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227 results on '"Demeter, Lisa M"'

11. HIV-1 reverse transcriptase mutants resistant to nonnucleoside reverse transcriptase inhibitors do not adversely affect DNA synthesis: Pre-steady-state and steady-state kinetic studies

Author

Domaoal, Robert A., Demeter, Lisa M., and Bambara, Robert A.

Subjects
DNA synthesis -- Analysis, DNA polymerases -- Analysis, Reverse transcriptase inhibitors -- Analysis, HIV infection -- Drug therapy, Health
Abstract

The polymerase function of 3 clinically occurring nonnucleoside reverse transcriptase inhibitor (NNRTI)-resistant RTs in greater detail, under both pre-steady-state and steady-state conditions is evaluated. Results indicate that the close proximity of the NNRTI-resistance mutations to the polymerase active site does not affect the interactions of the enzyme with the incoming nucleotide or the primer-template sufficiently to affect polymerization.

Published
2006

13. Antiretroviral drug resistance testing in adults infected with human immunodeficiency virus type 1: 2003 recommendations of an international AIDS society--USA panel. (HIV/AIDS)

Author

Hirsch, Martin S., Brun-Vezinet, Francoise, Clotet, Bonaventura, Conway, Brian, Kuritzkes, Daniel R., D'Aquila, Richard T., Demeter, Lisa M., Hammer, Scott M., Johnson, Victoria A., Loveday, Clive, Mellors, John W., Jacobsen, Donna M., and Richman, Douglas D.

Subjects
HIV infection -- Care and treatment, Drug resistance -- Genetic aspects, Drug resistance -- Physiological aspects, Clinical trials, Antiviral agents -- Testing, Health, Health care industry
Published
2003

14. The Y181C mutant of HIV-1 reverse transcriptase resistant to nonnucleoside reverse transcriptase inhibitors alters the size distribution of RNase H cleavages

Author

Archer, Richard H., Wisniewski, Michele, Bambara, Robert A., and Demeter, Lisa M.

Subjects
Reverse transcriptase -- Physiological aspects, HIV (Viruses) -- Physiological aspects, Mutation (Biology) -- Research, Biological sciences, Chemistry
Abstract

The effect of Y181C mutant on RNA 5'-end-directed RNase H cleavage reveals that the mutant preferentially cleaves toward the RNA 5' end of the RNA-DNA hybrid leading to smaller RNase H cleavage products.

Published
2001

17. Epidemiological and biological evidence for a compensatory effect of connection domain mutation N348I on M184V in HIV-1 reverse transcriptase

Author

von Wyl, VIktor, Ehteshami, Maryam, Symons, Jori, Burgisser, Philippe, Nijhuis, Monique, Demeter, Lisa M., Yerly, Sabine, Boni, Jurg, Klimkait, Thomas, Schuurman, Rob, Ledergerber, Bruno, Gotte, Matthias, and Gunthard, Huldrych F.

Subjects
Gene mutations -- Research, Reverse transcriptase -- Genetic aspects, Reverse transcriptase -- Research, HIV infection -- Genetic aspects, HIV infection -- Research, Zidovudine -- Dosage and administration, Zidovudine -- Complications and side effects, Lamivudine -- Dosage and administration, Lamivudine -- Complications and side effects, Drug resistance in microorganisms -- Genetic aspects, Drug resistance in microorganisms -- Research, Health
Published
2010

22. Antiretroviral Drug Resistance Testing in Adults With HIV Infection, Part 1

Author

Hirsch, Martin S., Conway, Brian, D'Aquila, Richard T., Brun-Vezinet, Francoise, Johnson, Victoria A., Clotet, Bonaventura, Demeter, Lisa M., Hammer, Scott M., Jacobsen, Donna M., Kuritzkes, Daniel R., Loveday, Clive, Mellors, John W., Vella, Stefano, and Richman, Douglas D.

Subjects
International AIDS Society -- Reports, HIV infection -- Drug therapy, Drug resistance in microorganisms -- Prevention, Antiviral agents -- Physiological aspects, HIV (Viruses) -- Genetic aspects
Abstract

Genetic testing of the virus in HIV-infected patients may be useful in guiding antiviral drug therapy to maximize effectiveness and reduce development of drug resistance. A panel of experts assembled by the International AIDS Society - USA recommends viral load and CD4+ T-cell count as immunologic guides for antiretroviral drug therapy. Poor patient compliance with treatment protocols contributes to the development of drug-resistant HIV. Resistance testing may be useful for determining the optimal drugs for use in treatment.

Published
1998

23. A controlled trial of two nucleoside analogues plus indinavir in persons with human immunodeficiency virus infection and CD4 cell counts of 200 per cubic millimeter or less

Author

Hammer, Scott M., Squires, Kathleen E., Hughes, Michael D., Grimes, Janet M., Demeter, Lisa M., Currier, Judith S., Eron, Joseph J., Jr., Feinberg, Judith E., Balfour, Henry H., Jr., Deyton, Lawrence R., Chodakewitz, Jeffrey A., and Fischl, Margaret A.

Subjects
Indinavir (Medication) -- Evaluation, Protease inhibitors -- Evaluation, Zidovudine -- Evaluation, Lamivudine -- Evaluation, HIV infection -- Drug therapy
Abstract

A protease inhibitor combined with two nucleoside analogs seems to be more effective than the nucleoside analogs alone in preventing the progression of HIV infection. These are all drugs used to treat HIV infection. A total of 1,156 HIV-infected patients were randomly assigned to take the nucleoside analogs zidovudine and lamivudine alone or combined with the protease inhibitor indinavir. The group taking all three drugs had half the risk of progressing to AIDS or dying compared to those taking the nucleoside analogs. They also experienced greater increases in their CD4 cell counts and greater decreases in HIV RNA levels.

Published
1997

27. Phase I study of atevirdine mesylate (U-87201E) monotherapy in HIV-1-infected patients

Author

Demeter, Lisa M., Meehan, Patricia M., Morse, Gene, Fischl, Margaret A., Para, Michael, Powderly, William, Leedom, John, Holden-Wiltse, Jeanne, Greisberger, Carol, Wood, Kenneth, Timpone, Joseph, Jr., Wathen, Lynne K., Nevin, Thomas, Resnick, Lionel, Batts, Donald H., and Reichman, Richard C.

Subjects
HIV infection -- Drug therapy, Reverse transcriptase inhibitors -- Evaluation, Health
Abstract

Further research is needed to determine whether atevirdine mesylate (U-87201E) is effective in treating HIV infection. This drug belongs to a class of AIDS drugs called non-nucleoside reverse transcriptase inhibitors. In a study of 34 HIV-infected patients, the drug did not substantially lower viral levels or increase T cell counts. However, in 41% of the patients, the virus became resistant to the drug. This resistance might not develop if the drug is given in combination with other AIDS drugs such as zidovudine.

Published
1998

31. Treatment of condyloma acuminatum with three different interferon-alpha preparations administered parenterally: a double-blind, placebo-controlled trial

Author

Reichman, Richard C., Oakes, David, Bonnez, William, Brown, Darron, Mattison, H. Reid, Bailey-Farchione, Allyson, Stoler, Mark H., Demeter, Lisa M., Tyring, Steven K., Miller, Lisa, Whitley, Richard, Carveth, Holly, Weidner, Melissa, Krueger, Gerald, and Choi, Anna

Subjects
Interferon alpha -- Health aspects, Interferon alpha -- Adverse and side effects, Condyloma acuminatum -- Care and treatment, Health
Abstract

Condyloma acuminatum is a sexually transmitted disease that causes anal and genital warts. It is caused by a human papillomavirus (HPV), and is becoming more common. Interferon has been shown to be more effective than placebo in treating HPV. Therefore, the effectiveness of three different interferon-alpha preparations, 2a, 2b and n1, in the treatment of condyloma was evaluated in 178 patients with the disease. Subcutaneous interferon-alpha reduced the size and number of warts by 50 percent when compared with placebo. All three interferon preparations were equally effective in treating the condition. Spontaneous regression of warts (without treatment) was more common among women than men. Also, interferon-alpha treatment was more effective in eliminating warts in women than in men. Interferon-alpha was associated with a higher incidence of fever, headache and chills than placebo. It is concluded that interferon-alpha reduced anogenital warts, although the rate of complete regression was low. Combination therapy, using several different treatments, should be evaluated further as a treatment for condyloma acuminatum. (Consumer Summary produced by Reliance Medical Information, Inc.)

Published
1990

37. Epidemiological and Biological Evidence for a Compensatory Effect of Connection Domain Mutation N348I on M184V in HIV-1 Reverse Transcriptase

Author

von Wyl, Viktor, Ehteshami, Maryam, Symons, Jori, Bürgisser, Philippe, Nijhuis, Monique, Demeter, Lisa M., Yerly, Sabine, Böni, Jürg, Klimkait, Thomas, Schuurman, Rob, Ledergerber, Bruno, Götte, Matthias, Günthard, Huldrych F., von Wyl, Viktor, Ehteshami, Maryam, Symons, Jori, Bürgisser, Philippe, Nijhuis, Monique, Demeter, Lisa M., Yerly, Sabine, Böni, Jürg, Klimkait, Thomas, Schuurman, Rob, Ledergerber, Bruno, Götte, Matthias, and Günthard, Huldrych F.

Abstract

Background. The connection domain mutation N348I confers resistance to zidovudine (AZT) and is associated with the lamivudine (3TC) mutation M184V. We explored the biochemical and virological influence of N348I in the context of M184V. Methods. Genotypic resistance data for patients receiving monotherapy or dual therapy with AZT, lamivudine (3TC), or AZT/3TC were analyzed. Rates of N348I emergence were compared between treatment groups. Mutant reverse transcriptases (RTs) containing M184V and/or N348I were generated to study enzymatic and virological properties. Results. We included 50 AZT-treated, 11 3TC-treated, and 10 AZT/3TC-treated patients. N348I was observed in 3 (6%), 0, and 4 (40%) of these patients, respectively. The rate of N348I emergence was increased by 5-fold in the AZT/3TC group (11.7 instances [95% confidence interval {CI}, 3.2-30.1 instances] per 100 person-years of receipt of AZT), compared with the rate noted for the AZT group (2.3 instances [95% CI, 0.4-6.8 instances] per 100 person-years of receipt of AZT; P = .04). Biochemical data show that N348I can partially compensate for the diminution in processive DNA synthesis and the reduction in AZT excision associated with M184V. Furthermore, virological analyses demonstrate that N348I confers low-level resistance to AZT and partly restores the reduced RT activity of the M184V variant. Conclusion. In vivo selection of N348I is driven by AZT and is further facilitated when 3TC is coadministered. Compensatory interactions between N348I and M184V help to explain these findings

Published
2017

38. HIV-1 Reverse Transcriptase Connection Domain Mutations: Dynamics of Emergence and Implications for Success of Combination Antiretroviral Therapy

Author

von Wyl, Viktor, Ehteshami, Maryam, Demeter, Lisa M., Bürgisser, Philippe, Nijhuis, Monique, Symons, Jori, Yerly, Sabine, Böni, Jürg, Klimkait, Thomas, Schuurman, Rob, Ledergerber, Bruno, Götte, Matthias, Günthard, Huldrych F., von Wyl, Viktor, Ehteshami, Maryam, Demeter, Lisa M., Bürgisser, Philippe, Nijhuis, Monique, Symons, Jori, Yerly, Sabine, Böni, Jürg, Klimkait, Thomas, Schuurman, Rob, Ledergerber, Bruno, Götte, Matthias, and Günthard, Huldrych F.

Abstract

Background. Factors promoting the emergence of human immunodeficiency virus type 1 (HIV-1) reverse transcriptase (RT) connection domain mutations and their effect on antiretroviral therapy (ART) are still largely undetermined.We investigated this matter by analyzing genotypic resistance tests covering 400 amino acid positions in the RT of HIV-1 subtype B viruses and corresponding treatment histories and laboratory measurements. Methods. The emergence of connection domain mutations was studied in 334 patients receiving monotherapy or dual therapy with thymidine analogues at the time of the genotypic resistance test. Response to subsequent combination ART (cART) was analyzed using Cox regression for 291 patients receiving unboosted protease inhibitors. Response was defined by ever reaching an HIV RNA level <50 copies/mL during the first cART. Results. The connection domain mutations N348I, R356K, R358K, A360V, and A371V were more frequently observed in ART-exposed than ART-naive patients, of which only N348I and A360V were nonpolymorphic (with a prevalence of <1.5% in untreated patients). N348I correlated with M184V and predominantly occurred in patients receiving lamivudine and zidovudine concomitantly. A360V was not associated with specific drug combinations and was found to emerge later than M184V or thymidine analogue mutations. Nonpolymorphic connection domain mutations were rarely detected in the absence of established drug resistance mutations in ART-exposed individuals (prevalence, <1%). None of the 5 connection domain mutations associated with treatment showed a statistically significant effect on response to cART. Conclusions. Despite their frequent emergence, connection domain mutations did not show large detrimental effects on response to cART. Currently, routine implementation of connection domain sequencing seems unnecessary for developed health care settings

Published
2017

39. Therapeutic drug monitoring: role for a pharmacist in multidisciplinary antiretroviral management

Author

Slish, Judianne C., Catanzaro, Linda M., Ma, Qing, Okusanya, Olanrewaju, Demeter, Lisa M., Albrecht, Mary, DiFrancesco, Robin, and Morse, Gene D.

Subjects
Homeopathy -- Materia medica and therapeutics, Highly active antiretroviral therapy -- Case studies -- Usage, Therapeutics -- Usage -- Case studies, HIV infection -- Risk factors -- Case studies, Pharmaceuticals and cosmetics industries, Usage, Case studies, Risk factors
Abstract

The current treatment guidelines for HIV pharmacotherapy recommend combinations of antiretrovirals (ARVs) to achieve optimal suppression of HIV replication. However, the initiation and long-term management of ARV therapy in a [...]

Published
2005

40. No Evidence for Decay of the Latent Reservoir in HIV‐1–Infected Patients Receiving Intensive Enfuvirtide‐Containing Antiretroviral Therapy

Author

Para, Michael, Lai, Jun, Siliciano, Janet D., Gandhi, Rajesh T., Eron, Joseph J., Bastow, Barbara, Bosch, Ronald J., Aga, Evgenia, Siliciano, Robert F., Albrecht, Mary, Dykes, Carrie, and Demeter, Lisa M.

Abstract

Human immunodeficiency virus type 1 (HIV-1) persists in a latent reservoir of infected resting memory CD4 cells in patients receiving antiretroviral therapy. We assessed whether multitarget therapy with enfuvirtide, 2 reverse-transcriptase inhibitors, and a ritonavir-boosted protease inhibitor leads to decay of this reservoir. Nineteen treatment-naive patients initiated this regimen; 9 experienced virologic suppression and continued enfuvirtide-containing therapy for at least 48 weeks. In enfuvirtide-treated patients with virological suppression, there was no decay of the latent reservoir (95% confidence interval for half-life, 11 months to infinity). The stability of the latent reservoir despite intensive therapy suggests that new strategies are needed to eradicate HIV-1 from this reservoir.

Published
2010
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43. A controlled trial of two nucleoside analogues plus indinavir in persons with human immunodeficiency virus infection and CD4 cell counts of 200 per cubic millimeter or less

Author

Currier, Judith S., Hughes, Michael D., Chodakewitz, Jeffrey A., Eron, Joseph J., Squires, Kathleen E., Grimes, Janet M., Hammer, Scott M., Feinberg, Judith E., Deyton, Lawrence R., Fischl, Margaret A., Balfour, Henry H., and Demeter, Lisa M.

Abstract

Background: The efficacy and safety of adding a protease inhibitor to two nucleoside analogues to treat human immunodeficiency virus type 1 (HIV-1) infection are not clear. We compared treatment with the protease inhibitor indinavir in addition to zidovudine and lamivudine with treatment with the two nucleosides alone in HIV-infected adults previously treated with zidovudine. Methods: A total of 1156 patients not previously treated with lamivudine or protease inhibitors were stratified according to CD4 cell count (50 or fewer vs. 51 to 200 cells per cubic millimeter) and randomly assigned to one of two daily regimens: 600 mg of zidovudine and 300 mg of lamivudine, or that regimen with 2400 mg of indinavir. Stavudine could be substituted for zidovudine. The primary end point was the time to the development of the acquired immunodeficiency syndrome (AIDS) or death. Results: The proportion of patients whose disease progressed to AIDS or death was lower with indinavir, zidovudine (or stavudine), and lamivudine (6 percent) than with zidovudine (or stavudine) and lamivudine alone (11 percent; estimated hazard ratio, 0.50; 95 percent confidence interval, 0.33 to 0.76; P 0.001). Mortality in the two groups was 1.4 percent and 3.1 percent, respectively (estimated hazard ratio, 0.43; 95 percent confidence interval, 0.19 to 0.99; P=0.04). The effects of treatment were similar in both CD4 cell strata. The responses of CD4 cells and plasma HIV-1 RNA paralleled the clinical results. Conclusions: Treatment with indinavir, zidovudine, and lamivudine as compared with zidovudine and lamivudine alone significantly slows the progression of HIV-1 disease in patients with 200 CD4 cells or fewer per cubic millimeter and prior exposure to zidovudine. (N Engl J Med 1997;337:725-33.)

Published
1997
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