Brief Report: No Evidence for Parvovirus B19 or Hepatitis E Virus as a Cause of Acute Liver Failure
Viral hepatitis A and B are known to cause acute liver failure. While nearly 20% of acute liver failure cases are of indeterminate etiology, screening for other viruses has not been uniformly performed. We looked for evidence for parvovirus B19 and hepatitis E virus in sera from U.S. acute liver failure patients. For B19, 78 patients’ sera, including 34 with indeterminate etiology, were evaluated by DNA dot-blot hybridization, reverse transcription polymerase chain reaction, and enzyme-linked immunosorbent assay for immunoglobin G and M antibodies; none showed evidence for infection. In like manner, 126 patients’ sera were analyzed for hepatitis E virus RNA by reverse transcription polymerase chain reaction and for hepatitis E virus immunoglobin G and M antibodies by enzyme-linked immunosorbent assay; no acute hepatitis E virus cases were identified. If a unique acute liver failure virus exists, it is neither of these candidate agents.
KeywordsParvovirus B19 Hepatitis E virus Acute liver failure Encephalopathy Polymerase chain reaction
The U.S. Acute Liver Failure Study Group (ALFSG), which participated in this study, includes William M. Lee (Principal Investigator), University of Texas Southwestern Medical Center, Dallas; Anne Larson, University of Washington, Seattle; Jeffery S. Crippin, Washington University, St. Louis, Missouri; Timothy J. Davern and Nathan Bass, University of California at San Francisco, San Francisco; Sukru Emre, Mt. Sinai Medical Center, New York; Timothy M. McCashland, University of Nebraska, Omaha; J. Eileen Hay, Mayo Clinic, Rochester, Minnesota; Natalie Murray, Baylor University Medical Center, Dallas, Texas; A. Obaid Shakil, University of Pittsburgh, Pittsburgh, Pennsylvania; Andres T. Blei, Northwestern University, Chicago, Illinois; Atif Zaman, Oregon Health Sciences University, Portland; Steven H. B. Han, University of California, Los Angeles; Robert J. Fontana, University of Michigan, Ann Arbor; Brendan McGuire, University of Alabama at Birmingham, Birmingham; Raymond Chung, Massachusetts General Hospital, Boston; Steven Lobritto, Robert Brown, and Michael Schilsky, Columbia-Presbyterian Medical Center, New York; M. Edwyn Harrison, Mayo Clinic Scottsdale, Phoenix, Arizona; Santiago Munoz, Albert Einstein Medical Center, Philadelphia, Pennsylvania; R. Todd Stravitz, Virginia Commonwealth University, Richmond; Lorenzo Rossaro, University of California, Davis Medical Center, Sacramento; and Raj Santayanarana, Mayo Clinic, Jacksonville, Florida. This work was presented in part at the DDW meeting, May 2004, in New Orleans, Louisiana (Gastroenterology 126 [Suppl 2]:A-706, abstract S1632, 2004). The authors from the U.S. ALFSG and from the National Heart, Lung and Blood Institute report no conflicts of interest with regard to this work. Drs. G. J. Dawson, G. G. Schlauder, and R.A. Gutierrez are employees of Abbott Laboratories.
The U.S. ALFSG has been funded by NIH Grants RO3 DK52827 and R01 DK58369, FDA Grant FD-R-001661, and generous grants from the Stephen B. Tips Fund of the Northwestern Medical Foundation, Chicago, Illinois, and from the Jeanne Roberts Fund of the Southwestern Medical Foundation, Dallas, Texas.
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