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Evolution of HIV-1 Integrase Following Selection of R263K With Further Dolutegravir Treatment: A Case Report From the P1093 Study
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Reported by Jules Levin
IAS 2015, July 19-22, 2015, Vancouver
Cindy Vavro,1 Paul Palumbo,2 Andrew Wiznia,3 Carmelita Alvero,4 Bobbie Graham,5 Terry Fenton,4 Rohan Hazra,6 Ellen Townley,7 Ann Buchanan,1 Joe Horton,1 Rolando Viani8 1GlaxoSmithKline, Research Triangle Park, NC, USA; 2Geisel School of Medicine at Dartmouth, Lebanon, NH, USA; 3Jacobi Medical Center, Bronx, NY, USA; 4Harvard School of Public Health, Boston, MA, USA; 5Frontier Science Research Foundation, Inc, Amherst, NY, USA; 6NICHD, Bethesda, MD, USA; 7HJF-DAIDS, NIAD, Bethesda, MD, USA; 8University of California San Diego, La Jolla, CA, USA
Hi Jules,
I spent a lot of time at this poster. What we have to decide is whether this very rare, anecdotal case of a non-adherent person is a typical one. Or whether we should best be guided by the Wainberg lab hypothesis (attached) and pay attention to the fact that today, 2 years after the approval of DTG by the FDA and hence its real-world use in such settings as inner city Washington and the Bronx, that there has not been a single case described from such settings and in clinical trials of resistance to either DTG or the NRTIs with which it has been co-utilized. This anecdotal case is similar to the SAILING patients who developed R263K, because some of them were on effective DTG monotherapy, which is the same mutation that we selected in the lab with DTG. It is also notable that this patient's viral load did not skyrocket if this was a true case of resistance. Rather, it is proof that DTG continues to be active despite the presence of the R263K mutation.
Feel free to circulate my views on this matter.
Regards,
Mark [Wainberg]
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