus nerve conduction velocity of the dorsal nerve of penis and penile brachial index was evaluated in HIV-1 infected asymptomatic and symptomatic men with and without an objective evidence of neuropathy. These studies revealed striking results in neuropathic group. Both asymptomatic and symptomatic patients with neuropathy exhibited a significant decrease (P < 0.0005) in the values of the nerve conduction velocity of the dorsal nerve of penis as well as penile brachial index in comparison with the controls of the same age group. However both types of non neuropathic patients showed a non significant difference in the above mentioned parameters with their respective controls. The latency of bulbocavernosus reflex showed no significant difference between the groups and was within the normal limits. A non significant association in the values of the study parameters among asymptomatic and symptomatic patients with and without neuropathy was also observed. These findings suggest an exclusively apparent sexual pathway for the penile dorsal nerve conduction and penile brachial index in both HIV-1 infected asymptomatic and AIDS positive men affected by neuropathic conditions, irrespective of their disease state. We thus conclude that a primary defective neuropathic mechanism may play an etiological role in the pathogenesis of erectile impotence in these patients.
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PMID:HIV-1 associated neuropathies in males; impotence and penile electrodiagnosis. 797 25

Human immunodeficiency virus infection commonly affects the nervous system, with the most important features being a dementing illness, a myelopathy, and a neuropathy. In the past year, important advances have been made in the epidemiology and treatment of these conditions. Moreover, a better understanding of the pathogenetic mechanisms has emerged, with particular emphasis being placed upon gp120, tumor necrosis factor, and quinolinic acid and other partly characterized neurotoxins. This review highlights these advances in the context of the clinical syndromes.
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PMID:The clinical spectrum and pathogenesis of HIV encephalopathy, myelopathy, and peripheral neuropathy. 808 14

Three HIV-infected patients developed cranial neuropathy as the initial manifestation of an AIDS-related large cell lymphoma. All were homosexual men known to be HIV seropositive for 3 to 4.5 years. At the time of presentation for neurological disease, the CD4 T-lymphocyte count was < 400 cells/mm3 in each. Initial manifestations were retro-orbital headache and oculomotor nerve palsy in two and an abducens nerve palsy in the other. Repeatedly negative CSF cytologies and recovery of the cranial neuropathy obscured the diagnosis. These patients illustrate that cranial neuropathy with HIV infection may herald the presence of an occult large cell lymphoma. Spontaneous or corticosteroid-associated improvement of the cranial neuropathy, absence of abnormalities on brain imaging studies, and negative CSF cytologies do not exclude this diagnosis. We suggest that a diligent and repeated search for lymphoma be considered in HIV-infected patients presenting with cranial neuropathy, including repeated CSF examinations, MRI of brain and spine (T1 and T2) with and without gadolinium enhancement, chest and abdominal CT scans, and bone marrow biopsy.
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PMID:Cranial neuropathy heralding otherwise occult AIDS-related large cell lymphoma. 810 48


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