ArticleNeuroImmune pharmacology and therapeutics2025
Neurovirulent and non-neurovirulent strains of HIV-1 and their Tat proteins induce differential cytokine-chemokine profiles.
Article in NeuroImmune pharmacology and therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- Selective reactivation of latent HIV using CyclinT1-Tat-containing virus-like particles.Virology · 2026Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Objectives: HIV-1 enters the central nervous system (CNS) early in infection, and a significant proportion of people with HIV experience CNS complications despite anti-retroviral therapy. Chronic immune dysfunction, inflammatory cytokines and chemokines, and viral proteins like Tat and gp120 released by HIV-1-infected immune cells are implicated in the pathogenesis of HIV-1-associated neurocognitive disorders (HAND). Methods: To elucidate the contribution of non-viral factors to CNS complications in people with HIV-1, a comparative analysis of neurovirulent subtype B (HIV-1 Results: HIV-1 Conclusions: These results confirm that both viral and non-viral immune factors mediate neuronal damage in people with HIV.
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Registered trials
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