Carl J Baldick
Affiliation: Bristol-Myers Squibb
- Hepatitis B virus quasispecies susceptibility to entecavir confirms the relationship between genotypic resistance and patient virologic responseCarl J Baldick
Bristol Myers Squibb Research and Development, 5 Research Parkway, Wallingford, CT 06492, USA
J Hepatol 48:895-902. 2008..Using >500 patient HBV isolates from several entecavir clinical trials, we show that phenotypic susceptibility correlates with genotypic resistance and patient virologic responses...
- A novel small molecule inhibitor of hepatitis C virus entryCarl J Baldick
Bristol Myers Squibb, Research and Development, Wallingford, Connecticut, United States of America
PLoS Pathog 6:e1001086. 2010..These results suggest that inhibitors of HCV entry could be added to replication inhibitors and interferons already in development...
- Ultrasensitive genotypic detection of antiviral resistance in hepatitis B virus clinical isolatesJie Fang
Bristol Myers Squibb Research and Development, Wallingford, CT, USA
Antimicrob Agents Chemother 53:2762-72. 2009..In summary, we established and validated an ultrasensitive method for measuring resistant HBV variants in clinical specimens, which enabled earlier, quantitative measurement of resistance to therapy...
- Two-year assessment of entecavir resistance in Lamivudine-refractory hepatitis B virus patients reveals different clinical outcomes depending on the resistance substitutions presentDaniel J Tenney
Bristol Myers Squibb Pharmaceutical Research Institute, 5 Research Parkway, Wallingford, CT 06492, USA
Antimicrob Agents Chemother 51:902-11. 2007..In summary, ETV was effective in LVD-refractory patients, with resistant sequences arising from a subset of patients harboring preexisting LVDr/ETVr variants and with approximately half of the patients experiencing a virologic rebound...
- Long-term monitoring shows hepatitis B virus resistance to entecavir in nucleoside-naïve patients is rare through 5 years of therapyDaniel J Tenney
Bristol Myers Squibb Company Research and Development, Wallingford, CT 06492, USA
Hepatology 49:1503-14. 2009..These findings support ETV as a primary therapy that enables prolonged treatment with potent viral suppression and minimal resistance...
- Comprehensive evaluation of hepatitis B virus reverse transcriptase substitutions associated with entecavir resistanceCarl J Baldick
Bristol Myers Squibb Research and Development, Wallingford, CT 06492, USA
Hepatology 47:1473-82. 2008....
- High-throughput screening and rapid inhibitor triage using an infectious chimeric Hepatitis C virusMichael J Wichroski
Bristol Myers Squibb Research and Development, Wallingford, Connecticut, United States of America
PLoS ONE 7:e42609. 2012..Leveraging results from this robust whole-virus assay represents a critical first step towards identifying inhibitors of novel targets to broaden the spectrum of antivirals for the treatment of HCV...
- Inhibition of hepatitis B virus polymerase by entecavirDavid R Langley
Bristol Myers Squibb Pharmaceutical Research Institute, 5 Research Parkway, Wallingford, CT 06443, USA
J Virol 81:3992-4001. 2007..Overall, these studies explain the potency, mechanism, and cross-resistance profile of ETV against HBV and account for the successful treatment of naive and LVD- or ADV-experienced chronic HBV patients...
- Entecavir resistance is rare in nucleoside naïve patients with hepatitis BRichard J Colonno
Bristol Myers Squibb Pharmaceutical Research Institute, Wallingford, CT 06492, USA
Hepatology 44:1656-65. 2006..These findings suggest that the rapid, sustained suppression of HBV replication, combined with a requirement for multiple substitutions, creates a high genetic barrier to ETVr in nucleoside naïve patients...
- Novel nonnucleoside inhibitor of hepatitis C virus RNA-dependent RNA polymeraseAnita Y M Howe
Infectious Diseases Wyeth Research, Pearl River, New York 10965, USA
Antimicrob Agents Chemother 48:4813-21. 2004..Fluorescence binding studies show that HCV-371 binds the NS5B with an apparent dissociation constant of 150 nM, leading to high selectivity and lack of cytotoxicity in the antiviral assays...
- Phosphorylation of human cytomegalovirus glycoprotein B (gB) at the acidic cluster casein kinase 2 site (Ser900) is required for localization of gB to the trans-Golgi network and efficient virus replicationMichael A Jarvis
Vaccine and Gene Therapy Institute, Oregon Health Sciences University, Portland, Oregon, USA
J Virol 78:285-93. 2004..Together, these results demonstrate that phosphorylation of gB at Ser900 is necessary for gB localization to the TGN, as well as for efficient viral replication, and further support the TGN as a site of HCMV envelopment...