@article {558,
	title = {Misdirected antibody responses against an N-terminal epitope on human rhinovirus VP1 as explanation for recurrent RV infections},
	journal = {FASEB J},
	volume = {26},
	number = {3},
	year = {2012},
	pages = {1001-8},
	type = {Journal Article},
	abstract = {Rhinoviruses (RVs) are the primary cause of upper respiratory tract infections, generally known as the common cold. Moreover, RV infections can trigger severe exacerbations of asthma and chronic obstructive pulmonary disease (COPD). We expressed the 4 major RV capsid proteins, VP1-VP4, in Escherichia coli and used these proteins as well as recombinant and synthetic VP1 fragments to study and map antibody responses in RV-infected humans. VP1, which on infection binds to ICAM 1, was identified as a major target for the memory immune response, residing in the IgG1 subclass and IgA class. Interestingly, this response was mainly directed against an N-terminal 20 mer peptide in VP1, P1a, which becomes exposed on intact RV only when it docks to its receptor ICAM 1. Molecular modeling using the 3-dimensional RV capsid structures revealed that P1a was localized inside the capsid and outside the areas involved in receptor binding or RV neutralization. Our results suggest misdirection of antibody responses against a nonprotective epitope as a mechanism how RV escapes immunity and causes recurrent infections. Based on these findings, it may be possible to design vaccines against RV infections and RV-induced respiratory diseases.},
	keywords = {Amino Acid Sequence Antibodies, Amino Acid Viral Proteins, Polyacrylamide Gel Enzyme-Linked Immunosorbent Assay Epitopes Host-Pathogen Interactions Humans Immunoglobulin A Immunoglobulin G Intercellular Adhesion Molecule-1 Molecular Sequence Data Recombinant Proteins Rhinovirus Seasons Sequence Homology, Viral Capsid Child Common Cold Electrophoresis},
	issn = {1530-6860},
	doi = {10.1096/fj.11-193557},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/22121050},
	author = {Niespodziana, K. and Napora, K. and Cabauatan, C. and Focke-Tejkl, M. and Keller, W. and Niederberger, V. and Tsolia, M. and Christodoulou, I. and Papadopoulos, N. G. and Valenta, R.}
}
