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Hepatitis C virus resistance to new specifically-targeted antiviral therapy: A public health perspective.

World journal of virology

Salvatierra K, Fareleski S, Forcada A, López-Labrador FX.
PMID: 24175225
World J Virol. 2013 Feb 12;2(1):6-15. doi: 10.5501/wjv.v2.i1.6.

Until very recently, treatment for chronic hepatitis C virus (HCV) infection has been based on the combination of two non-viral specific drugs: pegylated interferon-α and ribavirin, which is effective in, overall, about 40%-50% of cases. To improve the response...

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Salvatierra K, Fareleski S, Forcada A, et al. Hepatitis C virus resistance to new specifically-targeted antiviral therapy: A public health perspective. World J Virol. 2013;2(1):6-15doi: 10.5501/wjv.v2.i1.6.
Salvatierra, K., Fareleski, S., Forcada, A., & López-Labrador, F. X. (2013). Hepatitis C virus resistance to new specifically-targeted antiviral therapy: A public health perspective. World journal of virology, 2(1), 6-15. https://doi.org/10.5501/wjv.v2.i1.6
Salvatierra, Karina, et al. "Hepatitis C virus resistance to new specifically-targeted antiviral therapy: A public health perspective." World journal of virology vol. 2,1 (2013): 6-15. doi: https://doi.org/10.5501/wjv.v2.i1.6
Salvatierra K, Fareleski S, Forcada A, López-Labrador FX. Hepatitis C virus resistance to new specifically-targeted antiviral therapy: A public health perspective. World J Virol. 2013 Feb 12;2(1):6-15. doi: 10.5501/wjv.v2.i1.6. PMID: 24175225; PMCID: PMC3785043.
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New treatments for genotype 1 chronic hepatitis C - focus on simeprevir.

Therapeutics and clinical risk management

Kanda T, Nakamoto S, Wu S, Yokosuka O.
PMID: 24920913
Ther Clin Risk Manag. 2014 May 24;10:387-94. doi: 10.2147/TCRM.S50170. eCollection 2014.

Chronic hepatitis C virus (HCV) infection causes end-stage liver diseases and hepato cellular carcinoma. In the USA, Canada, and Japan, simeprevir - one of the second-generation HCV NS3/4A protease inhibitors - in combination with peginterferon α-2a or 2b plus...

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Kanda T, Nakamoto S, Wu S, et al. New treatments for genotype 1 chronic hepatitis C - focus on simeprevir. Ther Clin Risk Manag. 2014;10:387-94doi: 10.2147/TCRM.S50170.
Kanda, T., Nakamoto, S., Wu, S., & Yokosuka, O. (2014). New treatments for genotype 1 chronic hepatitis C - focus on simeprevir. Therapeutics and clinical risk management, 10387-94. https://doi.org/10.2147/TCRM.S50170
Kanda, Tatsuo, et al. "New treatments for genotype 1 chronic hepatitis C - focus on simeprevir." Therapeutics and clinical risk management vol. 10 (2014): 387-94. doi: https://doi.org/10.2147/TCRM.S50170
Kanda T, Nakamoto S, Wu S, Yokosuka O. New treatments for genotype 1 chronic hepatitis C - focus on simeprevir. Ther Clin Risk Manag. 2014 May 24;10:387-94. doi: 10.2147/TCRM.S50170. eCollection 2014. PMID: 24920913; PMCID: PMC4043814.
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Human pigmentation: A side effect adapted from a primitive organism's survival, acting through cell attachment with an affinity for the keratinocyte and for elastin: Part I.

Indian dermatology online journal

Arianayagam S, Ryan TJ.
PMID: 24860764
Indian Dermatol Online J. 2014 Apr;5(2):201-9. doi: 10.4103/2229-5178.131125.

Pigmentation featured millions of years ago and perhaps began with an amoeba frightening off a predator with some agent such as dopamine to prevent its attachment for phagocytosis by an enemy. This paper suggests that the environmental forces of...

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Arianayagam S, Ryan TJ. Human pigmentation: A side effect adapted from a primitive organism's survival, acting through cell attachment with an affinity for the keratinocyte and for elastin: Part I. Indian Dermatol Online J. 2014;5(2):201-9doi: 10.4103/2229-5178.131125.
Arianayagam, S., & Ryan, T. J. (2014). Human pigmentation: A side effect adapted from a primitive organism's survival, acting through cell attachment with an affinity for the keratinocyte and for elastin: Part I. Indian dermatology online journal, 5(2), 201-9. https://doi.org/10.4103/2229-5178.131125
Arianayagam, Sanju, and Ryan, Terence J. "Human pigmentation: A side effect adapted from a primitive organism's survival, acting through cell attachment with an affinity for the keratinocyte and for elastin: Part I." Indian dermatology online journal vol. 5,2 (2014): 201-9. doi: https://doi.org/10.4103/2229-5178.131125
Arianayagam S, Ryan TJ. Human pigmentation: A side effect adapted from a primitive organism's survival, acting through cell attachment with an affinity for the keratinocyte and for elastin: Part I. Indian Dermatol Online J. 2014 Apr;5(2):201-9. doi: 10.4103/2229-5178.131125. PMID: 24860764; PMCID: PMC4030357.
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The salivary secretome of the biting midge, Culicoides sonorensis.

PeerJ

Lehiy CJ, Drolet BS.
PMID: 24949243
PeerJ. 2014 Jun 05;2:e426. doi: 10.7717/peerj.426. eCollection 2014.

Culicoides biting midges (Diptera: Ceratopogonidae) are hematophagous insects with over 1400 species distributed throughout the world. Many of these species are of particular agricultural importance as primary vectors of bluetongue and Schmallenberg viruses, yet little is known about Culicoides...

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Lehiy CJ, Drolet BS. The salivary secretome of the biting midge, Culicoides sonorensis. PeerJ. 2014;2:e426doi: 10.7717/peerj.426.
Lehiy, C. J., & Drolet, B. S. (2014). The salivary secretome of the biting midge, Culicoides sonorensis. PeerJ, 2e426. https://doi.org/10.7717/peerj.426
Lehiy, Christopher J, and Drolet, Barbara S. "The salivary secretome of the biting midge, Culicoides sonorensis." PeerJ vol. 2 (2014): e426. doi: https://doi.org/10.7717/peerj.426
Lehiy CJ, Drolet BS. The salivary secretome of the biting midge, Culicoides sonorensis. PeerJ. 2014 Jun 05;2:e426. doi: 10.7717/peerj.426. eCollection 2014. PMID: 24949243; PMCID: PMC4060021.
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Campylobacter jejuni gene cj0511 encodes a serine peptidase essential for colonisation.

FEBS open bio

Karlyshev AV, Thacker G, Jones MA, Clements MO, Wren BW.
PMID: 24918062
FEBS Open Bio. 2014 May 09;4:468-72. doi: 10.1016/j.fob.2014.04.012. eCollection 2014.

According to MEROPS peptidase database, Campylobacter species encode 64 predicted peptidases. However, proteolytic properties of only a few of these proteins have been confirmed experimentally. In this study we identified and characterised a Campylobacter jejuni gene cj0511 encoding a...

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Karlyshev AV, Thacker G, Jones MA, et al. Campylobacter jejuni gene cj0511 encodes a serine peptidase essential for colonisation. FEBS Open Bio. 2014;4:468-72doi: 10.1016/j.fob.2014.04.012.
Karlyshev, A. V., Thacker, G., Jones, M. A., Clements, M. O., & Wren, B. W. (2014). Campylobacter jejuni gene cj0511 encodes a serine peptidase essential for colonisation. FEBS open bio, 4468-72. https://doi.org/10.1016/j.fob.2014.04.012
Karlyshev, A V, et al. "Campylobacter jejuni gene cj0511 encodes a serine peptidase essential for colonisation." FEBS open bio vol. 4 (2014): 468-72. doi: https://doi.org/10.1016/j.fob.2014.04.012
Karlyshev AV, Thacker G, Jones MA, Clements MO, Wren BW. Campylobacter jejuni gene cj0511 encodes a serine peptidase essential for colonisation. FEBS Open Bio. 2014 May 09;4:468-72. doi: 10.1016/j.fob.2014.04.012. eCollection 2014. PMID: 24918062; PMCID: PMC4050187.
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Computing the Amino Acid Specificity of Fluctuations in Biomolecular Systems.

Journal of chemical theory and computation

Hamacher K, McCammon JA.
PMID: 26626694
J Chem Theory Comput. 2006 May;2(3):873-8. doi: 10.1021/ct050247s.

We developed a new amino acid specific method for the computation of spatial fluctuations of proteins around their native structures. We show the consistency with experimental values and the increased performance in comparison to an established model, based on...

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Hamacher K, McCammon JA. Computing the Amino Acid Specificity of Fluctuations in Biomolecular Systems. J Chem Theory Comput. 2006;2(3):873-8doi: 10.1021/ct050247s.
Hamacher, K., & McCammon, J. A. (2006). Computing the Amino Acid Specificity of Fluctuations in Biomolecular Systems. Journal of chemical theory and computation, 2(3), 873-8. https://doi.org/10.1021/ct050247s
Hamacher, K, and McCammon, J A. "Computing the Amino Acid Specificity of Fluctuations in Biomolecular Systems." Journal of chemical theory and computation vol. 2,3 (2006): 873-8. doi: https://doi.org/10.1021/ct050247s
Hamacher K, McCammon JA. Computing the Amino Acid Specificity of Fluctuations in Biomolecular Systems. J Chem Theory Comput. 2006 May;2(3):873-8. doi: 10.1021/ct050247s. PMID: 26626694.
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Asunaprevir, a protease inhibitor for the treatment of hepatitis C infection.

Therapeutics and clinical risk management

Gentile I, Buonomo AR, Zappulo E, Minei G, Morisco F, Borrelli F, Coppola N, Borgia G.
PMID: 25061308
Ther Clin Risk Manag. 2014 Jun 26;10:493-504. doi: 10.2147/TCRM.S66731. eCollection 2014.

According to the World Health Organization, approximately 150 million people worldwide are chronic carriers of hepatitis C virus (HCV). HCV infection can evolve into cirrhosis of the liver and its complications, which are ultimately responsible for more than 350,000...

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Gentile I, Buonomo AR, Zappulo E, et al. Asunaprevir, a protease inhibitor for the treatment of hepatitis C infection. Ther Clin Risk Manag. 2014;10:493-504doi: 10.2147/TCRM.S66731.
Gentile, I., Buonomo, A. R., Zappulo, E., Minei, G., Morisco, F., Borrelli, F., Coppola, N., & Borgia, G. (2014). Asunaprevir, a protease inhibitor for the treatment of hepatitis C infection. Therapeutics and clinical risk management, 10493-504. https://doi.org/10.2147/TCRM.S66731
Gentile, Ivan, et al. "Asunaprevir, a protease inhibitor for the treatment of hepatitis C infection." Therapeutics and clinical risk management vol. 10 (2014): 493-504. doi: https://doi.org/10.2147/TCRM.S66731
Gentile I, Buonomo AR, Zappulo E, Minei G, Morisco F, Borrelli F, Coppola N, Borgia G. Asunaprevir, a protease inhibitor for the treatment of hepatitis C infection. Ther Clin Risk Manag. 2014 Jun 26;10:493-504. doi: 10.2147/TCRM.S66731. eCollection 2014. PMID: 25061308; PMCID: PMC4079632.
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Interferon-based combination treatment for chronic hepatitis C in the era of direct acting antivirals.

Annals of gastroenterology

Alexopoulou A, Karayiannis P.
PMID: 25608803
Ann Gastroenterol. 2015 Jan-Mar;28(1):55-65.

The development of protease inhibitors (PIs) such as telaprevir and boceprevir constitutes a milestone in chronic hepatitis C antiviral treatment since it has achieved sustained virological response (SVR) rates of up to 75% in naïve and 29-88% in treatment-experienced...

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Alexopoulou A, Karayiannis P. Interferon-based combination treatment for chronic hepatitis C in the era of direct acting antivirals. Ann Gastroenterol. 2015;28(1):55-65
Alexopoulou, A., & Karayiannis, P. (2015). Interferon-based combination treatment for chronic hepatitis C in the era of direct acting antivirals. Annals of gastroenterology, 28(1), 55-65.
Alexopoulou, Alexandra, and Karayiannis, Peter. "Interferon-based combination treatment for chronic hepatitis C in the era of direct acting antivirals." Annals of gastroenterology vol. 28,1 (2015): 55-65.
Alexopoulou A, Karayiannis P. Interferon-based combination treatment for chronic hepatitis C in the era of direct acting antivirals. Ann Gastroenterol. 2015 Jan-Mar;28(1):55-65. PMID: 25608803; PMCID: PMC4290005.
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A cross-sectional assessment of metabolic syndrome in HIV-infected people of low socio-economic status receiving antiretroviral therapy.

Diabetology & metabolic syndrome

Tiozzo E, Konefal J, Adwan S, Martinez LA, Villabona J, Lopez J, Cutrono S, Mehdi SM, Rodriguez A, Woolger JM, Lewis JE.
PMID: 25763112
Diabetol Metab Syndr. 2015 Mar 07;7:15. doi: 10.1186/s13098-015-0008-5. eCollection 2015.

BACKGROUND: Metabolic syndrome (MetS) is a constellation of symptoms used as a measure to identify patients at increased risk for cardiovascular disease, type 2 diabetes, and all-cause mortality. The results of prolonged life expectancy and cumulative toxic effects of...

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Tiozzo E, Konefal J, Adwan S, et al. A cross-sectional assessment of metabolic syndrome in HIV-infected people of low socio-economic status receiving antiretroviral therapy. Diabetol Metab Syndr. 2015;7:15doi: 10.1186/s13098-015-0008-5.
Tiozzo, E., Konefal, J., Adwan, S., Martinez, L. A., Villabona, J., Lopez, J., Cutrono, S., Mehdi, S. M., Rodriguez, A., Woolger, J. M., & Lewis, J. E. (2015). A cross-sectional assessment of metabolic syndrome in HIV-infected people of low socio-economic status receiving antiretroviral therapy. Diabetology & metabolic syndrome, 715. https://doi.org/10.1186/s13098-015-0008-5
Tiozzo, Eduard, et al. "A cross-sectional assessment of metabolic syndrome in HIV-infected people of low socio-economic status receiving antiretroviral therapy." Diabetology & metabolic syndrome vol. 7 (2015): 15. doi: https://doi.org/10.1186/s13098-015-0008-5
Tiozzo E, Konefal J, Adwan S, Martinez LA, Villabona J, Lopez J, Cutrono S, Mehdi SM, Rodriguez A, Woolger JM, Lewis JE. A cross-sectional assessment of metabolic syndrome in HIV-infected people of low socio-economic status receiving antiretroviral therapy. Diabetol Metab Syndr. 2015 Mar 07;7:15. doi: 10.1186/s13098-015-0008-5. eCollection 2015. PMID: 25763112; PMCID: PMC4356056.
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Computational Study of the Effects of Mutations A156T, D168V, and D168Q on the Binding of HCV Protease Inhibitors.

Journal of chemical theory and computation

Guo Z, Prongay A, Tong X, Fischmann T, Bogen S, Velazquez F, Venkatraman S, Njoroge FG, Madison V.
PMID: 26627036
J Chem Theory Comput. 2006 Nov;2(6):1657-63. doi: 10.1021/ct600151y.

The effect of the resistance mutations A156T, D168V, and D168Q in HCV protease on the binding of SCH 6, SCH 503034, VX-950, BILN-2061, and compound 1 was evaluated using the free energy perturbation (FEP) approach. All the inhibitors are...

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Guo Z, Prongay A, Tong X, et al. Computational Study of the Effects of Mutations A156T, D168V, and D168Q on the Binding of HCV Protease Inhibitors. J Chem Theory Comput. 2006;2(6):1657-63doi: 10.1021/ct600151y.
Guo, Z., Prongay, A., Tong, X., Fischmann, T., Bogen, S., Velazquez, F., Venkatraman, S., Njoroge, F. G., & Madison, V. (2006). Computational Study of the Effects of Mutations A156T, D168V, and D168Q on the Binding of HCV Protease Inhibitors. Journal of chemical theory and computation, 2(6), 1657-63. https://doi.org/10.1021/ct600151y
Guo, Zhuyan, et al. "Computational Study of the Effects of Mutations A156T, D168V, and D168Q on the Binding of HCV Protease Inhibitors." Journal of chemical theory and computation vol. 2,6 (2006): 1657-63. doi: https://doi.org/10.1021/ct600151y
Guo Z, Prongay A, Tong X, Fischmann T, Bogen S, Velazquez F, Venkatraman S, Njoroge FG, Madison V. Computational Study of the Effects of Mutations A156T, D168V, and D168Q on the Binding of HCV Protease Inhibitors. J Chem Theory Comput. 2006 Nov;2(6):1657-63. doi: 10.1021/ct600151y. PMID: 26627036.
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Studies on phenotypic expression patterns of proteases and protease inhibitors in benign compared to malignant prostate tissues.

Prostate cancer and prostatic diseases

Bjartell A, Paju A, Stenman UH, Väisänen V, Aumüller G, Diamandis E, Becker C, Lilja H.
PMID: 12497117
Prostate Cancer Prostatic Dis. 2000 Dec;3:S7. doi: 10.1038/sj.pcan.4500431.

No abstract available.

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Bjartell A, Paju A, Stenman UH, et al. Studies on phenotypic expression patterns of proteases and protease inhibitors in benign compared to malignant prostate tissues. Prostate Cancer Prostatic Dis. 2000;3:S7doi: 10.1038/sj.pcan.4500431.
Bjartell, A., Paju, A., Stenman, U. H., Väisänen, V., Aumüller, G., Diamandis, E., Becker, C., & Lilja, H. (2000). Studies on phenotypic expression patterns of proteases and protease inhibitors in benign compared to malignant prostate tissues. Prostate cancer and prostatic diseases, 3S7. https://doi.org/10.1038/sj.pcan.4500431
Bjartell, A, et al. "Studies on phenotypic expression patterns of proteases and protease inhibitors in benign compared to malignant prostate tissues." Prostate cancer and prostatic diseases vol. 3 (2000): S7. doi: https://doi.org/10.1038/sj.pcan.4500431
Bjartell A, Paju A, Stenman UH, Väisänen V, Aumüller G, Diamandis E, Becker C, Lilja H. Studies on phenotypic expression patterns of proteases and protease inhibitors in benign compared to malignant prostate tissues. Prostate Cancer Prostatic Dis. 2000 Dec;3:S7. doi: 10.1038/sj.pcan.4500431. PMID: 12497117.
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Clinical Pharmacologic Considerations for HIV-1 Protease Inhibitors.

Current infectious disease reports

Anderson PL, Fletcher CV.
PMID: 11470030
Curr Infect Dis Rep. 2001 Aug;3(4):381-387. doi: 10.1007/s11908-001-0079-3.

Many data associate low protease inhibitor plasma concentrations with suboptimal virologic responses, whereas relatively few data associate high plasma concentrations with increased likelihood of toxicity. Knowledge of relationships between concentrations and virologic response is important because significant variability in...

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Anderson PL, Fletcher CV. Clinical Pharmacologic Considerations for HIV-1 Protease Inhibitors. Curr Infect Dis Rep. 2001;3(4):381-387doi: 10.1007/s11908-001-0079-3.
Anderson, P. L., & Fletcher, C. V. (2001). Clinical Pharmacologic Considerations for HIV-1 Protease Inhibitors. Current infectious disease reports, 3(4), 381-387. https://doi.org/10.1007/s11908-001-0079-3
Anderson, Peter L., and Fletcher, Courtney V.. "Clinical Pharmacologic Considerations for HIV-1 Protease Inhibitors." Current infectious disease reports vol. 3,4 (2001): 381-387. doi: https://doi.org/10.1007/s11908-001-0079-3
Anderson PL, Fletcher CV. Clinical Pharmacologic Considerations for HIV-1 Protease Inhibitors. Curr Infect Dis Rep. 2001 Aug;3(4):381-387. doi: 10.1007/s11908-001-0079-3. PMID: 11470030.
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Showing 25 to 36 of 1337 entries