5′ leader defects drive persistent HIV-1 viremia on long-term ART

J Julia R. Box A Angelica Camilo-Contreras F Filippo Dragoni F Feng Yun Yue V Vitaliy Matveev J Jackson Foley J Jianwei Zhang (Biotech Drug Research Center, Shanghai Institute of Materia Medica, Chinese Academy of Sciences) Y Yan Wei Mok M Marlene DeSousa J Jun Lai (Department of Medicine, Johns Hopkins University School of Medicine) Z Zachary Mulcare Z Zachary Bakewell S Sebastien Poulin F Frederic Chano C Claude Fortin C Cecile Tremblay J Joel N. Blankson S Sonya Krishnan E Ethel D. Weld C Christie Basseth M Matthew M. Hamill (Johns Hopkins University School of Medicine, Baltimore) C Christopher J. Hoffmann E Eileen P. Scully J Joyce L. Jones A Andrea L. Cox W Wissam El Atrouni B Beverly Sha J Janet D. Siliciano (Department of Medicine, Johns Hopkins University School of Medicine) R Robert F. Siliciano (Department of Medicine, Johns Hopkins University School of Medicine) R Robert Reinhard J Jesper D. Gunst M Mario Ostrowski F Frank Maldarelli C Colin Kovacs F Francesco R. Simonetti (Department of Medicine, Johns Hopkins University School of Medicine)

Abstract

Abstract Traces of HIV-1 RNA can persist in plasma despite long-term suppressive antiretroviral therapy (ART). Some individuals develop nonsuppressible viremia (NSV), characterized by detectable HIV-1 RNA that raises concerns for virological failure, pathogenesis, and transmission. The sources of NSV remain poorly defined, in part due to limited tools to characterize plasma HIV-1 RNA. Both infectious and defective proviruses, including those with defects in the 5′ Leader (5′L), can contribute to NSV, but their relative contributions have not been quantified. Here we show that in over 50 participants, plasma viremia is markedly driven by highly clonal HIV-1 RNA populations carrying defects in the 5′L. Across individuals, dominant clones with 5′L defects clustered around the major splice donor (MSD) accounted for the vast majority of circulating HIV-1 RNA. To enable rapid, scalable profiling, we developed CLAWS (Capturing 5′ Leader Anomalies Without Sequencing), a digital PCR assay that distinguishes intact from defective 5′L RNA. CLAWS recapitulated sequencing-based estimates and detected low-abundance defective RNA early after ART initiation, revealing that defective genomes emerge early and become predominant during long-term therapy. These findings identify 5′L-defective genomes as the predominant driver of NSV and establish CLAWS as a practical tool for monitoring viremia in clinical and cure-related settings.

Article Details

Volume / Issue Vol. 17, Issue 1
Published June 08, 2026
ISSN 2041-1723
Publisher Nature Portfolio

Journal Info

Nature Communications

Nature Portfolio

ISSN: 2041-1723 Open Access Life Sciences

Authors (35)

J

Julia R. Box

A

Angelica Camilo-Contreras

F

Filippo Dragoni

F

Feng Yun Yue

V

Vitaliy Matveev

J

Jackson Foley

J

Jianwei Zhang

Biotech Drug Research Center, Shanghai Institute of Materia Medica, Chinese Academy of Sciences

Y

Yan Wei Mok

M

Marlene DeSousa

J

Jun Lai

Department of Medicine, Johns Hopkins University School of Medicine

Z

Zachary Mulcare

Z

Zachary Bakewell

S

Sebastien Poulin

F

Frederic Chano

C

Claude Fortin

C

Cecile Tremblay

J

Joel N. Blankson

S

Sonya Krishnan

E

Ethel D. Weld

C

Christie Basseth

M

Matthew M. Hamill

Johns Hopkins University School of Medicine, Baltimore

C

Christopher J. Hoffmann

E

Eileen P. Scully

J

Joyce L. Jones

A

Andrea L. Cox

W

Wissam El Atrouni

B

Beverly Sha

J

Janet D. Siliciano

Department of Medicine, Johns Hopkins University School of Medicine

R

Robert F. Siliciano

Department of Medicine, Johns Hopkins University School of Medicine

R

Robert Reinhard

J

Jesper D. Gunst

M

Mario Ostrowski

F

Frank Maldarelli

C

Colin Kovacs

F

Francesco R. Simonetti

Department of Medicine, Johns Hopkins University School of Medicine