Hepatitis C Virus and the Humoral Immune System
The purpose of this study is to measure specific chemokines, antibodies, and antibody-producing B cells in the blood of patients with hepatitis C virus (HCV) infection. Our hypothesis is that changes in chemokine levels affect the development of an effective immune response against HCV.
Hepatitis C Virus
|Study Design:||Observational Model: Case Control
Time Perspective: Prospective
|Official Title:||Hepatitis C Virus and the Humoral Immune System|
- Define the relationships between HCV infection, B cell phenotype, and B cell function [ Time Frame: 5 years ] [ Designated as safety issue: No ]Define the relationships between HCV infection, B cell phenotype, and B cell function
Biospecimen Retention: Samples With DNA
|Study Start Date:||September 2001|
|Study Completion Date:||May 2013|
|Primary Completion Date:||May 2013 (Final data collection date for primary outcome measure)|
current HCV infection, including intravenous drug users
cryoglobulinemia and without HCV infection
chronic liver disease
chronic liver disease not due to hepatitis C virus infection
Sustained Virologic responders
successfully treated for HCV infection
normal, healthy volunteers
The long-term goal of our research is to understand why immune complexes (ICs) are produced in patients infected with HCV, and whether these complexes affect virus interaction with target cells. We have found that many patients infected with HCV have an increased frequency of circulating B cells, but no evidence that the increased B cells are activated of proliferating. One possible mechanism for such an increase would be a change in levels of chemokines that influence B cell localization and trafficking. Our studies are aimed at testing the following hypotheses:
- One hypothesis is that HCV infection results in increased levels of specific cytokines and chemokines that may affect the motility and localization of immature and mature B cells. An alternative model is that HCV infection leads to chronic antigenic stimulation of B lymphocytes, and that the abnormalities of B cell function associated with HCV infection reflect this chronic antigenic stimulation.
- A second hypothesis is that autoantibodies and immune complexes present in HCV patient serum contribute to the persistence and spread of viral infection.
To test these hypotheses, we are measuring levels of chemokines, the frequency of circulating B cells (mature resting B cells, mature activated B cells, memory B cells, and immature B cells), and the levels and components of ICs in the blood of HCV-infected patients. Controls include healthy volunteers and patients with chronic liver disease unrelated to HCV infection. No interventions in patient care are planned. When patients elect to undergo standard antiviral therapies under the supervision of their hepatologists, we will study the outcomes of therapy (no virologic response, partial or transient virologic response, sustained virologic response) to determine whether any of the observed alterations in chemokine levels, B cell frequency or activation, or immune complex levels correlate with the patient's response to antiviral therapy.
Please refer to this study by its ClinicalTrials.gov identifier: NCT00219999
|United States, New York|
|Rockefeller University Hosital|
|New York, New York, United States, 10021|
|Principal Investigator:||Lynn B Dustin, PHD||Rockefeller University|