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Dialysis-membrane-dependent reduction and adsorption of circulating hepatitis C virus during hemodialysis
Mari Mizuno1, Terumi Higuchi, Mitsuru Yanai
1Department of Pathology, Nihon University School of Medicine, Tokyo, Japan.
Insights
Certain dialysis membranes, like polysulfone, can reduce hepatitis C virus (HCV) levels in patients undergoing hemodialysis (HD) through adsorption. This membrane-dependent effect offers a transient decrease in HCV viremia during HD treatment.
Area of Science:
- Nephrology
- Virology
- Biomaterials Science
Background:
- Chronic hemodialysis (HD) patients frequently have hepatitis C virus (HCV) infection, a leading cause of chronic liver disease.
- Observed decreases in serum HCV load post-HD prompted investigation into the underlying mechanisms.
Purpose of the Study:
- To investigate the impact of different dialysis membrane types on circulating HCV load.
- To elucidate the in vivo and in vitro effects of dialysis membranes on viral clearance.
Main Methods:
- Semiquantitative analysis of HCV RNA levels in patient serum and dialyzer membranes using RT-PCR before and after HD.
- In vitro dialysis and ultrafiltration experiments to assess HCV RNA in different fractions.
- Comparison of polysulfone (PS), hemophan, cuprophan (CU), and AN69 membranes.
Main Results:
- Polysulfone and hemophan membranes significantly reduced HCV RNA titers (10(-1)-10(-2) fold) in HD patients.
- Cuprophan membranes showed no effect, while AN69 had a variable effect on HCV viremia.
- In vitro studies confirmed HCV adsorption to PS membranes, but not CU membranes, with viral RNA recovered from the membrane itself, not the ultrafiltrate.
Conclusions:
- Dialysis membranes exhibit a capacity for adsorbing HCV during hemodialysis.
- This adsorption leads to a temporary reduction in circulating HCV levels in patients.
Background/Aims:
Patients on chronic hemodialysis (HD) are often infected with hepatitis C virus (HCV), a common cause of chronic liver disease. In some cases, however, decreases in the serum HCV load after HD have been documented. To better understand this phenomenon, we investigated the effects of various types of dialysis membrane on virus load in the circulation in vivo and in vitro.
Methods:
HCV RNA levels in patients' serum, filtrate and dialyzer membranes were analyzed semiquantitatively by reverse transcription-polymerase chain reaction (RT-PCR) before and after HD treatment with two to four different types of dialysis membrane. HCV RNA was also determined from each fraction in in vitro dialysis and ultrafiltration.
Results:
In HD patients treated with a polysulfone (PS) membrane and a hemophan membrane, the HCV RNA titer reproducibly decreased by a factor of 10(-1)-10(-2). In contrast, a cuprophan (CU) membrane had no detectable effect on HCV viremia, and HD with the AN69 membrane reduced HCV RNA levels in only a subset of the patients. In addition, a PS membrane, but not a CU membrane, reduced the level of circulating HCV in an in vitro assay. In both in vivo and in vitro experiments, HCV RNA was recovered from the PS membrane itself, but not from the ultrafiltrate.
Conclusions:
Membrane-dependent adsorption of HCV occurs during HD, causing a transient reduction in HCV in the circulation of patients.