Respiratory Syncytial Virus (RSV) is a widespread virus that causes respiratory tract infections. While anyone can be infected, it poses a particular risk to infants, young children, older adults, and those with weakened immune systems. For these groups, the virus is a primary cause of lower respiratory tract illnesses like pneumonia and bronchiolitis. Understanding the molecular biology of RSV is foundational for developing effective methods to diagnose, prevent, and treat the illnesses it causes.
The Viral Blueprint
The genetic instructions for RSV are encoded in a single strand of ribonucleic acid (RNA), distinguishing it as an RNA virus. This genetic material is housed within a protective envelope, a lipid membrane taken from a previously infected host cell. Embedded within this envelope are proteins fundamental to infection, the most significant being the Attachment (G) protein and the Fusion (F) protein. These are glycoproteins, meaning they have sugar molecules attached that can help shield them from the host’s immune system.
The G protein’s primary function is to locate and bind to specific cells in the human airway, initiating the infection process. Following this attachment, the F protein takes over. It is a type I fusion protein that can change its shape dramatically to merge the viral envelope with a host cell’s membrane, delivering the RNA genome into the cell’s interior.
The Infection Process
An RSV infection begins when a virus particle, transmitted through respiratory droplets, reaches the epithelial cells lining the nasopharynx. The virus’s G protein facilitates docking onto the host cell by binding to receptors on the cell surface, bringing the virus into close contact with the cell.
Once anchored, the F protein initiates membrane fusion. It undergoes a significant conformational change that exposes a fusion peptide, which inserts into the host cell’s membrane. The protein then refolds, pulling the viral envelope and the cell membrane together until they merge, allowing the viral RNA to enter the cytoplasm.
Inside the host cell, RSV hijacks the cell’s molecular machinery. The viral RNA is used as a template by an enzyme, RNA polymerase, to produce more copies of the viral genome and to create messenger RNA (mRNA). This mRNA is then read by the host’s ribosomes to synthesize new viral proteins, which assemble into new virus particles.
A defining characteristic of RSV infection is its method of spreading directly between cells. The F protein on an infected cell’s surface can trigger fusion with adjacent cells. This cell-to-cell fusion results in large, multinucleated cell masses known as syncytia, which contribute to the airway obstruction and inflammation of severe RSV disease.
The Body’s Molecular Defense
The body’s initial defense against RSV is the innate immune system, which provides a rapid response. When a cell detects viral RNA, it triggers the release of signaling molecules called interferons. These interferons alert neighboring cells to heighten their antiviral defenses to limit the spread of the infection.
Following the innate response, the adaptive immune system mounts a more targeted and lasting defense. This involves generating antibodies designed to recognize and neutralize the virus, primarily by targeting the F and G proteins. The F protein is highly conserved across RSV strains, making it a reliable target, while the G protein’s variability can help the virus evade pre-existing immunity.
While antibodies neutralize free-floating virus, another branch of the adaptive immune system deals with cells that are already infected. T-cells, a type of white blood cell, are trained to recognize viral proteins displayed on the surface of infected cells. Upon recognition, these T-cells directly kill the infected cells, preventing them from producing more virus and helping to clear the infection.
Molecular Tools for Detection and Treatment
The understanding of RSV’s molecular composition has led to precise tools for its diagnosis. The most sensitive method is the Polymerase Chain Reaction (PCR) test. This technique works by detecting the virus’s specific RNA sequence in a patient sample and amplifying it to detectable levels for reliable identification.
This molecular knowledge also underpins modern strategies for preventing severe RSV disease. Therapies using monoclonal antibodies, which are laboratory-produced antibodies, are an important preventative measure. Products like palivizumab and nirsevimab are composed of antibodies specifically engineered to target the conserved RSV F protein.
These therapeutic antibodies are administered to high-risk infants to provide passive immunity. They circulate in the bloodstream and bind to the F protein of any entering virus. This binding action physically obstructs the F protein, preventing the shape change required to fuse the viral and host cell membranes. By blocking this step, the antibodies neutralize the virus before it can establish an infection.