trimeric form and contains the major antigenic site ø. ø serves as a primary target of neutralizing antibodies in the body. after binding to its target on the host cell surface (its exact ligand remains unclear), pref undergoes a conformational change during which ø is lost. this change enables the protein to insert itself into the host cell membrane and leads to fusion of the viral and host cell membranes. a final conformational shift results in a more stable and elongated form of the protein (postfusion, postf). opposite of the rsv g protein, the rsv f protein also binds to and activates toll-like receptor 4 (tlr4), initiating the innate immune response and signal transduction.schematic image of rsv life cycle replication cycle following fusion of the viral and host cell membranes, the viral nucleocapsid (containing the viral genome) and the associated viral polymerase are delivered into the host cell cytoplasm. transcription and translation both occur within the cytoplasm. rna-dependent rna polymerase transcribes the genome into 10 segments of messenger rna (mrna) which is translated into structural proteins by host cell machinery. during replication of the negative-sense viral genome, rna-dependent rna polymerase synthesizes a positive-sense complement called the antigenome. this complementary strand is used as a template to construct genomic negative-sense rna, which is packaged into nucleocapsids and transported to the plasma membrane for assembly and particle budding. mechanism transmission rsv is highly contagious and can cause outbreaks from both community and hospital transmission. for each person infected with rsv, it is estimated that an average of 5 to 25 uninfected people will become infected. rsv can spread when an infected person coughs or sneezes, releasing contaminated droplets into the air. transmission usually occurs when these droplets come into contact with another person's eyes, nose, or mouth. rsv can also live for up to 25 minutes on contaminated skin (i.e. hands) and several hours on other surfaces like countertops and doorknobs. it has an incubation period of 2 to 8 days. once infected, people are usually contagious for 3 to 8 days. in infants and in people with weakened immune systems, however, the virus may continue to spread for up to 4 weeks (even after they are no longer showing symptoms). lumen of an obstructed bronchiole containing cellular debris and aggregates of sloughed epithelial cells pathogenesis following transmission through the nose or eyes, rsv infects ciliated columnar epithelial cells of the upper and lower airway. rsv continues to replicate within these bronchial cells for about 8 days. after the first several days, rsv-infected cells will become more rounded and ultimately slough into the smaller bronchioles of the lower airway. this sloughing mechanism is also thought to be responsible for the spread of virus from the upper to lower respiratory tract. infection causes generalized inflammation within the lungs, including the migration and infiltration of inflammatory cells (such as monocytes and t-cells), necrosis of the epithelial cell wall, edema, and increased mucous production. inflammation and cell damage tends to be patchy rather than diffuse. together, the sloughed epithelial cells, mucous plugs, and accumulated immune cells cause obstruction of the lower airway. diagnosis laboratory diagnosis a variety of laboratory tests are available for the diagnosis of rsv infection. while the american academy of pediatrics (aap) does not routinely recommend the use of lab testing to diagnosis rsv bronchiolitis (for which the treatment is largely supportive), confirmation of rsv infection may be warranted in high-risk groups if the result will guide clinical decisions. common identification techniques include antigen testing, molecular testing, and viral culture. antigen testing antigen testing involves detection of rsv antigen fragments (or pieces of molecular viral structures), usually from an nasopharyngeal swab or aspirate. this can be accomplished either by viewing fluorescently labeled antigens under a microscope (direct fluorescence assay, or dfa) or using a commercially available rapid antigen detection test (radt). overall, antigen testing is highly sensitive in young children (80–90%) but substantially less reliable in older children and adults, who have less viral shedding. antigen tests are also subject to higher false positive rates outside of the peak rsv season, such as in the summer months. in these scenarios, the use of either viral culture or nucleic acid amplification testing (naat) may aid in an accurate rsv diagnosis. rapid antigen detection tests (radt) are commonly used as point-of-care testing due to their ease of use and quick turnaround time (as little as 10 minutes). these include both enzyme immunosorbent assays (eia) and chromatographic immunoassays (cia). direct fluorescence assay (dfa) allows for direct microscopic examination of virus-infected cells. the sensitivity of dfa testing depends on an adequate specimen. molecular testing molecular assays, such as nucleic acid amplification tests (naats), enable sensitive detection of very small amounts of virus in nasopharyngeal swabs and aspirates. naat assays such as polymerase chain reaction (pcr) detect virus-specific genetic material, rather than viral antigens. they have a sensitivity and specificity approaching 100%. however, they tend to be more expensive and require more complex equipment than other testing methods, making them less practical in resource limited areas. polymerase chain reaction (pcr) is type of naat which allows a very small sample of genetic material to be rapidly amplified into millions of copies for study. pcr is more sensitive than either antigen testing or viral culture. therefore, it can be used to detect virus in those with lower viral shedding, such as older children and adults. it may also be used to detect the disease earlier in at-risk individuals (such as hospitalized or immunocompromised patients), when the viral burden may still be too low to be identified by traditional techniques. because of its sensitivity, pcr can also often detect asymptomatic carriers and may remain positive even days after an infection has clinically resolved. multi-pathogen panels are also available, which can detect the presence of multiple viral infections (including rsv) in a single patient. viral culture in traditional viral culture, a sample of the virus is introduced to different cell lines and allowed to replicate so it can be studied. benefits of this technique include the ability to perform genetic characterization, strain typing, and antiviral susceptibility testing. however, it is limited by its prolonged turnaround time of 3–7 days, making it less common in patient care and more common in research settings. serologic testing serology (the measurement of virus-specific antibodies in the serum) is not frequently used in rsv diagnosis. the time required for the body to mount a significant serologic response (and demonstrate a significant rise in antibodies that can be detected in serum) is usually not useful in guiding patient care. up to 30% of patients with documented rsv infection will have negative serology results. as such, this method is generally reserved for research and surveillance studies. imaging findings x-ray of a child with rsv bronchiolitis showing the typical bilateral perihilar fullness chest x-rays findings in children with rsv bronchiolitis are generally nonspecific and include perihilar markings, patchy hyperinflation, and atelectasis. however, the american academy of pediatrics (aap) does not recommend routine imaging for children with presumed rsv bronchiolitis because it does not change clinical outcomes and is associated with increased antibiotic use. chest x-ray is sometimes considered when the diagnosis of bronchiolitis is unclear or when there is an unexpected worsening. in adults with rsv infection, chest films are often normal or demonstrate nonspecific changes consistent with viral pneumonia, such as patchy bilateral infiltrates. differential diagnosis the differential diagnosis for individuals presenting with signs and symptoms of upper and lower respiratory tract infection includes other viral infections (such as rhinovirus, metapneumovirus, and influenza) and primary bacterial pneumonia. in children, inhaled foreign bodies and congenital conditions such as cystic fibrosis or asthma should also be considered. prevention general prevention measures the main prevention measure is to avoid close contact with infected individuals. in community and daycare settings, careful hand washing can help reduce transmission. in hospital settings, strict adherence to infection control measures can help prevent the spread of rsv to high-risk individuals. alcohol-based disinfectants are recommended for hand decontamination. immunoprophylaxis