ArticleJournal of neurovirology2007
Host and virus strain dependence in activation of human macrophages by human immunodeficiency virus type 1.
Article in Journal of neurovirology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- Article
- Siglecs facilitate HIV-1 infection of macrophages through adhesion with viral sialic acids.PloS one · 2011Article
- Antiretroviral therapy in macrophages: implication for HIV eradication.Antiviral chemistry & chemotherapy · 2009Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Human immunodeficiency virus type 1 (HIV-1)-associated neuropathogenesis occurs in a large minority of infected people. Presently, there are neither viral nor cellular markers that predict the development of brain disease during HIV-1 infection. This study was conducted to determine whether there exist systematic differences among human cell donors and virus strains for the activation of macrophage gene expression by HIV-1 that may contribute to neuropathogenesis. Four HIV-1, ADA and B-aL, which were isolated from peripheral tissues of acquired immunodeficiency syndrome (AIDS) patients, and DJV and YU-2, which were isolated from brains of patients with HIV-1-associated dementia, were compared for induction of expression of cellular genes associated with antiviral activity or inflammation in monocyte-derived macrophages from several donors. Virus replication and cytokine production were scored by enzyme-linked immunosorbent assay (ELISA) and cellular transcripts were measured by real-time polymerase chain reaction (PCR). ADA and B-aL productively infected cells from all donors tested and induced all cellular transcripts tested, illustrating a common response of macrophages to HIV-1 replication. In sharp contrast, the viruses associated with neuropathogenesis, DJV and YU-2, induced intense gene expression early after infection in cells from a subset of donors but DJV did not productively infect these cells. No such heterogeneity was observed in the responses of macrophages during high-level replication of any HIV-1 tested. The susceptibility to early activation by HIV-1 may reflect susceptibility to neuropathogenesis in AIDS.
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Registered trials
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