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Review
. 2025 Jul 31;39(14):e70858.
doi: 10.1096/fj.202500509RR.

Exploring Therapeutic Targets From Spreading Patterns Against Respiratory Syncytial Virus

Han Zhang  1   2 , Zhao Zhang  1   2 , Yixuan Yang  1   2 , Jingjing Pei  1   2
Affiliations
Review

Exploring Therapeutic Targets From Spreading Patterns Against Respiratory Syncytial Virus

Han Zhang et al. FASEB J. .

Abstract

Human respiratory syncytial virus (RSV) is a pathogen that causes severe respiratory illness in humans, primarily infecting infants, young children, the elderly, and adults with chronic health conditions. Each year, approximately 3.6 million children under the age of 5 are hospitalized worldwide, with over 100 000 fatalities reported. Currently, available RSV vaccines and antiviral drugs have several limitations, including inadequate immune persistence, limited applicability to specific populations, strict timing of treatment, and the risk of adverse reactions. RSV spreads through three main infection modes: syncytia formation, receptor-dependent infection of free viral particles, and transmission via actin filaments. These modes of transmission are key pathways that contribute to viral spread and pathogenicity while exposing potential targets for prevention and treatment. This is a complex process involving multiple aspects that remain not fully understood. Here, we review the mechanisms by which RSV infects and spreads within the host and explore the role of host factors in these processes, aiming to provide a theoretical and practical basis for identifying potential antiviral targets.

Keywords: respiratory syncytial virus (RSV); spreading patterns; therapeutic targets; viral protein receptor.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

FIGURE 1
FIGURE 1
The genetic and morphological structures of RSV. RSV is a complex virus with dual morphology. The left side is spherical in form, and the right side is filamentous in form.
FIGURE 2
FIGURE 2
The transmission model of receptor‐dependent infection of free viral particles. Two viral proteins, F and G, are involved in the adsorption process of RSV, where the G protein has three receptors in different host cells, including HSPG, CX3CR1, and CCR3, of which CX3CR1 and CCR3 are seven‐transmembrane proteins.
FIGURE 3
FIGURE 3
Mechanism of syncytial formation in RSV infection. (A) RSV infects the host cells. (B) Infected cells have F protein on their membrane surface. (C) Neighboring cells induce plasma membrane rearrangement and the fusion of cell membranes. (D) Cells ultimately undergo apoptosis, and viral particles are released.
FIGURE 4
FIGURE 4
Cell morphology changes during RSV infection. Actin filaments extend into broader, more continuous branches, forming channels that transport various substances. (A) Release of daughter virus particles through actin filament outgrowth. (B) Direct spread of RSV particles to other cells via intercellular bridges. (C) Activated ARP2/3 binds to the side branch of existing F‐actin, promoting the polymerization of branched actin filaments. The right side of the figure provides an enlarged view of the actin side branch, where the RSV M protein interacts with actin to facilitate the transport of viral particle components to the apical surface for release.
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