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1 toms and airway inflammation associated with rhinovirus infection.
2 s at baseline and on day 4 and 6 weeks after rhinovirus infection.
3 ng mostly children without wheezing and with rhinovirus infection.
4 S-CoV-2 circulation and were also present in rhinovirus infection.
5  are associated with adverse outcomes during rhinovirus infection.
6 erase chain reaction-confirmed SARS-CoV-2 or rhinovirus infection.
7 o died from respiratory failure with chronic rhinovirus infection.
8 abs (n = 165 participants) during and before rhinovirus infection.
9 s talk between AECs and MCs after epithelial rhinovirus infection.
10 asthma hospitalizations independent of human rhinovirus infection.
11 y subjects and treated with anti-IL-33 after rhinovirus infection.
12 n the asthmatic and healthy airways during a rhinovirus infection.
13  specific IgE antibodies was detected during rhinovirus infection.
14 ness, and reductions in lung function during rhinovirus infection.
15 pithelial PRR expression were induced during rhinovirus infection.
16 elates to exacerbations of asthma related to rhinovirus infection.
17 models of allergic airways disease and human rhinovirus infection.
18  of clinical illness that is associated with rhinovirus infection.
19 as been the lack of a small-animal model for rhinovirus infection.
20 -dominated assemblages increased the risk of rhinovirus infection.
21 xtracts from Echinacea angustifolia roots on rhinovirus infection.
22 th and the development of a murine model for rhinovirus infection.
23 f URT infections or symptoms associated with rhinovirus infection.
24 in nasal samples in natural and experimental rhinovirus infections.
25 l defense genes; 22 of these were induced by rhinovirus infections.
26 014) and were at 2.2-fold increased risk for rhinovirus infections.
27 with asthma experience more severe/prolonged rhinovirus infections.
28        Asthma exacerbations are triggered by rhinovirus infections.
29 infection by RSV group B, and no prior human rhinovirus infections.
30 d cost-effective means to reduce the risk of rhinovirus infections.
31 l during H1N1 infections compared with human rhinovirus infections (38 vs. 21%; odds ratio, 2.6; 95%
32 erval, 1.8-9; P < 0.001), but rates of human rhinovirus infection (90% each) and other viral infectio
33 depletion after allergen challenge or during rhinovirus infection abrogated exacerbation of inflammat
34                                    Following rhinovirus infection, all subjects developed nasal sympt
35 , which was induced by allergen challenge or rhinovirus infection and conditioned pDCs for proinflamm
36 e the protection of epithelial cells against rhinovirus infection and damage.
37 lation and again on Days 5, 15, and 42 after rhinovirus infection and DNA was extracted.
38        We used a human experimental model of rhinovirus infection and novel airway sampling technique
39 with exacerbation as the primary outcome and rhinovirus infection and respiratory illnesses as second
40 ent study collected individual data on human rhinovirus infection and sensitization to Alternaria and
41 f host double-stranded DNA (dsDNA) following rhinovirus infection and the exacerbation of type-2 alle
42 um was collected before and repeatedly after rhinovirus infection and virus and bacterial loads measu
43  methylated regions exhibit interaction with rhinovirus infection and/or specific blood cell types.
44 d by a history of wheezing and/or eczema and rhinovirus infection) and risk of development childhood
45 ma relate to the likelihood of exacerbation, rhinovirus infection, and respiratory illnesses during t
46 SV respiratory virus infection, asymptomatic rhinovirus infection, and virus-negative asymptomatic co
47            Deficient interferon responses to rhinovirus infection are present in childhood in asthmat
48                                              Rhinovirus infections are frequently followed by seconda
49       Infant respiratory syncytial virus and rhinovirus infections are known to be associated with an
50                                              Rhinovirus infections are the dominant cause of asthma e
51        Respiratory syncytial virus (RSV) and rhinovirus infections are the most common significant in
52                                              Rhinovirus infection at an early age has been associated
53 udies found that, during poliovirus or human rhinovirus infection, AUF1 is cleaved by the viral prote
54                                              Rhinovirus infection before SARS-CoV-2 exposure accelera
55 dren with histories of wheezing illness with rhinovirus infection before the third birthday had lower
56 ed in response to interferon stimulation and rhinovirus infection, but not SARS-CoV-2 infection.
57                                              Rhinovirus infections cause exacerbations of asthma.
58 m people with asthma are more susceptible to rhinovirus infection caused by deficient induction of th
59 vels of SRp20 relocalization observed during rhinovirus infection compared to poliovirus.
60 ated with increased severity and duration of rhinovirus infection compared with healthy subjects, sup
61 s a proinflammatory cytokine up-regulated by rhinovirus infection during acute exacerbations of asthm
62                       Clinically significant rhinovirus infection during infancy was more strongly as
63                                              Rhinovirus infection enhances detection of specific bact
64 mportant implications in the pathogenesis of rhinovirus infections, especially initiation of the host
65  SLPI and elafin significantly reduced after rhinovirus infection exclusively in subjects with COPD w
66                             Early-life human rhinovirus infection has been linked to asthma developme
67 s of the cytokine dysregulation that follows rhinovirus infection have implicated monocytic lineage c
68 daptive capacity (AC) during an experimental rhinovirus infection in 24 healthy and asthmatic human v
69 ue of the lungs has been demonstrated during rhinovirus infection in allergic individuals.
70 ron and PRR expression at baseline and after rhinovirus infection in atopic asthmatic patients and co
71 y increased IgE responsiveness 3 weeks after rhinovirus infection in atopic asthmatics.
72                            The prevalence of rhinovirus infection in children is high and presents a
73  airway interferon production in response to rhinovirus infection in children who are asthmatic, atop
74 on of tICAM453 was efficacious in preventing rhinovirus infection in chimpanzees subsequently challen
75                    Our findings suggest that rhinovirus infection in COPD alters the respiratory micr
76 ificantly reduced IL-6 and CXCL8 response to rhinovirus infection in COPD bronchial epithelial cells.
77 e to viral infection in experimental in vivo rhinovirus infection in healthy controls and patients wi
78 nse of circulating B cells upon experimental rhinovirus infection in healthy individuals and asthma p
79 s have features similar to those observed in rhinovirus infection in humans, including augmentation o
80 ate lymphoid cells (ILC2s) was expanded with rhinovirus infection in neonatal but not mature mice.
81                   Compared with mature mice, rhinovirus infection in neonatal mice increased lung IL-
82                           Here, we show that rhinovirus infection in patients with asthma leads to an
83                    Nevertheless, the role of rhinovirus infection in the initiation of asthma remains
84                            Participants with rhinovirus infection in the previous 30 days were at 48%
85 asthma exacerbation-related cytokines and by rhinovirus infection in vitro.
86 effects of inhaled fluticasone propionate on rhinovirus infection in vivo, in a mouse model.
87 ociated with adverse clinical outcomes after rhinovirus infection in vivo.
88       We sought to examine the prevalence of rhinovirus infections in relation to the atopic status o
89                                              Rhinovirus infection-increased numbers of subepithelial
90                                              Rhinovirus infection induced a dose- and time-dependent
91 nd polyinosinic-polycytidylic acid and human rhinovirus infection induced a potent antiviral protecti
92                   In parallel, we found that rhinovirus infection induced a rapid increase of intrace
93                                              Rhinovirus infection induced a time- and dose-dependent
94                                              Rhinovirus infection induced an amplified antiviral T(H)
95                                              Rhinovirus infection induced Il25, Il33, Il4, Il5, Il13,
96 lly-occurring exacerbations we identify that rhinovirus infection induces airway NET formation which
97                We sought to evaluate whether rhinovirus infection interferes with the mechanisms of a
98 P = .02), and risk allele in CDHR3 gene with rhinovirus infections (IRR, 1.10; 95% CI, 1.01-1.20, P =
99 dence that early activation of p38 kinase by rhinovirus infection is a key event in regulation of vir
100                                              Rhinovirus infection is a leading cause of exacerbation
101        Along with other respiratory viruses, rhinovirus infection is also a cause of exacerbations of
102                                              Rhinovirus infection is followed by significantly increa
103                                              Rhinovirus infection is now recognized as an important c
104        However, the inflammatory response to rhinovirus infection is poorly understood.
105                                     Frequent rhinovirus infections may enhance this protective gene p
106 respiratory tract infection, including human rhinovirus infections, may lead to increased duration of
107 Here we describe three novel mouse models of rhinovirus infection: minor-group rhinovirus infection o
108                                              Rhinovirus infection of airway epithelium induces ICAM-1
109 sociated with viral load during experimental rhinovirus infection of asthmatic patients.
110  models of rhinovirus infection: minor-group rhinovirus infection of BALB/c mice, major-group rhinovi
111                                              Rhinovirus infection of human primary BECs induced IL-33
112 tory T (Treg) cells, and we examined whether rhinovirus infection of the respiratory tract can block
113                  To test the hypothesis that rhinovirus infection of the upper airway may be associat
114 ovirus infection of BALB/c mice, major-group rhinovirus infection of transgenic BALB/c mice expressin
115                To investigate the effects of rhinovirus infection on the intracellular redox balance,
116  to the understanding of systemic effects of rhinovirus infections on B-cell responses in the periphe
117 layed an immune trajectory like that seen in rhinovirus infection or checkpoint inhibitor therapy for
118                                              Rhinovirus infection or dsRNA stimulation increased thym
119 among asymptomatic controls with presence of rhinovirus infection (OR, 4.23 [95% CI, 1.16-14.22]; P <
120 among asymptomatic controls with presence of rhinovirus infection (OR:4.23; 95%CI 1.16-14.22, p<0.05)
121 tures than does rhinovirus, and heterologous rhinovirus infection, or treatment with recombinant IFN-
122 ovirus RNA shedding, duration or severity of rhinovirus infections, or occurrence of rhinovirus RNA i
123 rial infections, but it is not known whether rhinovirus infections precipitate secondary bacterial in
124 r eczema, wheezing during acute illness, and rhinovirus infection; profile BC (38%), characterized by
125  and non-respiratory syncytial virus (mostly rhinovirus) infection; profile B (49%), which has the la
126                                        After rhinovirus infection, secondary bacterial infection was
127 ith atopic asthma are not at greater risk of rhinovirus infection than healthy individuals but suffer
128 t people with asthma are more susceptible to rhinovirus infection than people without the disease and
129  epidemiology and clinical manifestations of rhinovirus infection that have occurred as a result of t
130                                        After rhinovirus infection, there is a rise in bacterial burde
131                             At 15 days after rhinovirus infection, there was a sixfold increase in 16
132 del was validated by exposing the SAECs to a rhinovirus infection, to an inflammatory lung insult usi
133                                              Rhinovirus infection triggers acute asthma exacerbations
134 lergic airway hypersensitivity, we show that rhinovirus infection triggers dsDNA release associated w
135 lular redox balance, we also studied whether rhinovirus infection triggers the production of reactive
136                                        First rhinovirus infection was associated more frequently with
137 rticipants with SARS-CoV-2 infection, recent rhinovirus infection was associated with 9.6-fold lower
138 o contribute to the symptoms and sequelae of rhinovirus infection, we investigated the role of p38 ki
139                       Following experimental rhinovirus infection, we observed increased respiratory
140              Symptoms of LRT associated with rhinovirus infection were significantly more severe (p=0
141 fficient for neutrophilic inflammation after rhinovirus infection, whereas macrophages treated with I
142                The innate immune response to rhinovirus infection, which may play an important role i
143                                              Rhinovirus infections, which trigger increased expressio
144 ene-environment interactions (GEIs), such as rhinovirus infections, will improve detection of asthma

 
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