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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 PLoS+One
2017 ; 12
(3
): e0172953
Nephropedia Template TP
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English Wikipedia
The interdependencies of viral load, the innate immune response, and clinical
outcome in children presenting to the emergency department with respiratory
syncytial virus-associated bronchiolitis
#MMPMID28267794
Piedra FA
; Mei M
; Avadhanula V
; Mehta R
; Aideyan L
; Garofalo RP
; Piedra PA
PLoS One
2017[]; 12
(3
): e0172953
PMID28267794
show ga
Respiratory syncytial virus (RSV) causes significant infant morbidity and
mortality. For decades severe RSV-induced disease was thought to result from an
uncontrolled host response to viral replication, but recent work suggests that a
strong innate immune response early in infection is protective. To shed light on
host-virus interactions and the viral determinants of disease, copy numbers of
five RSV genes (NS1, NS2, N, G, F) were measured by quantitative real-time
polymerase chain reaction (qPCR) in nasal wash samples from children with
RSV-associated bronchiolitis. Correlations were sought with host
cytokines/chemokines and biomarkers. Associations with disposition from the
emergency department (hospitalized or sent home) and pulse oximetry O2 saturation
levels were also sought. Additionally, RNase P copy number was measured and used
to normalize nasal wash data. RSV gene copy numbers were found to significantly
correlate with both cytokine/chemokine and biomarker levels; and RNase
P-normalized viral gene copy numbers (NS1, NS2, N and G) were significantly
higher in infants with less severe disease. Moreover, three of the normalized
viral gene copy numbers (NS1, NS2, and N) correlated significantly with arterial
O2 saturation levels. The data support a model where a higher viral load early in
infection can promote a robust innate immune response that protects against
progression into hypoxic RSV-induced lower respiratory tract illness.