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HIV-1 replication can be suppressed with antiretroviral therapy (ART), but individuals who stop taking ART soon become viremic again. Some people experience extended times of detectable viremia despite optimal adherence to ART. In this issue of the JCI, White, Wu, and coauthors elucidate a source of nonsuppressible viremia (NSV) in treatment-adherent patients --clonally expanded T cells harboring HIV-1 proviruses with small deletions or mutations in the 5'-leader, the UTR that includes the major splice donor site of viral RNA. These mutations altered viral RNA-splicing efficiency and RNA dimerization and packaging, yet still allowed production of detectable levels of noninfectious virus particles. These particles lacked the HIV-1 Env surface protein required for cell entry and failed to form the mature capsid cone required for infectivity. These studies improve our understanding of NSV and the regulation of viral functions in the 5'-leader with implications for rationalized care in individuals with NSV., Low level viremia on therapy People living with HIV-1 (PLWH) who are not on therapy have virus particles in their blood that can be detected using a PCR assay, which [...]

HIV-1 genotypic resistance test were obtained on clinical samples from 116 patients with plasma, HIV RNA levels of less than 75 copies/mL. Genotypic validity was confirmed in 49 of 50 patients with a previous or follow-up genotype.

We report the isolation of West Nile (WN) virus from four patient serum samples submitted for diagnosis during an outbreak of WN fever in Israel in 2000. Sequencing and phylogenetic [...]