Skip to content
Open access

Siglec-1-targeted nanobodies restrict HIV-1 transmission and infection of dendritic cells

Jul 2026 · Journal of Virology · Vol 100 · 0 citations · 54 references
Medicine

TL;DR

Newly developed single-domain antibodies against Siglec-1 are used against Siglec-1 as a candidate inhibitor to limit HIV-1 transmission and support the development of host-directed nanobody-based strategies to reduce HIV-1 spread.

Abstract

ABSTRACT Human immunodeficiency virus 1 (HIV-1) remains a global health burden affecting over 39 million people worldwide, with approximately one million new infections occurring each year. Sexual transmission remains the predominant route of HIV-1 acquisition, during which the virus crosses mucosal barriers and interacts with host immune cells to facilitate infection. Dendritic cells (DCs) contribute to systemic viral spread and seeding of reservoirs by efficiently capturing HIV-1, leading to infection and subsequent transmission of the virus to CD4+ T cells. Siglec-1 (CD169) is a key receptor involved in HIV-1 capture, and its blockade may help prevent viral transmission. Here, we used newly developed single-domain antibodies, also known as nanobodies, against Siglec-1 as a candidate inhibitor to limit HIV-1 transmission. Using a Siglec-1-overexpressing cell line, we demonstrated that these nanobodies specifically blocked Siglec-1-mediated HIV-1 binding and transmission. Extending these findings to a more physiologically relevant context, the anti-Siglec-1 nanobodies neither induced immune nor cellular activation in DCs, indicating a favorable safety profile for functional applications. Most notably, the anti-Siglec-1 nanobody 2C2 effectively blocked HIV-1 binding as well as infection of DCs. Moreover, both replication-dependent and replication-independent HIV-1 transmission by DCs was also abrogated by the nanobody. Our findings not only underscore the relevance of Siglec-1 in HIV-1 capture but also highlight the therapeutic potential of utilizing host-targeting strategies against infectious diseases. IMPORTANCE Sexual transmission is the main route of human immunodeficiency virus 1 (HIV-1) infection, and novel interventions are needed to prevent this crucial first step. Mucosal dendritic cells play a key role by capturing HIV-1 via attachment receptors, leading to dendritic cell infection and subsequent transmission to T cells, thereby facilitating viral spread and establishment of infection. Here, we show that small, highly specific nanobodies targeting the attachment receptor Siglec-1 strongly interfere with this early stage of HIV-1 transmission. Siglec-1 nanobodies prevented HIV-1 binding to and infection of dendritic cells, thereby blocking transmission to T cells without inducing unwanted immune activation. Together, these findings identify Siglec-1 nanobodies as promising interventions and support the development of host-directed nanobody-based strategies to reduce HIV-1 spread. Sexual transmission is the main route of human immunodeficiency virus 1 (HIV-1) infection, and novel interventions are needed to prevent this crucial first step. Mucosal dendritic cells play a key role by capturing HIV-1 via attachment receptors, leading to dendritic cell infection and subsequent transmission to T cells, thereby facilitating viral spread and establishment of infection. Here, we show that small, highly specific nanobodies targeting the attachment receptor Siglec-1 strongly interfere with this early stage of HIV-1 transmission. Siglec-1 nanobodies prevented HIV-1 binding to and infection of dendritic cells, thereby blocking transmission to T cells without inducing unwanted immune activation. Together, these findings identify Siglec-1 nanobodies as promising interventions and support the development of host-directed nanobody-based strategies to reduce HIV-1 spread.

Read PDF

Similar papers

Open access

Inhibitors screeing against HIV-1 Nef-mediated MHC-I

Human immunodeficiency virus type 1 (HIV-1) remains a major global health challenge. Although current treatments effectively suppress viral replication, they are unable to eliminate infected cells. The viral accessory protein Nef contributes substantially to HIV-1 persistence: it downregulates multiple host immune rece...

Ke-Quan Wang · 0 citations
Open access Aug 2026

A new HIV-1 latency reversing agent activating HIV-Tat

D10 is the first Tat activator available and the first LRA that targets an HIV protein, and induces strong HIV production by latent cell lines and latent cells from people living with HIV-1.

P. Tong, Laetitia Marty, Nawel Chekrit et al. · 0 citations
Review Open access Sep 2026

Molecular mechanisms of HIV-1 entry into host cells and emerging therapeutic strategies

The global HIV/AIDS pandemic continues to pose a major public health challenge, underscoring the need for improved mechanistic understanding of viral infection and therapeutic intervention. HIV-1 infection is initiated by a highly orchestrated entry process that represents the first and most decisive determinant of pro...

Lamarana Jallow, P. Quashie · 0 citations
Open access

Characterization of a CRISPR/Cas9-based molecular recorder for HIV-1

HIV-SCRIBE is developed, a CRISPR-based molecular recorder in which a self-targeting guide RNA locus is placed under a Tat-responsive minimal HIV-1 5'LTR promoter, coupling Cas9-mediated cleavage and error-prone repair to Tat-driven transcriptional activation to generate a durable molecular record of HIV-1 reactivation...

Nahia Urturi Ortiz, M. Nonnemacher, Brian Wigdahl · 0 citations
#gene editing Open access Aug 2026

Triple-Target CRISPR Strategy to Block HIV Entry and Replication in Permissive Cells

The combination knockout of CCR5, MOGS, and viral sequences profoundly reduces HIV-1 replication in an ex vivo cellular model, that is, HIV-1-infected peripheral blood mononuclear human cells, thus offering a pathway to launch further preclinical studies.

Z. Safaei, Anna Bellizzi, Hong Liu et al. · 0 citations

Biophysical Investigation into the Mechanisms Regulating HIV-1 Envelope Glycoprotein Incorporation

Human Immunodeficiency Virus type-1 (HIV-1) infects CD4+ T cells and remains a global pandemic due to our incomplete understanding of the molecular mechanisms underlying its highly coordinated and regulated assembly process and the strategies it uses for immune evasion. For HIV-1 to produce infectious particles, the vi...

Austin R. Clark · 0 citations

We use cookies to run the site and, with your consent, for analytics and to show ads. See our Cookie Policy.