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• W2085688788 abstract "Respiratory viral infections, such as those from respiratory syncytial virus (RSV) or human rhinovirus (HRV), have been implicated in the development of asthma and atopic disease, as well as in causing asthma exacerbations.1Sly P.D. Kusel M. Holt P.G. Do early-life viral infections cause asthma?.J Allergy Clin Immunol. 2010; 125: 1202-1205Abstract Full Text Full Text PDF PubMed Scopus (111) Google Scholar However, the mechanisms through which viruses lead to atopic disease and asthma exacerbations remain elusive. By using a mouse model and the rodent parainfluenza virus type 1 (Sendai virus), we have shown that the development of postviral atopic disease requires cross-linking of FcεRI on lung dendritic cells by antiviral (ie, anti–Sendai virus) IgE.2Grayson M.H. Cheung D. Rohlfing M.M. Kitchens R. Spiegel D.E. Tucker J. et al.Induction of high-affinity IgE receptor on lung dendritic cells during viral infection leads to mucous cell metaplasia.J Exp Med. 2007; 204: 2759-2769Crossref PubMed Scopus (168) Google Scholar Human studies have documented that anti-RSV IgE is made as part of the antiviral response to RSV infection and that the level of IgE correlated with the subsequent risk for wheeze.3Welliver R.C. Wong D.T. Sun M. Middleton Jr., E. Vaughan R.S. Ogra P.L. The development of respiratory syncytial virus-specific IgE and the release of histamine in nasopharyngeal secretions after infection.N Engl J Med. 1981; 305: 841-846Crossref PubMed Scopus (415) Google Scholar Other viral infections appear to also drive antiviral IgE production, such as anti-H1N1 IgE, which was shown to persist even after clearance of the initial viral infection.4Smith-Norowitz T.A. Kusonruksa M. Wong D. Norowitz M.M. Joks R. Durkin H.G. et al.Long-term persistence of IgE anti-influenza A HIN1 virus antibodies in serum of children and adults following influenza A vaccination with subsequent H1N1 infection: a case study.J Inflamm Res. 2012; 5: 111-116Crossref PubMed Scopus (15) Google Scholar HRV is a nonenveloped, single-stranded RNA virus belonging to the family Picornaviridae and is one of the most prevalent respiratory viral pathogens associated with the development of asthma. In fact, in at least 1 study, HRV infection conferred a greater risk of asthma than did RSV.5Jackson D.J. Gangnon R.E. Evans M.D. Roberg K.A. Anderson E.L. Pappas T.E. et al.Wheezing rhinovirus illnesses in early life predict asthma development in high-risk children.Am J Respir Crit Care Med. 2008; 178: 667-672Crossref PubMed Scopus (1002) Google Scholar However, it is not known whether humans make antiviral IgE against HRV. Indirect evidence that anti-HRV IgE may play a role in asthma exacerbations comes from the recent Inner-City Anti-IgE Therapy for Asthma study, where removal of IgE by treatment with omalizumab markedly and significantly abrogated exacerbations of asthma.6Busse W.W. Morgan W.J. Gergen P.J. Mitchell H.E. Gern J.E. Liu A.H. et al.Randomized trial of omalizumab (anti-IgE) for asthma in inner-city children.N Engl J Med. 2011; 364: 1005-1015Crossref PubMed Scopus (706) Google Scholar Therefore, we hypothesized that part of the immune response to HRV would include the development of antiviral anti-HRV IgE. While HRV infection is ubiquitous, there are more than 150 HRV serotypes with many more distinct HRV strains circulating in the human population. These HRV strains belong to 3 genetic clades (A, B, and C). Rhinoviruses elicit serotype-specific antibody responses, and individuals are typically infected repeatedly with different strains.7Jartti T. Lee W.M. Pappas T. Evans M. Lemanske Jr., R.F. Gern J.E. Serial viral infections in infants with recurrent respiratory illnesses.Eur Respir J. 2008; 32: 314-320Crossref PubMed Scopus (155) Google Scholar To test our hypothesis and to avoid issues involving differences in serotypes, we used a laboratory strain of HRV (HRV-39, ATCC VR-340) that is not found naturally circulating, and developed an ELISA to detect anti-HRV39 specific IgE in the sera from subjects who had or did not have a history of being exposed to HRV39. The study protocol was approved by the institutional review board at the participating institutions, and peripheral blood was obtained following informed consent. HRV39 was propagated in HeLa cells to a concentration of 2 × 107 PFU/mL similar to what we have done with other Picornoviruses.8Richards A.L. Jackson W.T. Intracellular vesicle acidification promotes maturation of infectious poliovirus particles.PLoS Pathog. 2012; 8: e1003046Crossref PubMed Scopus (110) Google Scholar Ultraviolet-inactivated virus at a 1:10 dilution in PBS, or control (PBS alone), was fixed to the bottom of wells of 96-well enzyme immunoassay/radioimmunoassay (EIA/RIA) plates (Costar 9018) overnight at 4°C. After overnight incubation, the plates were washed with PBS/0.05% Tween 20, blocked with PBS and 10% FCS, and then incubated for 2 hours at room temperature with 0.1 mL subject serum samples. Serum of adult subjects with (n = 8) or without (n = 2) neutralizing antibodies to HRV39 was compared with cord blood serum (n = 4) from deidentified donors as a negative control.9Proud D. Gwaltney Jr., J.M. Hendley J.O. Dinarello C.A. Gillis S. Schleimer R.P. Increased levels of interleukin-1 are detected in nasal secretions of volunteers during experimental rhinovirus colds.J Infect Dis. 1994; 169: 1007-1013Crossref PubMed Scopus (129) Google Scholar Five subjects had an atopic history (2 with allergic rhinitis, 1 with mild asthma, 1 with atopic dermatitis and allergic rhinitis, and 1 asymptomatic with a history of positive skin testing), and 3 of these had neutralizing antibodies to HRV39 (the 3 subjects with a history of allergic rhinitis). The plates were then washed and incubated for an additional hour at room temperature with 0.1 mL of biotin-labeled goat anti-human IgE (Kirkegaard and Perry 16-10-04) diluted 1:500 in PBS/10%FCS. Following an additional washing, 0.1 mL of ExtraAvidin-Peroxidase (Sigma, St Louis, Mo; E2886) diluted 1:500 in PBS/10%FCS was added and incubated for 30 minutes. Tetramethylbenzidine was then used to develop the staining, and the resulting OD at 450 nm was read on a plate reader (Bio-Tek Instruments, Winooski, Vt; ELx808 Absorbance Microplate Reader). Total serum IgE level in the subject's serum was also determined by using a commercially available ELISA kit (eBioscience, San Diego, Calif; 88-50610-22) according to the manufacturer's instructions. As shown in Fig 1, A, anti-HRV39 IgE could be detected in all samples to varying degrees. Importantly, this was specific and dose dependent (Fig 1, B). Significantly higher levels were found in the serum of subjects with neutralizing antibodies to HRV39 (OD, 0.62-2.95) than in those with no neutralizing antibodies (OD, 0.73-0.99, P = .026) or cord blood (OD, 0.43-0.62, P = .0039). It is interesting to note that patients with no known exposure to the virus generally had lower OD values than did those with reported exposure (note dotted line in Fig 1, A). Whether this is due to cross-reactivity between rhinovirus serotypes or distant exposure is unknown. There was no relationship between atopic status and the presence of HRV39 specific IgE (1.69 ± 0.29 [mean OD ± SEM] for nonatopic subjects vs 1.41 ± 0.43 for atopic subjects, P = .60; in Fig 1, compare triangles [atopic subjects] and circles [nonatopic subjects]). As shown in Fig 1, B (right panel), the ELISA is specific for HRV39 because the addition of HRV39 to subject's serum significantly inhibited binding to the level seen in subjects without an exposure history. We believe that OD values above 1.5 represent the presence of anti-HRV39 IgE, while those between 1.5 and 1.0 are indeterminate, and those below 1.0 indicate no evidence of anti-HRV39 IgE. Importantly, total IgE levels did not correlate with anti-HRV39 specific IgE (Fig 1, C, Pearson P > .05). To our knowledge, this study is the first to show that IgE antibodies against rhinovirus (at least a laboratory strain) can be found in the sera of human subjects who have been exposed to that serotype, and adds to a growing body of evidence supporting a role for antiviral IgE as part of the natural antiviral immune response. It is important to stress that these data alone do not support the hypothesis that antiviral IgE is causative in the development of postviral atopic disease, but do begin to provide potential mechanistic explanations for why omalizumab might reduce asthma exacerbations outside of the pollen season. Furthermore, based on our studies in mice, these data support the model in which IgE against a respiratory virus drives the de novo development of postviral atopic disease (such as asthma), and provides some tantalizing evidence that the pathways identified in mice might be operative in humans. These data provide the initial support for further investigations focusing on preexposure/postexposure to HRV (and other respiratory viruses) and the role of antiviral IgE in the immune response to respiratory viruses, as well as the development and exacerbation of atopic diseases. We acknowledge the limitation of the small sample size, as well as the issue of potential cross-reactivity of anti-HRV39 IgE with other HRV strains. It is interesting to note that anti–HIV-1 IgE has been shown to inhibit HIV-1 production in infected PBMC cultures.10Pellegrino M.G. Bluth M.H. Smith-Norowitz T. Fikrig S. Volsky D.J. Moallem H. et al.HIV type 1-specific IgE in serum of long-term surviving children inhibits HIV type 1 production in vitro.AIDS Res Hum Retroviruses. 2002; 18: 363-372Crossref PubMed Scopus (30) Google Scholar Whether antiviral IgE is a purposeful or maladaptive immune response, it nonetheless appears to contribute to the exacerbation and perhaps development of atopic disease. Taken together, our study helps to shed light on the role viral infections might play in the development and exacerbation of atopic disease, and provides some additional rationale for future studies exploring therapeutic strategies to reduce or prevent the development of atopic disease." @default.
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• W2085688788 title "Rhinovirus specific IgE can be detected in human sera" @default.
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