Analysis of Measles Virus Binding Sites of the CD46 Gene in Patients with Subacute Sclerosing Panencephalitis (original) (raw)

Journal Article

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1

Department of Pediatrics, Graduate School of Medical Sciences, Kyushu University

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Fukuoka

Reprints or correspondence: Dr. Koichi Kusuhara, Dept. of Pediatrics, Graduate School of Medical Sciences, Kyushu University, 3-1-1, Maidashi, Higashi-ku, Fukuoka 812-8582, Japan (kkusuhar@pediatr.med.kyushu-u.ac.jp).

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Department of Pediatrics, Graduate School of Medical Sciences, Kyushu University

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Fukuoka

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Department of Pediatrics, Graduate School of Medical Sciences, Kyushu University

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Fukuoka

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Department of Pediatrics, Graduate School of Medical Sciences, Kyushu University

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Fukuoka

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Department of Pediatrics, Osaka City University Medical School

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Division of Neurology, Kanagawa Children's Medical Center

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Yokohama

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Division of Neurology, National Children's Hospital

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Tokyo

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Division of Pediatrics, National Iwaki Hospital

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Aomori

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Division of Neurology, Shizuoka Children's Hospital

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Shizuoka

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Division of Child Neurology, Institute of Neurological Sciences, Tottori University

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Yonago

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Japan

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Received:

15 September 1999

Revision received:

27 December 1999

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Koichi Kusuhara, Yuka Sasaki, Futoshi Nakao, Kenji Ihara, Hideji Hattori, Sumimasa Yamashita, Kenji Nihei, Nobuo Koide, Hideo Aiba, Kenzo Takeshita, Toshiro Hara, Analysis of Measles Virus Binding Sites of the CD46 Gene in Patients with Subacute Sclerosing Panencephalitis, The Journal of Infectious Diseases, Volume 181, Issue 4, April 2000, Pages 1447–1449, https://doi.org/10.1086/315386
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Abstract

Measles virus (MV) binding sites of the CD46 gene were sequenced in patients with subacute sclerosing panencephalitis (SSPE) and in controls. There were 3 novel polymorphisms, including C/T at nucleotide position 38 (C/T38), G/A at position 176 (G/A176), and C/T at position 453 (C/T453), at allele frequencies of .97 : .03, .99 : .01, and .97 : .03, respectively. The G/A176 polymorphism causes an Arg/Gln amino acid change within the essential binding sites of MV, whereas the C/A38 polymorphism causes a Ser/Phe change outside the MV binding sites. The C/T453 polymorphism does not produce an amino acid change. Two of the 40 SSPE patients and 2 of the 32 controls had both C/T38 and C/T453 polymorphisms in heterozygous patterns. One control subject, but no SSPE patients, had the G/A176 polymorphism in a heterozygous pattern. Thus, it is not likely that CD46 gene alteration has a role as a host susceptibility factor in the development of SSPE.

© 2000 by the Infectious Diseases Society of America

Topic:

• amino acids
• polymorphism
• binding sites
• gene frequency
• genes
• heterozygote
• measles virus
• nucleotides
• phenylalanine
• subacute sclerosing panencephalitis
• glutamine
• cd46 antigen
• host (organism)

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