| pubmed-article:8269391 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8269391 | lifeskim:mentions | umls-concept:C0019704 | lld:lifeskim |
| pubmed-article:8269391 | lifeskim:mentions | umls-concept:C0021311 | lld:lifeskim |
| pubmed-article:8269391 | lifeskim:mentions | umls-concept:C0006104 | lld:lifeskim |
| pubmed-article:8269391 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:8269391 | pubmed:dateCreated | 1994-1-31 | lld:pubmed |
| pubmed-article:8269391 | pubmed:abstractText | Direct infection of the central nervous system by human immunodeficiency virus type 1 (HIV-1), the causative agent of AIDS, was not appreciated in the early years of the AIDS epidemic. Neurological complications associated with AIDS were largely attributed to opportunistic infections that arose as a result of the immunocompromised state of the patient and to depression. In 1985, several groups succeeded in isolating HIV-1 directly from brain tissue. Also that year, the viral genome was completely sequenced, and HIV-1 was found to belong to a neurotropic subfamily of retrovirus known as the Lentivirinae. These findings clearly indicated that direct HIV-1 infection of the central nervous system played a role in the development of AIDS-related neurological disease. This review summarizes the clinical manifestations of HIV-1 infection of the central nervous system and the related neuropathology, the tropism of HIV-1 for specific cell types both within and outside of the nervous system, the possible mechanisms by which HIV-1 damages the nervous system, and the current strategies for diagnosis and treatment of HIV-1-associated neuropathology. | lld:pubmed |
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