# A contemporary strain of RSV activates primary human monocytes after abortive infection

## TL;DR

This study shows that RSV can activate human monocytes, leading to increased inflammation and immune responses.

## Contribution

The study reveals that RSV infection activates monocytes through abortive infection, promoting cytokine and chemokine secretion.

## Key findings

- Primary monocytes and THP-1 cells are permissive to abortive RSV infection.
- RSV infection increases proinflammatory cytokines like IP-10, IL-6, and CCL2.
- Monocytes express CD80, CD86, and HLA-DR after RSV infection or paracrine stimulation.

## Abstract

Respiratory syncytial virus (RSV) is a leading cause of lower respiratory tract infections worldwide, particularly affecting infants, older adults, and immunocompromised individuals. Understanding the cellular immune response to RSV infection is essential for developing effective treatments for infection and its complications. In this study, we investigated the susceptibility of blood-derived primary monocytes and monocytic THP-1 cells to infection with a contemporary RSV A-ON1 strain and characterized the subsequent cytokine and chemokine secretion, as well as the expression of surface markers involved in antigen presentation. Our findings demonstrate that primary monocytes and related THP-1 cells are permissive to abortive infection by RSV, leading to increased expression of proinflammatory cytokines and chemokines, including IP-10, IL-6, and CCL2. Furthermore, primary monocytes expressed CD80, CD86, and HLA-DR upon direct infection or through potential paracrine stimulation. Collectively, these findings demonstrate the activation of monocytes by RSV infection, suggesting their contributory role in orchestrating early immune responses during infection.