| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
32 Favors Recovery from Hepatitis B1
* Department of Medicine, Johns Hopkins University, Baltimore, MD 21205;
Cancer and Inflammation Program, Laboratory of Experimental Immunology, Science Applications International Corp.-Frederick, National Cancer Institute, Frederick, MD 21702;
Los Angeles Biomedical Research Institute at Harbor, University of California Medical Center and David Geffen School of Medicine, Los Angeles, CA 90509;
Viral Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD 20852;
¶ Gulf States Hemophilia Center, University of Texas Health Science Center, Houston, TX 77030; and
|| Laboratory of Genomic Diversity, National Cancer Institute, Frederick, MD 21702
Recovery from acute hepatitis B virus (HBV) infection occurs in 95% of adult-acquired infections. A 32-bp deletion in CCR5 (CCR5
32), which encodes for a nonfunctional receptor, increases the likelihood of recovery. Using 181 subjects with persistent HBV infection and 316 who had recovered, we tested the hypothesis that an epistatic interaction between functional polymorphisms in RANTES (a CCR5 ligand) and CCR5 impacts recovery. Specific models designed to assess individual contributions of compound genotypes demonstrated that the only combination associated with recovery from an HBV infection was RANTES –403A with CCR532 (odds ratio 0.36, p = 0.02). Because the phenotypic consequence of –403A is reported to be higher levels of RANTES, we propose a model in which excess RANTES in combination with low CCR5 favors recovery from an HBV infection, which will require validation through functional testing.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Data in this manuscript were collected by the Multicenter AIDS Cohort Study, with centers (principal investigators) at The Johns Hopkins University Bloomberg School of Public Health (Joseph B. Margolick, Lisa Jacobson); Howard Brown Health Center and Northwestern University Medical School (John Phair); University of California, Los Angeles (Roger Detels); and University of Pittsburgh (Charles Rinaldo). The Multicenter AIDS Cohort Study is funded by the National Institute of Allergy and Infectious Diseases, with additional supplemental funding from the National Cancer Institute and the National Heart, Lung, and Blood Institute (UO1-AI-35042, 5-MO1-RR-00722 (GCRC), UO1-AI-35043, UO1-AI-37984, UO1-AI-35039, UO1-AI-35040, UO1-AI-37613, UO1-AI-35041). Website located at http://www.statepi.jhsph.edu/macs/macs.html
The content of this publication does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the U.S. Government. The publisher or recipient acknowledges rights of the U.S. Government to retain a nonexclusive, royalty-free license in and to any copyright covering the article.
1 This work was supported by National Institutes of Health Grant DA00441 and by the investigators in the Pathogenesis of Infectious Diseases Award from the Burroughs Wellcome Fund (to C.L.T.). This project has been funded in whole or in part with federal funds from the National Cancer Institute, National Institutes of Health, under Contract N01-CO-12400. This research was supported in part by the Intramural Research Program of the National Institutes of Health, National Cancer Institute, Center for Cancer Research. Multicenter Hemophilia Cohort Study is supported by National Cancer Institute Contract N02-CP-55504 with RTI International. Hemophilia Growth and Development Study is supported by the Bureau of Maternal and Child Health and Resources Development (MCJ-060570), the National Institute of Child Health and Human Development (NO1-HD-4-3200), the Centers for Disease Control and Prevention, and the National Institute of Mental Health. Additional support has been provided by grants from the National Center for Research Resources of the National Institutes of Health to the New York Hospital-Cornell Medical Center Clinical Research Center (MO1-RR06020); Mount Sinai General Clinical Research Center, New York (MO1-RR00071); University of Iowa Clinical Research Center (MO1-RR00059); University of Texas Health Science Center, Houston (MO1-RR02558); and R01-HD-4-1224.
2 Address correspondence and reprint requests to Dr. Mary Carrington, Cancer and Inflammation Program, Science Applications International Corp.-Frederick, National Cancer Institute, Frederick, MD 21702. E-mail address: carringt{at}ncifcrf.gov
3 Abbreviations used in this paper: HBV, hepatitis B virus; anti-HBc, Ab to hepatitis B core Ag; anti-HBs, Ab to hepatitis B surface Ag; CI, confidence interval; HBsAg, hepatitis B surface Ag; OR, odds ratio; SNP, single nucleotide polymorphism.
This article has been cited by other articles:
|
|
 |
|
  R.-h. Cha, S. H. Yang, H. S. Kim, S. M. Kim, M. H. Park, J. Ha, and Y. S. Kim Genetic interactions between the donor and the recipient for susceptibility to acute rejection in kidney transplantation: polymorphisms of CCR5 Nephrol. Dial. Transplant., September 1, 2009; 24(9): 2919 - 2925. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
