Human respiratory syncytial virus (hRSV) RNA quantification in nasopharyngeal secretions identifies the hRSV etiologic role in acute respiratory tract infections of hospitalized infants.

Human respiratory syncytial virus (hRSV) detection in nasopharyngeal aspirates (NPAs) from infants with acute respiratory tract infection (ARTI) does not prove the hRSV etiology of the current ARTI episode. HRSV RNA quantification may help in affording this issue. hRSV was detected by quantitative reverse transcription-PCR in NPAs taken upon admission to hospital and, whenever possible, at discharge and subsequent medical visits. Prospective study, including 63 infants affected by either hRSV upper or lower ARTI. Based on the kinetics of viral load, hRSV etiology was identified in 25 infants in whom hRSV load dropped from 2.5 x 10(6) upon admission (presence of respiratory symptoms) to 7.5 x 10(2)RNAcopies/ml NPA upon discharge (absence of symptoms) after a median time of 5 days, and in 19 infants, in whom hRSV load was determined at admission only, in association with clinical symptoms (2.4 x 10(6)copies/ml). Furthermore, low levels of hRSV RNA (<1 x 10(5)copies/ml NPA) identified 14 patients with non-hRSV ARTI. Finally, in 14 infants with hRSV coinfections or sequential infections, hRSV quantification defined the hRSV role in the current ARTI episode. hRSV RNA quantification is critical in defining the hRSV role in respiratory infections.