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Clinical and Developmental Immunology
Volume 2012 (2012), Article ID 580696, 9 pages
http://dx.doi.org/10.1155/2012/580696
Research Article

CD4 T-Cell-Independent Antibody Response Reduces Enterovirus 71 Lethality in Mice by Decreasing Tissue Viral Loads

1Institute of Basic Medical Sciences, Medical College, National Cheng Kung University, Tainan 701, Taiwan
2Department of Microbiology and Immunology, Medical College, National Cheng Kung University, Tainan 701, Taiwan
3National Institute of Infectious Diseases and Vaccinology, National Health Research Institutes, Tainan 701, Taiwan
4Statistical Analysis Laboratory, Department of International Business Management, Tainan University of Technology, Tainan 701, Taiwan
5Center of Excellence for Infectious Diseases and Signaling Research, National Cheng Kung University, Tainan 701, Taiwan

Received 15 March 2012; Revised 9 September 2012; Accepted 10 September 2012

Academic Editor: David Kaplan

Copyright © 2012 Li-Chiu Wang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Enterovirus 71 (EV71) has induced fatal encephalitis in hundreds of thousands of infants and young children in the Asia-Pacific region since the past decade. Lymphocyte and antibody responses have been suspected to aggravate EV71-induced neurological symptoms, so anti-inflammatory agents have been used to treat patients with neurological symptoms. In the present study, we found that mice deficient in CD4+ T cells were resistant to EV71 infection as wild-type mice, whereas mice deficient in B cells were highly susceptible to viral infection. Compensation of CD4 T-cell function by other immune cells was not likely, because wild-type mice depleted of CD4+ T cells were also resistant to viral infection. Infected CD4 T-cell-deficient mice produced virus-specific neutralizing antibodies, IgM and IgG. Moreover, adoptive transfer of the virus-specific antibody produced by infected CD4 T-cell-deficient mice protected B-cell-deficient mice from infection by reducing tissue viral loads. Collectively, our results show that the CD4 T-cell-independent antibody response promotes the survival of EV71-infected mice and suggest great potential for the use of vaccines and neutralizing antibodies to reduce fatal symptoms in patients.