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. 2007 Jun;39(2):119-24.
doi: 10.1016/j.jcv.2007.03.009. Epub 2007 Apr 23.

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

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

Giulia Campanini et al. J Clin Virol. 2007 Jun.

Abstract

Background: 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.

Objectives: hRSV was detected by quantitative reverse transcription-PCR in NPAs taken upon admission to hospital and, whenever possible, at discharge and subsequent medical visits.

Study design: Prospective study, including 63 infants affected by either hRSV upper or lower ARTI.

Results: 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.

Conclusions: hRSV RNA quantification is critical in defining the hRSV role in respiratory infections.

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Figures

Fig. 1
Fig. 1
Sensitivity of the quantitative RT-PCR method in detecting: (A) hRSV subgroup A plasmid; (B) hRSV subgroup B plasmid dilutions; and (C): C+, C and plasmid subgroup A dilutions used for quantification; lanes 1–10: clinical subgroup A (lanes 3, 4, 5, 8, and 9) and B (lanes 1 and 6) strains. (D) Quantification curve. MW, molecular weight markers; N (lanes 2, 7, 10), negative samples; RNA Ic, armored RNA internal control; C+, positive control; C, negative control.
Fig. 2
Fig. 2
Individual and median levels of viral load in the four groups of infants examined upon admission to hospital and during follow-up. For group IV, both minimal and maximal viral loads observed in NPAs during the follow-up period of six infants are reported.

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