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Journal of Virology, July 2005, p. 9192-9196, Vol. 79, No. 14
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.14.9192-9196.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Mannose Binding Lectin Genotypes Influence Recovery from Hepatitis B Virus Infection

Chloe L. Thio,1* Timothy Mosbruger,1 Jacquie Astemborski,1 Spencer Greer,1 Gregory D. Kirk,2 Stephen J. O'Brien,3 and David L. Thomas1

Departments of Medicine,1 Epidemiology, Johns Hopkins University, Baltimore, Maryland,2 Laboratory of Genomic Diversity, National Cancer Institute, Frederick, Maryland3

Received 22 February 2005/ Accepted 14 March 2005

Mannose binding lectin (MBL) is a central component of the innate immune response and thus may be important for determining hepatitis B virus (HBV) persistence. Since single-nucleotide polymorphisms (SNPs) in the gene encoding MBL (mbl2) alter the level of functional MBL, we hypothesized that mbl2 genotypes are a determinant of HBV persistence or recovery from viral infection. We tested this hypothesis by using a nested case control design with 189 persons with HBV persistence matched to 338 individuals who had naturally recovered from HBV infection. We determined genotypes of two promoter and three exon 1 SNPs in mbl2 and grouped these genotypes according to the amount of functional MBL production. We found that the promoter SNP –221C, which leads to deficient MBL production, was more common in those subjects with viral persistence (odds ratio [OR], 1.38; 95% confidence interval [CI], 1.01 to 1.89; P = 0.04). Those subjects homozygous for the combination of promoter and exon 1 genotypes associated with the highest amount of functional MBL had significantly increased odds of recovery from infection (OR, 0.55; 95% CI, 0.37 to 0.84; P = 0.005). Conversely, those homozygous for the combination of promoter and exon 1 genotypes which produce the lowest amount of functional MBL were more likely to have viral persistence (OR, 1.76; 95% CI, 1.02 to 3.01; P = 0.04). These data are consistent with the hypothesis that functional MBL plays a central role in the pathogenesis of acute hepatitis B.

* Corresponding author. Mailing address: 1503 E. Jefferson Street, Baltimore, MD 21231. Phone: (410) 955-0349. Fax: (410) 614-7564. E-mail: cthio{at}jhmi.edu.

Journal of Virology, July 2005, p. 9192-9196, Vol. 79, No. 14
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.14.9192-9196.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

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