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Journal of Virology, April 2001, p. 3462-3468, Vol. 75, No. 7
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.7.3462-3468.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Naturally Occurring Deletional Mutation in the C-Terminal Cytoplasmic Tail of CCR5 Affects Surface Trafficking of CCR5

Tatsuo Shioda,1,* Emi E. Nakayama,1 Yuetsu Tanaka,2 Xiaomi Xin,3 Huanliang Liu,1 Ai Kawana-Tachikawa,3 Atsushi Kato,4 Yuko Sakai,3 Yoshiyuki Nagai,4 and Aikichi Iwamoto3

Research Institute for Microbial Diseases, Osaka University, Osaka,1 Ryukyu University, Okinawa,2 and Institute of Medical Science, University of Tokyo,3 and National Institute of Infectious Diseases,4 Tokyo, Japan

Received 20 September 2000/Accepted 22 December 2000

CCR5 is an essential coreceptor for the cellular entry of R5 strains of human immunodeficiency virus type 1 (HIV-1). CCR5-893(-) is a single-nucleotide deletion mutation which is observed exclusively in Asians (M. A. Ansari-Lari, et al., Nat. Genet. 16:221-222, 1997). This mutant gene produces a CCR5 which lacks the entire C-terminal cytoplasmic tail. To assess the effect of CCR5-893(-) on HIV-1 infection, we generated a recombinant Sendai virus expressing the mutant CCR5 and compared its HIV-1 coreceptor activity with that of wild-type CCR5. Although the mutant CCR5 has intact extracellular domains, its coreceptor activity was much less than that of wild-type CCR5. Flow cytometric analyses and confocal microscopic observation of cells expressing the mutant CCR5 revealed that surface CCR5 levels were greatly reduced in these cells, while cytoplasmic CCR5 levels of the mutant CCR5 were comparable to that of the wild type. Peripheral blood CD4+ T cells obtained from individuals heterozygous for this allele expressed very low levels of CCR5. These data suggest that the CCR5-893(-) mutation affects intracellular transport of CCR5 and raise the possibility that this mutation also affects HIV-1 transmission and disease progression.

* Corresponding author. Mailing address: Department of Viral Infections, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamada-oka, 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, April 2001, p. 3462-3468, Vol. 75, No. 7
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.7.3462-3468.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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