TRIM5α H43Y Polymorphism and Susceptibility to HIV-1 Infection: A Meta-Analysis.

TRIM5α is an antiviral factor that can greatly limit HIV-1 infection. Although several researchers have investigated whether TRIM5α H43Y polymorphism influences the risk of HIV-1 infection, no definite conclusion has ever been drawn. In this research, we performed a meta-analysis to generate a more robust estimate of the association between TRIM5α H43Y and susceptibility to HIV-1 infection.

Designed transcription activator-like effector proteins efficiently induced the expression of latent HIV-1 in latently infected cells.

HIV latency is the foremost barrier to clearing HIV infection from patients. Reactivation of latent HIV-1 represents a promising strategy to deplete these viral reservoirs. Here, we report a novel approach to reactivate latent HIV-1 provirus using artificially designed transcription activator-like effector (TALE) fusion proteins containing a DNA-binding domain specifically targeting the HIV-1 promoter and the herpes simplex virus-based transcriptional activator VP64 domain.

Dilazep synergistically reactivates latent HIV-1 in latently infected cells.

The long-lived latently infected cells persist in spite of prolonged highly active anti-retroviral therapy and present a major barrier to a cure of human immunodeficiency virus type 1 (HIV-1) infection. Elimination of this reservoir requires reactivation of the latent virus. None of the current agents can safely and effectively reactivate latent HIV-1 reservoirs.