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Journal of Virology, June 2000, p. 5452-5459, Vol. 74, No. 12
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Polymorphism in the Interleukin-4 Promoter Affects Acquisition of Human Immunodeficiency Virus Type 1 Syncytium-Inducing Phenotype

Emi E. Nakayama,1 Yoshihiko Hoshino,1 Xiaomi Xin,1,2 Huanliang Liu,1 Mieko Goto,1 Nobukazu Watanabe,1 Hitomi Taguchi,1 Akihiro Hitani,1 Ai Kawana-Tachikawa,1 Masao Fukushima,2 Kaneo Yamada,3 Wataru Sugiura,4 Shin-Ichi Oka,5 Atsushi Ajisawa,6 Hironori Sato,4 Yutaka Takebe,4 Tetsuya Nakamura,1 Yoshiyuki Nagai,2,4 Aikichi Iwamoto,1 and Tatsuo Shioda1,*

Department of Infectious Diseases1 and Department of Viral Infection,2 Institute of Medical Science, University of Tokyo, St. Marianna University School of Medicine,3 AIDS Research Center, National Institute of Infectious Diseases,4 AIDS Clinical Center, International Medical Center of Japan,5 and Department of Infectious Diseases, Tokyo Metropolitan Komagome Hospital,6 Tokyo, Japan

Received 29 July 1999/Accepted 21 March 2000

The emergence of syncytium-inducing (SI) variants of human immunodeficiency virus type 1 (HIV-1) in infected individuals is an indicator of poor prognosis and is often correlated with faster CD4+ cell depletion and rapid disease progression. Interleukin-4 (IL-4) is a pleiotropic cytokine with various immune-modulating functions including induction of immunoglobulin E (IgE) production in B cells, down-regulation of CCR5 (a coreceptor for HIV-1 non-SI [NSI] strains), and up-regulation of CXCR4 (a coreceptor for HIV-1 SI variants). Here we show that homozygosity of a polymorphism in the IL-4 promoter region, IL-4 -589T, is correlated with increased rates of SI variant acquisition in HIV-1-infected individuals in Japan. This mutation was also shown to be associated with elevated serum IgE levels in HIV-1-infected individuals, especially in those at advanced stages of disease. In contrast, neither a triallele polymorphism in IL-10, another Th2 cytokine, nor a biallele polymorphism in the RANTES promoter affected acquisition of the SI phenotype. This finding suggested that IL-4-589T increases IL-4 production in the human body and thus accelerates the phenotypic switch of HIV-1 from NSI to SI and possibly disease progression of AIDS.

* Corresponding author. Present address: Department of Viral Infections, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamadaoka, Suita, Osaka 565-0871, Japan. Phone: 81-6-6879-8346. Fax: 81-6-6879-8347. E-mail: shioda{at}biken.osaka-u.ac.jp.

Journal of Virology, June 2000, p. 5452-5459, Vol. 74, No. 12
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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