Respiratory Syncytial Virus Disease

RSV enters through the nasal mucosa via respiratory droplets. The viral envelope's G protein binds to cellular receptors on ciliated epithelial cells, while the F protein initiates fusion between viral and host membranes. This fusion allows the viral nucleocapsid to enter the host cell cytoplasm, beginning the infection cycle.

After entry, RSV transcribes its RNA genome into mRNA, directing viral protein production for capsid assembly and genome replication. The virus uses the host's cellular machinery to complete replication in the cytoplasm. New virions then bud off from the host cell membrane to infect neighboring cells.

The host immune system releases inflammatory cytokines in response to RSV, damaging the respiratory lining. This causes cellular debris and mucus accumulation in the airways, obstructing airflow and impairing normal breathing. Epithelial necrosis and mucus hypersecretion further reduce lung compliance and mucociliary clearance.

RSV is an enveloped virus with a lipid bilayer encasing a ribonucleoprotein core. Its viral envelope displays two critical glycoproteins: the attachment glycoprotein (RSV-G) for initial adherence to host cells, and the fusion glycoprotein (RSV-F) for membrane fusion. These surface proteins are essential for viral entry and immune recognition.

Although RSV primarily targets infants and young children, elderly and immunocompromised individuals also face serious health risks. In young children, severe lower respiratory tract involvement such as bronchiolitis is common and can progress to pneumonia or respiratory failure. Globally, millions of cases result in hospitalizations and mortality, particularly in resource-limited settings.

Monoclonal antibodies such as palivizumab and nirsevimab target the fusion protein to prevent cellular entry and viral spread. By blocking the F protein's function, these therapeutic agents reduce the virus's ability to fuse with host membranes and establish infection, offering prophylactic protection for high-risk populations.

Host immune responses include early polymorphonuclear infiltration followed by lymphomononuclear responses. Viral replication and immune-mediated cytotoxicity lead to epithelial necrosis and mucus hypersecretion. While these responses attempt to control infection, they also contribute to airway obstruction and reduced lung function, similar to complications seen in cytomegalovirus disease.