Respiratory Syncytial Virus (RSV): Overview and Key Facts

Respiratory Syncytial Virus (RSV) is a virus that primarily causes respiratory infections, especially in the lower respiratory tract. It is a major cause of such infections in infants and young children. The virus tends to spread widely during winter in temperate climates and during the rainy season in tropical regions.

Classification

RSV belongs to the Pneumovirus genus of the Paramyxoviridae family. The virus gets its name from the ability of its surface F protein to induce fusion between the membranes of adjacent cells, leading to the formation of large multinucleated cells or syncytia.

Structure

RSV is an enveloped virus with a diameter ranging from 120 to 200 nm. Its envelope consists of lipoproteins, primarily the F (fusion), G (attachment), and SH proteins. The F and G proteins are crucial for the virus to bind and fuse with host cells, allowing infection.

Genome

RSV has a single-stranded negative-sense RNA genome consisting of approximately 15,000 nucleotides. It encodes 10 genes that translate into 11 proteins. Four viral proteins, including nucleoprotein (N), phosphoprotein (P), matrix protein (M), and large protein (L), are essential for the transcription, replication, and budding of the virus. The RNA genome forms a ribonucleoprotein (RNP) complex, which serves as a template for RNA synthesis. To date, 10 genotypes of HRSV-A (GA1-GA7, SAA1, NA1, NA2) and various HRSV-B genotypes (GB1-GB4, SAB1-SAB3, BA1-BA6) have been identified.

Replication and Life Cycle

RSV enters host cells by fusing with the cell membrane, a process initiated by the G protein binding to extracellular matrix components called glycosaminoglycans (GAGs). The F protein interacts with the RhoA protein, facilitating viral attachment. Once inside the cell, the virus releases its nucleocapsid and genome into the cytoplasm, where replication and gene expression take place. The M2-2 gene regulates the switch from transcription to genome RNA synthesis, with the polymerase binding to the 3' end of the genome. The viral genes are transcribed into mRNA, which follows a start-stop-restart mechanism. Replication produces a complementary positive-strand RNA, called the antigenome, which serves as a template for creating new viral genomes. Both the genome and antigenome are coated with N proteins, preparing them for further RNA synthesis. The matrix (M) protein regulates viral assembly, interacting with F, G, and nucleocapsid proteins to form mature viruses that bud off from the cell membrane.

Diagnosis, Transmission, and Epidemiology

RSV's incubation period is typically 4 to 6 days, though it can range from 2 to 8 days. The virus spreads easily through direct contact, and it can survive for extended periods on surfaces like hands and countertops. In childcare settings, the virus can spread rapidly between infants. RSV is identical to the coryza virus in chimpanzees, and transmission between humans and primates is common. While RSV has been isolated from animals like cattle, sheep, and goats, these are not considered significant transmission vectors. The virus can persist for 2 to 8 days, but symptoms may last up to 3 weeks.

Prevention and Treatment

Although RSV is widespread globally, complete prevention is difficult. However, a monoclonal antibody treatment, Palivizumab, can be used for high-risk infants. Palivizumab targets the F protein of RSV and is administered before RSV season to prevent infection in infants with premature birth, heart, or lung conditions. Its high cost limits its use. Currently, treatment options for RSV are largely supportive. Medications such as epinephrine, bronchodilators, steroids, antibiotics, and ribavirin have shown limited efficacy. Salbutamol may be helpful in cases with bronchospasm, and nasal cannulas can be used to increase airflow and moisture for patients experiencing respiratory distress.