I have two problems with the news, out of Kenilworth, tonight, that a study at Duke (funded by Schering-Plough) has likely-identified the gene variant which dictates that current Hep-C treatments are largely ineffective in many people of color. [My backgrounder -- on this sad state of affairs -- here.]
I am always in favor of learning, and knowing, more -- don't misunderstand -- but I am surprised that both the PI, and the press reports (see below) characterize the (predominantly) African Americans' gene sequence as containing a "spelling mistake" -- when in fact, the mistake (if there one be) is that our current standard treatment (here, Schering-Plough's $915 million a year franchise) fails to address a very common biological variant.
My second concern is that this new test will be used by diagnostic companies, that sign license agreements with Schering-Plough (as owner of the IP), to encourage doctors to keep more patients on standard regimens, when it is shown that they are likely to respond to treatment (i.e., in the stilted-language of the researchers -- have no spelling errors in their alleles -- near Interleukin-28B).
My understanding is that the next generation of Hep C treatments -- primarily Vertex's teleprevir -- is not dependent on this gene variant receptivity. In fact, as I understand it, should Vertex win FDA approval for teleprevir, much of Schering-Plough's $900 million per year franchise becomes "trailing edge". Some of Schering's current offerings will still be prescribed with teleprevir, but at nothing like the pace now seen.
So, this hub-bub about a test may be used to delay the transfer of Hep C non-responders into Vertex-sponsored teleprevir investigational studies -- or at least I fear that sad outcome. What do you think? Let me know -- in the comments. Here is the Reuter's version of the story -- and a pull-quote, from it [emphasis supplied]:
. . . .Hepatitis C is a blood-borne liver disease that can lead to chronic liver problems, liver cancer, cirrhosis and death. The virus affects an estimated 3.2 million people in the United States alone and 170 million worldwide.
Treatment typically involves 48 weeks of interferon plus the antiviral drug ribavirin. Some patients develop such taxing side effects that they stop treatment. Blacks are less likely to respond than whites.
Until now, no one has known why.'SPELLING MISTAKE'
According to Goldstein's study, published in the journal Nature, it may be because of a "spelling mistake" -- a one-letter error in the genetic code near the Interleukin-28B or IL28B gene, which plays a role in fighting off infections.
"If you look at individuals with the good response genotype, about 80 percent of them will be cured. If you look at individuals with the poor-response genotype, about 30 percent of them will be cured," Goldstein said in a telephone interview. "That is just a huge, huge difference."
The discovery came from a clinical trial of 1,671 people with the most common form of the disease in the United States and Europe who were taking the two most common hepatitis C therapies.
It was funded by Schering-Plough, maker of one of two standard hepatitis C regimens. . . .
A spelling mistake? Really? Why is it that the less dominant, "TT" allele, at IL 28B, is a "mistake"? C'mon, now FDA -- let's get Vertex's teleprevir to market STAT! [or, ASAP, if one prefers.]
LATER: The New York Times does a better job with the story -- correctly pointing out that this is likely the result of either milder strains of hepatitis (or similar viral agents) in ancient Africa, or of more potent ones in East Asia, and to a lesser extent, Europe, in our collective, but very-distant, evolutionary past.
