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Clinical Chemistry 51: 1091-1092, 2005; 10.1373/clinchem.2005.051706
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(Clinical Chemistry. 2005;51:1091-1092.)
© 2005 American Association for Clinical Chemistry, Inc.

Editorials

Mass Spectrometry for Genotyping Hepatitis C Virus: A Promising New Approach

Linda Cook1,2 and Keith R. Jerome1,2,a

1 Department of Laboratory Medicine, University of Washington Medical Center, Seattle, WA
2 Program in Infectious Diseases, Fred Hutchinson Cancer Research Center, Seattle, WA

aAddress correspondence to this author at: Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue N, D3-100, Seattle, WA 98109. Fax 206-667-4411; e-mail kjerome@fhcrc.org.

The first 20% of the full text of this article appears below.

Hepatits C virus (HCV) infection is a growing health problem worldwide, with more than 170 million individuals currently infected(1). Because no vaccine is currently available, the mainstay of control is treatment of infected individuals. Although the first attempts at treatment with interferon-{alpha} produced sustained responses in only ~25% of patients, more recent combination treatment regimens consisting of pegylated interferon-{alpha} plus ribavirin have led to sustained response rates approaching 60%(2)(3). In spite of intense study, the specific HCV gene(s) controlling the response to combination therapy have not been identified. Instead, the best predictor is the HCV genotype of the strain present in the patient(4). HCV is an extremely diverse virus, with 6 major genotypes and more than 60 subtypes identified(5)(6). Genotype 1 is the most common genotype in the United States and Europe, and genotypes 2 and 3 are also common in these areas. Frequently, the virus within a given infected individual diverges during the course of chronic infection into multiple viral lineages with related sequences (known as quasispecies). Less frequently, an individual may become infected with a mixture of 2 or more genotypes. In spite of the wide sequence variation present in HCV, multiple studies have clearly shown a lower response rate to combination therapy with pegylated interferon-{alpha} plus ribavirin for patients who are infected with genotype 1 compared with the other genotypes(7). Thus, 2 therapeutic schemes are used: a 48-week course of therapy for patients infected with genotype-1 HCV and a 24-week course for those infected with other genotypes of the virus(8). The dramatically . . . [Full Text of this Article]






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