Respiratory Syncytial Virus (RSV) is a common pathogen causing respiratory tract infections and is a leading cause of hospitalizations in infants and older adults worldwide. It is responsible for seasonal outbreaks of lower respiratory tract illnesses, such as bronchiolitis and pneumonia, particularly in vulnerable populations. Understanding the history of its recognition reveals how this mid-twentieth-century mystery ailment was identified and how scientific efforts have focused on prevention.
The Decade of Discovery
The pathogen now known as Respiratory Syncytial Virus was first identified in the mid-1950s. Its initial isolation occurred in 1956 during an investigation into an outbreak of coryza, or common cold-like symptoms, among a colony of laboratory chimpanzees. Researchers recovered a novel agent from these animals and initially named it the Chimpanzee Coryza Agent (CCA).
The crucial connection to human disease was established in 1957 by virologist Robert M. Chanock. Chanock and his colleagues found that the CCA was indistinguishable from a virus isolated from human infants suffering from severe respiratory illnesses. This confirmed that the chimpanzee agent was the cause of serious lower respiratory tract disease in children, identifying the viral culprit previously known only by its symptoms.
How the Virus Got Its Name
The virus was named Respiratory Syncytial Virus based on a unique characteristic of its interaction with host cells. The term “syncytial” refers to its ability to cause infected cells to fuse together, creating a large, abnormal, multinucleated mass known as a syncytium. This cellular fusion is a direct result of the fusion protein (F protein), one of the virus’s surface proteins, which merges the viral envelope with the cell membrane.
When the F protein is expressed on the surface of an infected cell, it causes that cell to merge with its neighbors. This process results in the formation of a single giant cell containing the nuclei of multiple fused cells, visible under a microscope. This distinct cytopathic effect provided the descriptive classification for the pathogen.
Timeline of Prevention Methods
Following its discovery, early medical efforts focused primarily on supportive care, such as oxygen therapy and mechanical ventilation, to manage severe symptoms in hospitalized infants. A major setback occurred in the 1960s when a formalin-inactivated vaccine resulted in enhanced disease upon natural infection in vaccinated children. This event delayed the development of safe and effective preventative measures for decades.
A significant breakthrough came in the late 1990s with the introduction of the monoclonal antibody Palivizumab. This injectable offered passive immunity by directly targeting and neutralizing the RSV F protein. However, it required monthly injections throughout the RSV season. Due to its cost and complex regimen, Palivizumab was reserved mostly for high-risk populations, such as premature infants and those with chronic heart or lung conditions.
The year 2023 marked a turning point with the approval of multiple new preventative tools. A single-dose, long-acting monoclonal antibody, Nirsevimab, was licensed for all infants entering their first RSV season, offering simpler, season-long protection. This new antibody binds to the prefusion form of the F protein and has a longer half-life than Palivizumab.
The first RSV vaccines were also approved for specific populations, including older adults and pregnant women. The maternal vaccine is administered during late pregnancy, transferring protective antibodies to the fetus and providing passive immunity to the newborn for the first six months of life. These recent developments represent the first successful preventative strategies to protect infants and the elderly since the virus was identified nearly 70 years ago.