M A Winters

Summary

Affiliation: Stanford University
Country: USA

Publications

  1. ncbi Development of elvitegravir resistance and linkage of integrase inhibitor mutations with protease and reverse transcriptase resistance mutations
    Mark A Winters
    AIDS Research Center, Veterans Affairs Palo Alto Health Care System, Palo Alto, California, United States of America
    PLoS ONE 7:e40514. 2012
  2. ncbi Rare one and two amino acid inserts adjacent to codon 103 of the HIV-1 reverse transcriptase (RT) affect susceptibility to non-nucleoside RT inhibitors
    Mark A Winters
    Center for AIDS Research, Stanford University, Stanford, CA, USA
    Antivir Ther 10:363-6. 2005
  3. ncbi New two-amino acid insertion near codon 70 of the HIV type 1 protease gene
    Mark A Winters
    Division of Infectious Diseases, Stanford University Medical Center, Stanford, California 94305, USA
    AIDS Res Hum Retroviruses 21:311-3. 2005
  4. ncbi Insertions in the human immunodeficiency virus type 1 protease and reverse transcriptase genes: clinical impact and molecular mechanisms
    Mark A Winters
    Division of Infectious Diseases and Geographic Medicine, Stanford University, 300 Pasteur Drive, Room S-146, Stanford, California 94305-5107, USA
    Antimicrob Agents Chemother 49:2575-82. 2005
  5. ncbi Impact of highly active antiretroviral therapy on hepatitis C virus protease quasispecies diversity in HIV co-infected patients
    Mark A Winters
    AIDS Research Center, VA Palo Alto Health Care System, Palo Alto, California 94304, USA
    J Med Virol 82:791-8. 2010
  6. ncbi Variants other than aspartic acid at codon 69 of the human immunodeficiency virus type 1 reverse transcriptase gene affect susceptibility to nuleoside analogs
    M A Winters
    Division of Infectious Diseases and Geographic Medicine, Stanford University, Stanford, California, USA
    Antimicrob Agents Chemother 45:2276-9. 2001
  7. ncbi Genotypic, phenotypic, and modeling studies of a deletion in the beta3-beta4 region of the human immunodeficiency virus type 1 reverse transcriptase gene that is associated with resistance to nucleoside reverse transcriptase inhibitors
    M A Winters
    Stanford University, Stanford, California 94305, USA
    J Virol 74:10707-13. 2000
  8. ncbi Frequency of antiretroviral drug resistance mutations in HIV-1 strains from patients failing triple drug regimens. The Terry Beirn Community Programs for Clinical Research on AIDS
    M A Winters
    Stanford University, Calif, USA
    Antivir Ther 5:57-63. 2000
  9. ncbi Maternal-fetal pharmacokinetics and dynamics of a single intrapartum dose of maraviroc in rhesus macaques
    Mark A Winters
    AIDS Research Center, VA Palo Alto Health Care System, Palo Alto, California 94304, USA
    Antimicrob Agents Chemother 54:4059-63. 2010
  10. ncbi Use of dried clinical samples for storing and detecting influenza RNA
    Mark Winters
    VA Palo Alto Health Care System, Palo Alto, CA, USA
    Influenza Other Respi Viruses 5:413-7. 2011

Collaborators

Detail Information

Publications35

  1. ncbi Development of elvitegravir resistance and linkage of integrase inhibitor mutations with protease and reverse transcriptase resistance mutations
    Mark A Winters
    AIDS Research Center, Veterans Affairs Palo Alto Health Care System, Palo Alto, California, United States of America
    PLoS ONE 7:e40514. 2012
    ..Continued appearance of new INI DRMs after initial INI failure suggests a potent, highly dynamic selection of INI resistant strains that is unaffected by co-location with PI and RTI DRMs...
  2. ncbi Rare one and two amino acid inserts adjacent to codon 103 of the HIV-1 reverse transcriptase (RT) affect susceptibility to non-nucleoside RT inhibitors
    Mark A Winters
    Center for AIDS Research, Stanford University, Stanford, CA, USA
    Antivir Ther 10:363-6. 2005
    ..These results suggest that inserts in the NNRTI-binding pocket contribute to NNRTI resistance, but are tolerated only under specific genetic conditions...
  3. ncbi New two-amino acid insertion near codon 70 of the HIV type 1 protease gene
    Mark A Winters
    Division of Infectious Diseases, Stanford University Medical Center, Stanford, California 94305, USA
    AIDS Res Hum Retroviruses 21:311-3. 2005
    ..Susceptibility of this strain to protease inhibitors was similar to that of non-insert-containing strains with comparable resistance mutations and one or more other major PI mutations...
  4. ncbi Insertions in the human immunodeficiency virus type 1 protease and reverse transcriptase genes: clinical impact and molecular mechanisms
    Mark A Winters
    Division of Infectious Diseases and Geographic Medicine, Stanford University, 300 Pasteur Drive, Room S-146, Stanford, California 94305-5107, USA
    Antimicrob Agents Chemother 49:2575-82. 2005
  5. ncbi Impact of highly active antiretroviral therapy on hepatitis C virus protease quasispecies diversity in HIV co-infected patients
    Mark A Winters
    AIDS Research Center, VA Palo Alto Health Care System, Palo Alto, California 94304, USA
    J Med Virol 82:791-8. 2010
    ..These results suggest ARV treatment for HIV would not affect the efficacy of HCV PI treatment...
  6. ncbi Variants other than aspartic acid at codon 69 of the human immunodeficiency virus type 1 reverse transcriptase gene affect susceptibility to nuleoside analogs
    M A Winters
    Division of Infectious Diseases and Geographic Medicine, Stanford University, Stanford, California, USA
    Antimicrob Agents Chemother 45:2276-9. 2001
    ..These results suggest that the T69D mutation is not the only codon 69 variant associated with drug resistance and that ddC is not the only drug affected...
  7. ncbi Genotypic, phenotypic, and modeling studies of a deletion in the beta3-beta4 region of the human immunodeficiency virus type 1 reverse transcriptase gene that is associated with resistance to nucleoside reverse transcriptase inhibitors
    M A Winters
    Stanford University, Stanford, California 94305, USA
    J Virol 74:10707-13. 2000
    ..These results suggest that the deletion in the RT gene contributes to resistance to several nucleoside analogs through a complex interaction with other mutations in the RT gene...
  8. ncbi Frequency of antiretroviral drug resistance mutations in HIV-1 strains from patients failing triple drug regimens. The Terry Beirn Community Programs for Clinical Research on AIDS
    M A Winters
    Stanford University, Calif, USA
    Antivir Ther 5:57-63. 2000
    ..These protease gene mutations and a similarly limited set of RT gene mutations appear to be responsible for treatment failure in antiretroviral therapy...
  9. ncbi Maternal-fetal pharmacokinetics and dynamics of a single intrapartum dose of maraviroc in rhesus macaques
    Mark A Winters
    AIDS Research Center, VA Palo Alto Health Care System, Palo Alto, California 94304, USA
    Antimicrob Agents Chemother 54:4059-63. 2010
    ..The low concentrations of fetal maraviroc and short pharmacokinetic profile in infants suggest that a single maternal intrapartum dose of maraviroc would not be effective in reducing the risk of MTCT of HIV...
  10. ncbi Use of dried clinical samples for storing and detecting influenza RNA
    Mark Winters
    VA Palo Alto Health Care System, Palo Alto, CA, USA
    Influenza Other Respi Viruses 5:413-7. 2011
    ....
  11. ncbi Clinical impact of the M184V mutation on switching to didanosine or maintaining lamivudine treatment in nucleoside reverse-transcriptase inhibitor-experienced patients
    Mark A Winters
    Division of Infectious Diseases and Geographic Medicine, Stanford University, Stanford, California 94305, USA
    J Infect Dis 188:537-40. 2003
    ..These results show that ddI continues to provide activity against viruses with the M184V/I mutation and suggest that the presence of the M184V/I mutation should not preclude the use of ddI in nucleoside-experienced patients...
  12. ncbi A 6-basepair insert in the reverse transcriptase gene of human immunodeficiency virus type 1 confers resistance to multiple nucleoside inhibitors
    M A Winters
    Center for AIDS Research at Stanford, Stanford University, Stanford, California 94305 5107, USA
    J Clin Invest 102:1769-75. 1998
    ..These results establish that inserts, like point mutations, are selected in vivo during antiretroviral therapy and provide resistance to multiple nucleoside analogs...
  13. ncbi Changes in CD4+ and CD8+ T cell subsets in response to highly active antiretroviral therapy in HIV type 1-infected patients with prior protease inhibitor experience
    C M Gray
    Center for AIDS Research at Stanford, Division of Infectious Disease and Geographic Medicine, Stanford University School of Medicine, California 94305, USA
    AIDS Res Hum Retroviruses 14:561-9. 1998
    ..Overall, drug-experienced patients responding to HAART displayed increased numbers of naive and memory CD4+ subsets, and reduced CD8+ cell activation with a loss of TCR skewing...
  14. ncbi Reproducibility of human immunodeficiency virus type 1 (HIV-1) protease and reverse transcriptase sequencing of plasma samples from heavily treated HIV-1-infected individuals
    R W Shafer
    Division of Infectious Diseases and Geographic Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA
    J Virol Methods 86:143-53. 2000
    ..These results suggest that HIV-1 protease and RT sequencing of circulating plasma virus is highly reproducible but that the sensitivity at detecting mutations may be low if those mutations are present as minor variants...
  15. ncbi Multiple concurrent reverse transcriptase and protease mutations and multidrug resistance of HIV-1 isolates from heavily treated patients
    R W Shafer
    Stanford University Medical Center, California 94305, USA
    Ann Intern Med 128:906-11. 1998
    ..Drug resistance of HIV-1 is an obstacle to the long-term efficacy of antiretroviral therapy...
  16. ncbi The prognostic significance of serum viral load, codon 215 reverse transcriptase mutation and CD4+ T cells on progression of HIV disease in a double-blind study of thymopentin
    T C Merigan
    Center for AIDS Research, Stanford University Medical Center, California 94305, USA
    AIDS 10:159-65. 1996
    ..The retrospective evaluation of thymopentin treatment effect on subjects in high risk groups for progression was a secondary objective...
  17. ncbi Genotypic correlates of a virologic response to stavudine after zidovudine monotherapy
    N S Shulman
    Division of Infectious Diseases, Stanford University Medical Center, Stanford, California 94305, USA
    J Acquir Immune Defic Syndr 27:377-80. 2001
    ..We conclude that in patients with prior ZDV treatment, those with only one ZDV mutation, particularly at position 70, can still get reasonable virologic activity from d4T. Those with more mutations are not likely to have much benefit...
  18. ncbi Human immunodeficiency virus type 1 protease genotypes and in vitro protease inhibitor susceptibilities of isolates from individuals who were switched to other protease inhibitors after long-term saquinavir treatment
    M A Winters
    Center for AIDS Research at Stanford, Stanford University, Stanford, California 94305, USA
    J Virol 72:5303-6. 1998
    ..These results suggest that mutations selected in vivo by initial saquinavir therapy may provide more cross-resistance to the other protease inhibitors than has been previously reported...
  19. ncbi Frequency of class I HLA-restricted anti-HIV CD8+ T cells in individuals receiving highly active antiretroviral therapy (HAART)
    C M Gray
    Center for AIDS Research, Division of Infectious Diseases and Geographic Medicine, Stanford University Medical Center, Stanford, CA 94305
    J Immunol 162:1780-8. 1999
    ..In conclusion, this study provides evidence that persistently replicating viral populations are probably required to maintain high frequencies of HIV-1 epitope-specific CD8+ T cells in asymptomatic chronically infected individuals..
  20. ncbi HIV-1 drug resistance genotype results in patients with plasma samples with HIV-1 RNA levels less than 75 copies/mL
    Yumi Mitsuya
    Division of Infectious Diseases, Department of Medicine, Stanford University, Stanford 94305, and Kaiser-Permanente Medical Care Program-Northern California, Oakland, CA, USA
    J Acquir Immune Defic Syndr 43:56-9. 2006
    ..Genotype validity was confirmed in 49 of 50 patients with a previous or follow-up genotype. The belief that genotypic resistance testing is unreliable in samples with low-level viremia should be reassessed...
  21. ncbi Panel of prototypical infectious molecular HIV-1 clones containing multiple nucleoside reverse transcriptase inhibitor resistance mutations
    Elizabeth Johnston
    Division of Infectious Diseases, Stanford University, Stanford, CA, USA
    AIDS 19:731-3. 2005
    ..Testing the activity of new antiretroviral compounds against this panel of drug-resistant clones will determine their relative activity against many clinically relevant NRTI-resistant viruses...
  22. ncbi Restructuring the neuronal stress response with anti-glucocorticoid gene delivery
    D Kaufer
    Department of Biological Sciences, Stanford University, Stanford, California, USA
    Nat Neurosci 7:947-53. 2004
    ..Our findings elucidate three principal steps in the neuronal stress-response pathway, all of which are amenable to therapeutic intervention...
  23. ncbi Subtle decreases in stavudine phenotypic susceptibility predict poor virologic response to stavudine monotherapy in zidovudine-experienced patients
    Nancy S Shulman
    Stanford University School of Medicine, California 94305, USA
    J Acquir Immune Defic Syndr 31:121-7. 2002
    ..d4T susceptibility greater than 1.4-fold change was associated with failure to achieve significant viral load reduction after 8 weeks of d4T monotherapy...
  24. ncbi Nonnucleoside reverse transcriptase inhibitor phenotypic hypersusceptibility can be demonstrated in different assays
    Nancy S Shulman
    Center for AIDS Research, Division of Infectious Diseases, Stanford University, Stanford, CA 97305, USA
    J Acquir Immune Defic Syndr 39:78-81. 2005
    ..In fact, there was a report that a commercial multicycle assay did not readily detect hypersusceptibility...
  25. ncbi Impact of interferon-ribavirin treatment on hepatitis C virus (HCV) protease quasispecies diversity in HIV- and HCV-coinfected patients
    Aarthi Chary
    AIDS Research Center, Veterans Affairs Palo Alto Health Care System, Palo Alto, California 94304, USA
    J Infect Dis 202:889-93. 2010
    ..The effect of prior interferon-ribavirin treatment on HCV NS3 will likely not impact HCV PI efficacy in HIV-coinfected patients receiving ART...
  26. ncbi Potent efficacy of entecavir (BMS-200475) in a duck model of hepatitis B virus replication
    Patricia L Marion
    Division of Gastroenterology, Stanford University School of Medicine, Stanford, California 94305 5187, USA
    Antimicrob Agents Chemother 46:82-8. 2002
    ..ETV and 3TC were both well tolerated in all treated animals. These results show that ETV is a highly potent and effective antiviral in the DHBV duck model...
  27. ncbi Functional correlates of insertion mutations in the protease gene of human immunodeficiency virus type 1 isolates from patients
    E Y Kim
    Center for AIDS Research, Stanford University, Stanford, California 94305 5107, USA
    J Virol 75:11227-33. 2001
    ....
  28. ncbi Association of a novel human immunodeficiency virus type 1 protease substrate cleft mutation, L23I, with protease inhibitor therapy and in vitro drug resistance
    Elizabeth Johnston
    Division of Infectious Diseases, Department of Medicine, Stanford University, Stanford, California 94305, USA
    Antimicrob Agents Chemother 48:4864-8. 2004
    ..In combination with other drug resistance mutations, L23I was associated with multidrug resistance and a compensatory increase in replication capacity...
  29. ncbi Hepatitis C virus protease gene diversity in patients coinfected with human immunodeficiency virus
    Mark A Winters
    Division of Infectious Diseases and Geographic Medicine, Stanford University, California, USA
    J Virol 80:4196-9. 2006
    ..01). Significant variability exists within HCV protease gene variants at the patient level and could affect the effectiveness of HCV protease inhibitors...
  30. ncbi N88D facilitates the co-occurrence of D30N and L90M and the development of multidrug resistance in HIV type 1 protease following nelfinavir treatment failure
    Yumi Mitsuya
    Division of Infectious Diseases, Department of Medicine, Stanford University, Stanford, California 94305, USA
    AIDS Res Hum Retroviruses 22:1300-5. 2006
    ....
  31. ncbi More on the treatment-tropism relationship: the impact of prior antiretroviral treatment on HIV coreceptor tropism among subjects entering AIDS clinical trials group 175
    Nancy S Shulman
    J Infect Dis 196:328-9; author reply 329-30. 2007
  32. ncbi "Wide-open" 1.3 A structure of a multidrug-resistant HIV-1 protease as a drug target
    Philip Martin
    Department of Biochemistry and Molecular Biology, Wayne State University School of Medicine, Detroit, Michigan 48201, USA
    Structure 13:1887-95. 2005
    ..A third key structural change of the protease is due to the mutations from longer to shorter amino acid side chains at positions 82 and 84...
  33. ncbi Increasing prevalence of HIV-1 reverse transcriptase mutation K65R correlates with tenofovir utilization
    Ron M Kagan
    Antivir Ther 9:827-8. 2004
  34. ncbi HIV-1 protease variants from 100-fold drug resistant clinical isolates: expression, purification, and crystallization
    John F Vickrey
    Department of Biochemistry and Molecular Biology, Wayne State University School of Medicine, 540 E. Canfield Avenue, Detroit, MI 48201, USA
    Protein Expr Purif 28:165-72. 2003
    ..Here, we report the expression, purification, and crystallization of clinical isolates of HIV-1 protease that have been characterized to be more than 100 times less susceptible to US FDA approved protease inhibitors...
  35. ncbi Crystal structures of a multidrug-resistant human immunodeficiency virus type 1 protease reveal an expanded active-site cavity
    Bradley C Logsdon
    Department of Biochemistry and Molecular Biology, Wayne State University School of Medicine, Detroit, Michigan, USA
    J Virol 78:3123-32. 2004
    ..This MDR 769 protease represents a new antiviral target, presenting the possibility of designing novel inhibitors with activity against the open and expanded protease forms...