Research article

MBL2 and Hepatitis C Virus Infection among Injection Drug Users

Elizabeth E Brown¹ , Mingdong Zhang¹ , Rebecca Zarin-Pass¹ , Toralf Bernig² , Fan-Chen Tseng¹ , Nianqing Xiao³ , Meredith Yeager³ , Brian R Edlin^4,5 , Stephen J Chanock^1,2 and Thomas R O'Brien¹

¹Division of Cancer Epidemiology and Genetics, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA

²Center for Cancer Research, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland, USA

³SAIC-Frederick, Inc., Core Genotyping Facility, Advanced Technology Center, National Cancer Institute, Gaithersburg, Maryland, USA

⁴Center for the Study of Hepatitis C, Weill Medical College of Cornell University, New York, New York, USA

⁵Urban Health Study, University of California, San Francisco, USA

author email corresponding author email

BMC Infectious Diseases 2008, 8:57doi:10.1186/1471-2334-8-57

Published:	1 May 2008

Abstract

Background

Genetic variations in MBL2 that reduce circulating levels and alter functional properties of the mannose binding lectin (MBL) have been associated with many autoimmune and infectious diseases. We examined whether MBL2 variants influence the outcome of hepatitis C virus (HCV) infection.

Methods

Participants were enrolled in the Urban Health Study of San Francisco Bay area injection drug users (IDU) during 1998 through 2000. Study subjects who had a positive test for HCV antibody were eligible for the current study. Participants who were positive for HCV RNA were frequency matched to those who were negative for HCV RNA on the basis of ethnicity and duration of IDU. Genotyping was performed for 15 single nucleotide polymorphisms in MBL2. Statistical analyses of European American and African American participants were conducted separately.

Results

The analysis included 198 study subjects who were positive for HCV antibody, but negative for HCV RNA, and 654 IDUs who were positive for both antibody and virus. There was no significant association between any of the genetic variants that cause MBL deficiency and the presence of HCV RNA. Unexpectedly, the MBL2 -289X promoter genotype, which causes MBL deficiency, was over-represented among European Americans who were HCV RNA negative (OR = 1.65, 95% CI 1.05–2.58), although not among the African Americans.

Conclusion

This study found no association between genetic variants that cause MBL deficiency and the presence of HCV RNA. The observation that MBL2 -289X was associated with the absence of HCV RNA in European Americans requires validation.