The Journal of Experimental Medicine
Avanti Polar Lipids
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Published online 9 June 2003 doi:10.1084/jem.20021457
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© Rockefeller University Press, 0022-1007/2003/6/1779 $5.00
The Journal of Experimental Medicine, Volume 197, Number 12, 1779-1785

Brief Definitive Report

 Unmutated Immunoglobulin M Can Protect Mice from Death by Influenza Virus Infection

Yuichi Harada1, Masamichi Muramatsu2, Toshikatsu Shibata1,3, Tasuku Honjo2 and Kazumichi Kuroda3

1 Department of Virology and Immunology, Osaka University of Pharmaceutical Sciences, Takatsuki 569-1094, Japan
2 Department of Medical Chemistry, Graduate School of Medicine, Kyoto University, Kyoto 606-8501, Japan
3 Department of Immunology and Microbiology, Nihon University School of Medicine, Tokyo 173-8610, Japan

Address correspondence to Kazumichi Kuroda, Department of Immunology and Microbiology, Nihon University School of Medicine, Oyaguchi-kamicho, Itabashi-ku, Tokyo 173-8610, Japan. Phone: 81-3-3972-8111; Fax: 81-3-3972-9560; E-mail: kkuroda{at}med.nihon-u.ac.jp

To elucidate the role of class switch recombination (CSR) and somatic hypermutation (SHM) in virus infection, we have investigated the influence of the primary and secondary infections of influenza virus on mice deficient of activation-induced cytidine deaminase (AID), which is absolutely required for CSR and SHM. In the primary infection, AID deficiency caused no significant difference in mortality but did cause difference in morbidity. In the secondary infection with a lethal dose of influenza virus, both AID-/- and AID+/- mice survived completely. However, AID-/- mice could not completely block replication of the virus and their body weights decreased severely whereas AID+/- mice showed almost complete prevention from the reinfection. Depletion of CD8+ T cells by administration of an anti-CD8 monoclonal antibody caused slightly severer body weight loss but did not alter the survival rate of AID-/- mice in secondary infection. These results indicate that unmutated immunoglobulin (Ig)M alone is capable of protecting mice from death upon primary and secondary infections. Because the titers of virus-neutralizing antibodies were comparable between AID-/- and AID+/- mice at the time of the secondary infection, a defect of AID-/- mice in protection of morbidity might be due to the absence of either other Ig classes such as IgG, high affinity antibodies with SHM, or both.

Key Words: AID • class-switch recombination • somatic hypermutation • antiviral immunity • antibody


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