Loading
HIV Infections / Neurocognitive Disorders / RNA, Viral · Journal article
Emerging Microbes & Infections · February 3, 2026
Encouraging direction, but not yet definitive.
This cross-sectional study of 24 ART-treated people with HIV found that HIV RNA and HIV-derived peptides (Env, Pol) persist in cerebrospinal fluid of those with HAND (n=14) despite undetectable plasma viral load and pharmacologically adequate ART drug concentrations. No productive infection was established, suggesting latent viral expression rather than active replication may drive neuroinflammation and cognitive decline in suppressed patients.
Cross-sectional study. 24 people with HIV on antiretroviral therapy recruited from Institute of Infectious Diseases Emilio Ribas in Brazil from December 2014 to March 2016. Participants with cognitive impairments affecting consent capacity required authorization from legal guardian aged 18 or older.. Intervention: Paired plasma and cerebrospinal fluid sampling with measurement of HIV RNA, ART drug concentrations, and viral peptides; viral outgrowth assay. Compared with: Cognitively normal participants (n=10) versus HAND participants (n=14). n = 24. Institute of Infectious Diseases Emilio Ribas in Brazil.
HIV RNA was undetectable in plasma but present in CSF from HAND participants (n=14), indicating compartmentalized viral persistence HIV-derived peptides (Env and Pol) were detected exclusively in HAND samples, accompanied by early reduction in β-tau Tenofovir and lamivudine levels were higher in plasma; dolutegravir trended higher in CSF; all CSF drug concentrations exceeded their IC50 values
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
Clinicians should recognize that cognitive decline in ART-treated people with HIV may reflect latent CNS HIV infection with non-replicative viral expression rather than virological failure. This suggests that standard plasma viral load monitoring may not adequately assess CNS pathology and could inform development of CNS-penetrating strategies or biomarker monitoring for HAND.
Cross-sectional study showing HIV RNA and derived peptides persist in cerebrospinal fluid of HAND patients despite undetectable plasma viral load and adequate ART penetration, suggesting latent infection may drive neuroinflammation, but lacks comparator group and causal evidence.
As stated by the source record.
Quoted from the source exactly as published.
Clinicians should recognize that cognitive decline in ART-treated people with HIV may reflect latent CNS HIV infection with non-replicative viral expression rather than virological failure. This suggests that standard plasma viral load monitoring may not adequately assess CNS pathology and could inform development of CNS-penetrating strategies or biomarker monitoring for HAND.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
Despite effective antiretroviral therapy (ART), HIV-associated neurocognitive disorders (HAND) persist in people with HIV (PWH). The central nervous system (CNS) may act as a viral reservoir due to limited ART penetration and virological discordance between plasma and cerebrospinal fluid (CSF). In a cross-sectional study of 24 ART-treated PWH, participants were stratified as cognitively normal (CN, n = 10) or HAND (n = 14), including asymptomatic neurocognitive impairment (ANI, n = 3), mild neurocognitive disorder (MND, n = 9), and HIV-associated dementia (HAD, n = 2). HIV RNA was quantified in paired plasma and CSF by RT-ddPCR. CSF peptidome profiling was performed using mass spectrometry, and ART concentrations were measured by LC-MS/MS. HIV infectivity in CSF was assessed via viral outgrowth assays. HIV RNA was undetectable in plasma but present in CSF from HAND participants, indicating compartmentalized viral persistence. Tenofovir and lamivudine levels were higher in plasma, whereas dolutegravir trended higher in CSF. Nevertheless, all CSF drug concentrations exceeded their IC50 values in effectively suppressing active HIV replication. Peptidomic analysis identified HIV-derived peptides (e.g. Env and Pol) exclusively in HAND samples, accompanied by an early reduction in β-tau. Although HIV RNA and peptides were detectable, no productive infection was established by CSF in permissive immune cells. Together, despite pharmacologically sufficient ART penetration, HIV persists in the CSF of PWH with HAND. These findings suggest that the latent HIV infection with non-replicative viral expression, rather than residual active HIV replication, may contribute to neuroinflammation and cognitive decline in PWH on suppressive ART.
Taken from the source record, never inferred. Follow any of these and new work involving them reaches your briefing.