Levels of human immunodeficiency virus type 1 (HIV-1) replication in macrophages determines the severity of murine HIV-1 encephalitis

被引：0

作者：

Nukuna A. ^{[1
,2
,4
]}

Gendelman H.E. ^{[1
,2
,3
]}

Limoges J. ^{[1
,3
]}

Rasmussen J. ^{[1
,2
]}

Poluektova L. ^{[1
,2
]}

Ghorpade A. ^{[1
,2
]}

Persidsky Y. ^{[1
,2
]}

机构：

[1] Ctr. Neurovirol./Neurodegen. Disord., Univ. of Nebraska Medical Center, Nebraska Medical Center, Omaha

[2] Department of Pathology/Microbiology, Univ. of Nebraska Medical Center, Nebraska Medical Center, Omaha

[3] Department of Internal Medicine, Univ. of Nebraska Medical Center, Nebraska Medical Center, Omaha

[4] Creighton Univ. School of Medicine, Omaha, NE

来源：

Journal of NeuroVirology | 2004年 / 10卷 / Suppl 1期

关键词：

Animal model; Encephalitis; HIV-1; Viral strain;

D O I：

10.1080/753312757

中图分类号：

学科分类号：

摘要：

The presence of specific neuroinvasive strains and necessity for brain viral replication for disease progression remain controversial issues in neuro-AIDS research. To investigate these questions, the authors injected human monocyte-derived macrophages (MDMs) infected with diverse viral strains were injected into the caudate and putamen of severe combined immunodeficient (SCID) mice. Independent of viral strain, infected MDMs became immunologically activated and elicited profound inflammatory reactions in brain areas most affected in humans. The intensity of neuropathologic changes, including microglial reactions, paralleled levels of viral infection and numbers of infected MDMs. The data suggest that HIV-1-associated neurological disease is related to the level of productive viral infection in activated macrophages. Virus infection, per se, may affect the ability of macrophages to respond to immune stimuli by overproduction of proinflammatory factors and neurotoxins, leading to neuronal dysfunction. © 2004 Journal of NeuroVirology.

引用

页码：82 / 90

页数：8

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