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2. The Authors Reply

Author

Crane, H. M., Heckbert, S. R., Drozd, D. R., Budoff, M. J., Delaney, J. A. C., Rodriguez, C., Paramsothy, P., Lober, W. B., Burkholder, G., Willig, J. H., Mugavero, M. J., Mathews, W. C., Crane, P. K., Moore, R. D., Napravnik, S., Eron, J. J., Hunt, P., Geng, E., Hsue, P., Barnes, G. S., McReynolds, J., Peter, I., Grunfeld, C., Saag, M. S., and Kitahata, M. M.

Published
2014
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3. Lessons Learned From the Design and Implementation of Myocardial Infarction Adjudication Tailored for HIV Clinical Cohorts

Author

Crane, H. M., Heckbert, S. R., Drozd, D. R., Budoff, M. J., Delaney, J. A. C., Rodriguez, C., Paramsothy, P., Lober, W. B., Burkholder, G., Willig, J. H., Mugavero, M. J., Mathews, W. C., Crane, P. K., Moore, R. D., Napravnik, S., Eron, J. J., Hunt, P., Geng, E., Hsue, P., Barnes, G. S., McReynolds, J., Peter, I., Grunfeld, C., Saag, M. S., and Kitahata, M. M.

Published
2014
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6. Anemia risk factors among people living with HIV across the United States in the current treatment era: a clinical cohort study

Author

Harding, B. N., primary, Whitney, B. M., additional, Nance, R. M., additional, Ruderman, S. A., additional, Crane, H. M., additional, Burkholder, G., additional, Moore, R. D., additional, Mathews, W. C., additional, Eron, J. J., additional, Hunt, P. W., additional, Volberding, P., additional, Rodriguez, B., additional, Mayer, K. H., additional, Saag, M. S., additional, Kitahata, M. M., additional, Heckbert, S. R., additional, and Delaney, J. A. C., additional

Published
2020
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10. Comparison of Kaposi Sarcoma Risk in Human Immunodeficiency Virus-Positive Adults Across 5 Continents: A Multiregional Multicohort Study

Author

Rohner E., Butikofer L., Schmidlin K., Sengayi M., Maskew M., Giddy J., Garone D., Moore R. D., D'Souza G., Goedert J. J., Achenbach C., Gill M. J., Kitahata M. M., Patel P., Silverberg M. J., Castilho J., McGowan C., Chen Y. -M. A., Law M., Taylor N., Paparizos V., Bonnet F., Verbon A., Fatkenheuer G., Post F. A., Sabin C., Mocroft A., Le Moing V., Dronda F., Obel N., Grabar S., Spagnuolo V., Antinori A., Quiros-Roldan E., Mussini C., Miro J. M., Meyer L., Hasse B., Konopnicki D., Roca B., Barger D., Raben D., Clifford G. M., Franceschi S., Brockmeyer N., Chakraborty R., Egger M., Bohlius J., Judd A., Zangerle R., Touloumi G., Warszawski J., Dabis F., Krause M. M., Ghosn J., Leport C., Wittkop L., Reiss P., Wit F., Prins M., Bucher H., Gibb D., Del Amo J., Thorne C., Kirk O., Stephan C., Perez-Hoyos S., Hamouda O., Bartmeyer B., Chkhartishvili N., Noguera-Julian A., Monforte A. D., Prieto L., Conejo P. R., Soriano-Arandes A., Battegay M., Kouyos R., Tookey P., Casabona J., Castagna A., Konopnick D., Goetghebuer T., Sonnerborg A., Teira R., Garrido M., Haerry D., De Wit S., Costagliola D., D'Arminio-Monforte A., Chene G., Schwimmer C., Termote M., Campbell M., Frederiksen C. M., Friis-Moller N., Kjaer J., Brandt R. S., Berenguer J., Bouteloup V., Cozzi-Lepri A., Davies M. -A., Dorrucci M., Dunn D., Furrer H., Guiguet M., Lambotte O., Leroy V., Lodi S., Matheron S., Monge S., Nakagawa F., Paredes R., Phillips A., Puoti M., Schomaker M., Smit C., Sterne J., Thiebaut R., Torti C., Van Der Valk M., Tanser F., Vinikoor M., MacEte E., Wood R., Stinson K., Fatti G., Phiri S., Chimbetete C., Malisita K., Eley B., Fritz C., Hobbins M., Kamenova K., Fox M., Prozesky H., Technau K., Sawry S., Benson C. A., Bosch R. J., Kirk G. D., Boswell S., Mayer K. H., Grasso C., Hogg R. S., Harrigan P. R., Montaner J. S. G., Yip B., Zhu J., Salters K., Gabler K., Buchacz K., Brooks J. T., Gebo K. A., Carey J. T., Rodriguez B., Horberg M. A., Thorne J. E., Rabkin C., Margolick J. B., Jacobson L. P., Klein M. B., Rourke S. B., Rachlis A. R., Cupido P., Hunter-Mellado R. F., Mayor A. M., Deeks S. G., Martin J. N., Saag M. S., Mugavero M. J., Willig J., Eron J. J., Napravnik S., Crane H. M., Drozd D. R., Haas D., Rebeiro P., Turner M., Bebawy S., Rogers B., Justice A. C., Dubrow R., Fiellin D., Gange S. J., Anastos K., Althoff K. N., McKaig R. G., Freeman A. M., Lent C., Van Rompaey S. E., Morton L., McReynolds J., Lober W. B., Abraham A. G., Lau B., Zhang J., Jing J., Modur S., Wong C., Hogan B., Desir F., Liu B., You B., Cahn P., Cesar C., Fink V., Sued O., Dell'Isola E., Perez H., Valiente J., Yamamoto C., Grinsztejn B., Veloso V., Luz P., De Boni R., Wagner S. C., Friedman R., Moreira R., Pinto J., Ferreira F., Maia M., De Menezes Succi R. C., MacHado D. M., De Fatima Barbosa Gouvea A., Wolff M., Cortes C., Rodriguez M. F., Allendes G., Pape J. W., Rouzier V., Marcelin A., Perodin C., Luque M. T., Padgett D., Madero J. S., Ramirez B. C., Belaunzaran P., Vega Y. C., Gotuzzo E., Mejia F., Carriquiry G., McGowan C. C., Shepherd B. E., Sterling T., Jayathilake K., Person A. K., Rebeiro P. F., Giganti M., Duda S. N., Maruri F., Vansell H., Ly P. S., Khol V., Zhang F. J., Zhao H. X., Han N., Lee M. P., Li P. C. K., Lam W., Chan Y. T., Kumarasamy N., Saghayam S., Ezhilarasi C., Pujari S., Joshi K., Gaikwad S., Chitalikar A., Merati T. P., Wirawan D. N., Yuliana F., Yunihastuti E., Imran D., Widhani A., Tanuma J., Oka S., Nishijima T., Choi J. Y., Na S., Kim J. M., Sim B. L. H., Gani Y. M., David R., Kamarulzaman A., Syed Omar S. F., Ponnampalavanar S., Azwa I., Ditangco R., Uy E., Bantique R., Wong W. W., Ku W. W., Wu P. C., Ng O. T., Lim P. L., Lee L. S., Ohnmar P. S., Avihingsanon A., Gatechompol S., Phanuphak P., Phadungphon C., Kiertiburanakul S., Sungkanuparph S., Chumla L., Sanmeema N., Chaiwarith R., Sirisanthana T., Kotarathititum W., Praparattanapan J., Kantipong P., Kambua P., Ratanasuwan W., Sriondee R., Nguyen K. V., Bui H. V., Nguyen D. T. H., Nguyen D. T., Cuong D. D., An N. V., Luan N. T., Sohn A. H., Ross J. L., Petersen B., Cooper D. A., Law M. G., Jiamsakul A., Boettiger D. C., Ellis D., Bloch M., Agrawal S., Vincent T., Allen D., Smith D., Rankin A., Baker D., Templeton D. J., Jackson E., McCallum K., Ryder N., Sweeney G., Cooper D., Carr A., MacRae K., Hesse K., Finlayson R., Gupta S., Langton-Lockton J., Shakeshaft J., Brown K., Idle S., Arvela N., Varma R., Lu H., Couldwell D., Eswarappa S., Smith D. E., Furner V., Cabrera G., Fernando S., Cogle A., Lawrence C., Mulhall B., Boyd M., Petoumenos K., Puhr R., Huang R., Han A., Gunathilake M., Payne R., O'Sullivan M., Croydon A., Russell D., Cashman C., Roberts C., Sowden D., Taing K., Marshall P., Orth D., Youds D., Rowling D., Latch N., Warzywoda E., Dickson B., Donohue W., Moore R., Edwards S., Boyd S., Roth N. J., Lau H., Read T., Silvers J., Zeng W., Hoy J., Watson K., Bryant M., Price S., Woolley I., Giles M., Korman T., Williams J., Nolan D., Allen A., Guelfi G., Mills G., Wharry C., Raymond N., Bargh K., Templeton D., Medical Microbiology & Infectious Diseases, Global Health, Infectious diseases, APH - Aging & Later Life, AII - Infectious diseases, APH - Global Health, Graduate School, APH - Digital Health, APH - Personalized Medicine, Bohlius, Julia, Cohere In, Eurocoord, Castagna, Antonella, Rohner, E, Butikofer, L, Schmidlin, K, Sengayi, M, Maskew, M, Giddy, J, Garone, D, Moore, R, D'Souza, G, Goedert, J, Achenbach, C, Gill, M, Kitahata, M, Patel, P, Silverberg, M, Castilho, J, Mcgowan, C, Chen, Y, Law, M, Taylor, N, Paparizos, V, Bonnet, F, Verbon, A, Fatkenheuer, G, Post, F, Sabin, C, Mocroft, A, Le Moing, V, Dronda, F, Obel, N, Grabar, S, Spagnuolo, V, Antinori, A, Quiros-Roldan, E, Mussini, C, Miro, J, Meyer, L, Hasse, B, Konopnicki, D, Roca, B, Barger, D, Raben, D, Clifford, G, Franceschi, S, Brockmeyer, N, Chakraborty, R, Egger, M, Bohlius, J, Judd, A, Zangerle, R, Touloumi, G, Warszawski, J, Dabis, F, Krause, M, Ghosn, J, Leport, C, Wittkop, L, Reiss, P, Wit, F, Prins, M, Bucher, H, Gibb, D, Del Amo, J, Thorne, C, Kirk, O, Stephan, C, Perez-Hoyos, S, Hamouda, O, Bartmeyer, B, Chkhartishvili, N, Noguera-Julian, A, Monforte, A, Prieto, L, Conejo, P, Soriano-Arandes, A, Battegay, M, Kouyos, R, Tookey, P, Casabona, J, Castagna, A, Konopnick, D, Goetghebuer, T, Sonnerborg, A, Teira, R, Garrido, M, Haerry, D, De Wit, S, Costagliola, D, D'Arminio-Monforte, A, Chene, G, Schwimmer, C, Termote, M, Campbell, M, Frederiksen, C, Friis-Moller, N, Kjaer, J, Brandt, R, Berenguer, J, Bouteloup, V, Cozzi-Lepri, A, Davies, M, Dorrucci, M, Dunn, D, Furrer, H, Guiguet, M, Lambotte, O, Leroy, V, Lodi, S, Matheron, S, Monge, S, Nakagawa, F, Paredes, R, Phillips, A, Puoti, M, Schomaker, M, Smit, C, Sterne, J, Thiebaut, R, Torti, C, Van Der Valk, M, Tanser, F, Vinikoor, M, Macete, E, Wood, R, Stinson, K, Fatti, G, Phiri, S, Chimbetete, C, Malisita, K, Eley, B, Fritz, C, Hobbins, M, Kamenova, K, Fox, M, Prozesky, H, Technau, K, Sawry, S, Benson, C, Bosch, R, Kirk, G, Boswell, S, Mayer, K, Grasso, C, Hogg, R, Harrigan, P, Montaner, J, Yip, B, Zhu, J, Salters, K, Gabler, K, Buchacz, K, Brooks, J, Gebo, K, Carey, J, Rodriguez, B, Horberg, M, Thorne, J, Rabkin, C, Margolick, J, Jacobson, L, Klein, M, Rourke, S, Rachlis, A, Cupido, P, Hunter-Mellado, R, Mayor, A, Deeks, S, Martin, J, Saag, M, Mugavero, M, Willig, J, Eron, J, Napravnik, S, Crane, H, Drozd, D, Haas, D, Rebeiro, P, Turner, M, Bebawy, S, Rogers, B, Justice, A, Dubrow, R, Fiellin, D, Gange, S, Anastos, K, Althoff, K, Mckaig, R, Freeman, A, Lent, C, Van Rompaey, S, Morton, L, Mcreynolds, J, Lober, W, Abraham, A, Lau, B, Zhang, J, Jing, J, Modur, S, Wong, C, Hogan, B, Desir, F, Liu, B, You, B, Cahn, P, Cesar, C, Fink, V, Sued, O, Dell'Isola, E, Perez, H, Valiente, J, Yamamoto, C, Grinsztejn, B, Veloso, V, Luz, P, De Boni, R, Wagner, S, Friedman, R, Moreira, R, Pinto, J, Ferreira, F, Maia, M, De Menezes Succi, R, Machado, D, De Fatima Barbosa Gouvea, A, Wolff, M, Cortes, C, Rodriguez, M, Allendes, G, Pape, J, Rouzier, V, Marcelin, A, Perodin, C, Luque, M, Padgett, D, Madero, J, Ramirez, B, Belaunzaran, P, Vega, Y, Gotuzzo, E, Mejia, F, Carriquiry, G, Shepherd, B, Sterling, T, Jayathilake, K, Person, A, Giganti, M, Duda, S, Maruri, F, Vansell, H, Ly, P, Khol, V, Zhang, F, Zhao, H, Han, N, Lee, M, Li, P, Lam, W, Chan, Y, Kumarasamy, N, Saghayam, S, Ezhilarasi, C, Pujari, S, Joshi, K, Gaikwad, S, Chitalikar, A, Merati, T, Wirawan, D, Yuliana, F, Yunihastuti, E, Imran, D, Widhani, A, Tanuma, J, Oka, S, Nishijima, T, Choi, J, Na, S, Kim, J, Sim, B, Gani, Y, David, R, Kamarulzaman, A, Syed Omar, S, Ponnampalavanar, S, Azwa, I, Ditangco, R, Uy, E, Bantique, R, Wong, W, Ku, W, Wu, P, Ng, O, Lim, P, Lee, L, Ohnmar, P, Avihingsanon, A, Gatechompol, S, Phanuphak, P, Phadungphon, C, Kiertiburanakul, S, Sungkanuparph, S, Chumla, L, Sanmeema, N, Chaiwarith, R, Sirisanthana, T, Kotarathititum, W, Praparattanapan, J, Kantipong, P, Kambua, P, Ratanasuwan, W, Sriondee, R, Nguyen, K, Bui, H, Nguyen, D, Cuong, D, An, N, Luan, N, Sohn, A, Ross, J, Petersen, B, Cooper, D, Jiamsakul, A, Boettiger, D, Ellis, D, Bloch, M, Agrawal, S, Vincent, T, Allen, D, Smith, D, Rankin, A, Baker, D, Templeton, D, Jackson, E, Mccallum, K, Ryder, N, Sweeney, G, Carr, A, Macrae, K, Hesse, K, Finlayson, R, Gupta, S, Langton-Lockton, J, Shakeshaft, J, Brown, K, Idle, S, Arvela, N, Varma, R, Lu, H, Couldwell, D, Eswarappa, S, Furner, V, Cabrera, G, Fernando, S, Cogle, A, Lawrence, C, Mulhall, B, Boyd, M, Petoumenos, K, Puhr, R, Huang, R, Han, A, Gunathilake, M, Payne, R, O'Sullivan, M, Croydon, A, Russell, D, Cashman, C, Roberts, C, Sowden, D, Taing, K, Marshall, P, Orth, D, Youds, D, Rowling, D, Latch, N, Warzywoda, E, Dickson, B, Donohue, W, Edwards, S, Boyd, S, Roth, N, Lau, H, Read, T, Silvers, J, Zeng, W, Hoy, J, Watson, K, Bryant, M, Price, S, Woolley, I, Giles, M, Korman, T, Williams, J, Nolan, D, Allen, A, Guelfi, G, Mills, G, Wharry, C, Raymond, N, and Bargh, K

Subjects
Male, viruses, HIV Infections, Men who have sex with men, Cohort Studies, 0302 clinical medicine, Risk Factors, Antiretroviral therapy, Cohort study, HIV, Kaposi sarcoma, Adolescent, Adult, Anti-Retroviral Agents, CD4 Lymphocyte Count, Female, HIV-1, Humans, Middle Aged, Sarcoma, Kaposi, Viral Load, Young Adult, 030212 general & internal medicine, Articles and Commentaries, Incidence (epidemiology), Hazard ratio, virus diseases, Sarcoma, 3. Good health, Infectious Diseases, 030220 oncology & carcinogenesis, Cohort, Coinfection, Microbiology (medical), antiretroviral therapy, 610 Medicine & health, Kaposi, 03 medical and health sciences, SDG 3 - Good Health and Well-being, 360 Social problems & social services, medicine, cohort study, business.industry, medicine.disease, Confidence interval, business, Demography
Abstract

Background We compared Kaposi sarcoma (KS) risk in adults who started antiretroviral therapy (ART) across the Asia-Pacific, South Africa, Europe, Latin, and North America. Methods We included cohort data of human immunodeficiency virus (HIV)-positive adults who started ART after 1995 within the framework of 2 large collaborations of observational HIV cohorts. We present incidence rates and adjusted hazard ratios (aHRs). Results We included 208140 patients from 57 countries. Over a period of 1066572 person-years, 2046 KS cases were diagnosed. KS incidence rates per 100000 person-years were 52 in the Asia-Pacific and ranged between 180 and 280 in the other regions. KS risk was 5 times higher in South African women (aHR, 4.56; 95% confidence intervals [CI], 2.73-7.62) than in their European counterparts, and 2 times higher in South African men (2.21; 1.34-3.63). In Europe, Latin, and North America KS risk was 6 times higher in men who have sex with men (aHR, 5.95; 95% CI, 5.09-6.96) than in women. Comparing patients with current CD4 cell counts ≥700 cells/µL with those whose counts were

Published
2017

11. HIV-1 Expression Within Resting CD4+ T Cells After Multiple Doses of Vorinostat

Author

Eron, J. J., Bateson, R., Richman, D. D., Anderson, E. M., Margolis, D. M., Bosch, R. J., Kearney, M. F., Kuruc, J. D., Robertson, K. R., Coffin, J. M., Strain, M. C., Hazuda, D. J., Crooks, A. M., Tripathy, M. K., Kashuba, A. D., Archin, N. M., Dahl, N. P., and Yang, K.-H.

Subjects
genetic structures, sense organs
Abstract

Background. A single dose of the histone deacetylase inhibitor vorinostat (VOR) up-regulates HIV RNA expression within resting CD4+ T cells of treated, aviremic human immunodeficiency virus (HIV)–positive participants. The ability of multiple exposures to VOR to repeatedly disrupt latency has not been directly measured, to our knowledge.

Published
2014
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12. Associations of T cell activation and inflammatory biomarkers with virological response to darunavir/ritonavir plus raltegravir therapy

Author

Berzins, B. I., Rinaldo, C. R., Taiwo, B., Zheng, L., Kuritzkes, D. R., Eron, J. J., Kim, P. S., Matining, R. M., Lederman, M. M., Jennings, A., and Wilson, C. C.

Subjects
biochemical phenomena, metabolism, and nutrition
Abstract

One of the goals of antiretroviral therapy (ART) is to attenuate HIV-induced systemic immune activation and inflammation. We determined the dynamics of biomarkers of immune activation, microbial translocation and inflammation during initial ART with a nucleos(t)ide-sparing regimen of darunavir/ritonavir plus raltegravir. We also evaluated associations between these biomarkers and the virological response to the regimen.

Published
2013
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13. Temporal Trends in Presentation and Survival for HIV-Associated Lymphoma in the Antiretroviral Therapy Era

Author

Burkholder, G. A., Napravnik, S., Deeks, S. G., Patel, M. R., Gopal, S., Reid, E. G., Yanik, E. L., Rodriguez, B., Richards, K. L., Achenbach, C. J., Moore, R. D., Cole, S. R., Mayer, K. H., Eron, J. J., and Kitahata, M. M.

Subjects
hemic and lymphatic diseases
Abstract

Lymphoma is the leading cause of cancer-related death among HIV-infected patients in the antiretroviral therapy (ART) era.

Published
2013
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15. Ten-year Survival by Race/Ethnicity and Sex Among Treated, HIV-infected Adults in the United States

Author

Lesko, C. R., primary, Cole, S. R., additional, Miller, W. C., additional, Westreich, D., additional, Eron, J. J., additional, Adimora, A. A., additional, Moore, R. D., additional, Mathews, W. C., additional, Martin, J. N., additional, Drozd, D. R., additional, Kitahata, M. M., additional, Edwards, J. K., additional, and Mugavero, M. J., additional

Published
2015
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16. Predictive Value of Pharmacokinetics-Adjusted Phenotypic Susceptibility on Response to Ritonavir-Enhanced Protease Inhibitors (PIs) in Human Immunodeficiency Virus-Infected Subjects Failing Prior PI Therapy

Author

Park, J.-G., Pakes, G. E., Eron, J. J., Aweeka, F., Bastow, B., Wu, H., Richman, D. D., Yu, S., and Haubrich, R.

Abstract

The activities of protease inhibitors in vivo may depend on plasma concentrations and viral susceptibility. This nonrandomized, open-label study evaluated the relationship of the inhibitory quotient (IQ [the ratio of drug exposure to viral phenotypic susceptibility]) to the human immunodeficiency virus type 1 (HIV-1) viral load (VL) change for ritonavir-enhanced protease inhibitors (PIs). Subjects on PI-based regimens replaced their PIs with ritonavir-enhanced indinavir (IDV/r) 800/200 mg, fosamprenavir (FPV/r) 700/100 mg, or lopinavir (LPV/r) 400/200 mg twice daily. Pharmacokinetics were assessed at day 14; follow-up lasted 24 weeks. Associations between IQ and VL changes were examined. Fifty-three subjects enrolled, 12 on IDV/r, 33 on FPV/r, and 8 on LPV/r. Median changes (n-fold) (FC) of 50% inhibitory concentrations (IC50s) to the study PI were high. Median 2-week VL changes were −0.7, −0.1, and −1.0 log10 for IDV/r, FPV/r, and LPV/r. With FPV/r, correlations between the IQ and the 2-week change in VL were significant (Spearman's r range, −0.39 to −0.50; P ≤ 0.029). The strongest correlation with response to FPV/r was the IC50 FC (r = 0.57; P = 0.001), which improved when only adherent subjects were included (r = 0.68; P = 0.001). In multivariable analyses of the FPV/r arm that included FC, one measure of the drug concentration, corresponding IQ, baseline VL, and CD4, the FC to FPV was the only significant predictor of VL decline (P < 0.001). In exploratory analyses of all arms, the area under the concentration-time curve IQ was correlated with the week 2 VL change (r = −0.72; P < 0.001). In conclusion, in PI-experienced subjects with highly resistant HIV-1, short-term VL responses to RTV-enhanced FPV/r correlated best with baseline susceptibility. The IQ improved correlation in analyses of all arms where a greater range of virologic responses was observed.

Published
2009
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17. Major Coexisting Human Immunodeficiency Virus Type 1 env Gene Subpopulations in the Peripheral Blood Are Produced by Cells with Similar Turnover Rates and Show Little Evidence of Genetic Compartmentalization

Author

Price, R. W., Schnell, G. L., Patel-Chhabra, M., Ince, W. L., Eron, J. J., Harrington, P. R., Menezes, P., Swanstrom, R. I., and Burch, C. L.

Subjects
virus diseases
Abstract

A distinctive feature of chronic human immunodeficiency virus type 1 (HIV-1) infection is the presence of multiple coexisting genetic variants, or subpopulations, that comprise the HIV-1 population detected in the peripheral blood. Analysis of HIV-1 RNA decay dynamics during the initiation of highly active antiretroviral therapy (HAART) has been a valuable tool for modeling the life span of infected cells that produce the bulk HIV-1 population. However, different HIV-1 target cells may have different turnover rates, and it is not clear whether the bulk HIV-1 RNA decay rate actually represents a composite of the decay rates of viral subpopulations compartmentalized in different cellular subsets with different life spans. Using heteroduplex tracking assays targeting the highly variable V3 or V4-V5 regions of the HIV-1 env gene in eight subjects, we found that all detectable coexisting HIV-1 variants in the peripheral blood generally decayed at similar rates during the initiation of HAART, suggesting that all of the variants were produced by cells with similar life spans. Furthermore, single genome amplification and coreceptor phenotyping revealed that in two subjects coexisting HIV-1 variants with distinct CXCR4 or CCR5 coreceptor phenotypes decayed with similar rates. Also, in nine additional subjects, recombination and a lack of genetic compartmentalization between X4 and R5 variants were observed, suggesting an overlap in host cell range. Our results suggest that the HIV-1 env subpopulations detectable in the peripheral blood are produced by cells with similar life spans and are not genetically isolated within particular cell types.

Published
2009
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18. Dose Separation Does Not Overcome the Pharmacokinetic Interaction between Fosamprenavir and Lopinavir/Ritonavir

Author

Kashuba, A. D. M., Eron, J. J., Kalvass, L. A., Ngo, L. T., Corbett, A. H., Lim, M. L., Tien, H.-C., and Patterson, K. B.

Abstract

Previous investigations have shown a significant negative two-way drug interaction between fosamprenavir (FPV) and lopinavir/ritonavir (LPV/RTV) in both human immunodeficiency virus (HIV)-infected patients and seronegative volunteers. This randomized, nonblinded, three-way crossover study of HIV-seronegative adult volunteers investigated dose separation and increased doses of RTV as a means to overcome the interaction between FPV and LPV/RTV. Eleven HIV-seronegative volunteers were given FPV plus LPV/RTV at 700 mg plus 400/100 mg every 12 hours (q12h) simultaneously for 10 days and then randomized to receive each of three 7-day treatments in one of six possible sequences, as follows: FPV plus LPV/RTV at 700 mg plus 400 mg/100 mg q12h simultaneously, FPV/RTV at 700 mg/100 mg q12h plus LPV/RTV at 400 mg/100 mg q12h, with doses separated by 4 h, and FPV/RTV at 1,400 mg/200 mg in the morning plus LPV/RTV at 800 mg/200 mg in the evening. Pharmacokinetic sampling was performed on day 8 of each treatment, and samples were analyzed for FPV, amprenavir (APV), LPV, and RTV concentrations by high-performance liquid chromatography-tandem mass spectrometry. Geometric mean ratios (GMR [with 95% confidence intervals]) for the 4- and 12-h dose separation strategies compared to simultaneous administration were calculated for the areas under the concentration-time curves from 0 to 24 h. Compared to simultaneous administration, RTV exposures increased with both 4-h and 12-h dose separation strategies (GMR, 5.30 [3.66 to 7.67] and 4.45 [3.09 to 6.41], respectively). LPV exposures also significantly increased with both 4-h and 12-h dose separation strategies (GMR, 1.76 [1.34 to 2.32] and 1.43 [1.02 to 2.01], respectively). However, both the 4- and 12-h strategies resulted in greater reductions in APV exposure (0.67 [0.54 to 0.83] and 0.77 [0.59 to 0.99], respectively) compared to simultaneous administration. Additional investigations are warranted to determine the optimal dosing of FPV with LPV/RTV.

Published
2006
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19. Multiple V1/V2 env Variants Are Frequently Present during Primary Infection with Human Immunodeficiency Virus Type 1

Author

Swanstrom, R., Eron, J. J., Fiscus, S. A., Ritola, K., Hicks, C. B., Kitrinos, K. M., Nelson, J. A. E., Pilcher, C. D., and Hoffman, N. G.

Abstract

Human immunodeficiency virus type 1 (HIV-1) exists as a complex population of multiple genotypic variants in persons with chronic infection. However, acute HIV-1 infection via sexual transmission is a low-probability event in which there is thought to be low genetic complexity in the initial inoculum. In order to assess the viral complexity present during primary HIV-1 infection, the V1/V2 and V3 variable regions of the env gene were examined by using a heteroduplex tracking assay (HTA) capable of resolving these genotypic variants. Blood plasma samples from 26 primary HIV-1-infected subjects were analyzed for their level of diversity. Half of the subjects had more than one V1/V2 viral variant during primary infection, indicating the frequent transmission of multiple variants. This observation is inconsistent with the idea of infrequent transmission based on a small transmitting inoculum of cell-free virus. In chronically infected subjects, the complexity of the viral populations was even greater in both the V1/V2 and the V3 regions than in acutely infected subjects, indicating that in spite of the presence of multiple variants in acute infection, the virus does pass through a genetic bottleneck during transmission. We also examined how well the infecting virus penetrated different anatomical compartments by using the HTA. Viral variants detected in blood plasma were compared to those detected in seminal plasma and/or cerebral spinal fluid of six individuals. The virus in each of these compartments was to a large extent identical to virus in blood plasma, a finding consistent with rapid penetration of the infecting variant(s). The low-probability transmission of multiple variants could be the result of transient periods of hyperinfectiousness or hypersusceptibility. Alternatively, the inefficient transfer of a multiply infected cell could account for both the low probability of transmission and the transfer of multiple variants.

Published
2004
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20. Lymphoma Immune Reconstitution Inflammatory Syndrome in the Center for AIDS Research Network of Integrated Clinical Systems Cohort

Author

Gopal, S., primary, Patel, M. R., additional, Achenbach, C. J., additional, Yanik, E. L., additional, Cole, S. R., additional, Napravnik, S., additional, Burkholder, G. A., additional, Mathews, W. C., additional, Rodriguez, B., additional, Deeks, S. G., additional, Mayer, K. H., additional, Moore, R. D., additional, Kitahata, M. M., additional, Richards, K. L., additional, and Eron, J. J., additional

Published
2014
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21. HIV-1 Expression Within Resting CD4+ T Cells After Multiple Doses of Vorinostat

Author

Archin, N. M., primary, Bateson, R., additional, Tripathy, M. K., additional, Crooks, A. M., additional, Yang, K.-H., additional, Dahl, N. P., additional, Kearney, M. F., additional, Anderson, E. M., additional, Coffin, J. M., additional, Strain, M. C., additional, Richman, D. D., additional, Robertson, K. R., additional, Kashuba, A. D., additional, Bosch, R. J., additional, Hazuda, D. J., additional, Kuruc, J. D., additional, Eron, J. J., additional, and Margolis, D. M., additional

Published
2014
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22. Pharmacokinetic Study of Human Immunodeficiency Virus Protease Inhibitors Used in Combination with Amprenavir

Author

Lou, Y., Eron, J. J., Stein, D. S., Lang, W., Haubrich, R., Sadler, B. M., and Gillotin, C.

Subjects
biochemical phenomena, metabolism, and nutrition
Abstract

In an open-label, randomized, multicenter, multiple-dose pharmacokinetic study, we determined the steady-state pharmacokinetics of amprenavir with and without coadministration of indinavir, nelfinavir, or saquinavir soft gel formulation in 31 human immunodeficiency virus type 1-infected subjects. The results indicated that amprenavir plasma concentrations were decreased by saquinavir soft gel capsule (by 32% for area under the concentration-time curve at steady state [AUCss] and 37% for peak plasma concentration at steady state [Cmax,ss]) and increased by indinavir (33% for AUCss). Nelfinavir significantly increased amprenavir minimum drug concentration at steady state (by 189%) but did not affect amprenavir AUCss or Cmax,ss. Nelfinavir and saquinavir steady-state pharmacokinetics were unchanged by coadministration with amprenavir compared with the historical monotherapy data. Concentrations of indinavir, coadministered with amprenavir, in plasma decreased in both single-dose and steady-state evaluations. The changes in amprenavir steady-state pharmacokinetic parameters, relative to those for amprenavir alone, were not consistent among protease inhibitors, nor were the changes consistent with potential interactions in CYP3A4 metabolism or P-glycoprotein transport. No dose adjustment of either protease inhibitor in any of the combinations studied is needed.

Published
2001
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23. Temporal Trends in Presentation and Survival for HIV-Associated Lymphoma in the Antiretroviral Therapy Era

Author

Gopal, S., primary, Patel, M. R., additional, Yanik, E. L., additional, Cole, S. R., additional, Achenbach, C. J., additional, Napravnik, S., additional, Burkholder, G. A., additional, Reid, E. G., additional, Rodriguez, B., additional, Deeks, S. G., additional, Mayer, K. H., additional, Moore, R. D., additional, Kitahata, M. M., additional, Eron, J. J., additional, and Richards, K. L., additional

Published
2013
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25. Erratum: Administration of vorinostat disrupts HIV-1 latency in patients on antiretroviral therapy

Author

Archin, N. M., primary, Liberty, A. L., additional, Kashuba, A. D., additional, Choudhary, S. K., additional, Kuruc, J. D., additional, Crooks, A. M., additional, Parker, D. C., additional, Anderson, E. M., additional, Kearney, M. F., additional, Strain, M. C., additional, Richman, D. D., additional, Hudgens, M. G., additional, Bosch, R. J., additional, Coffin, J. M., additional, Eron, J. J., additional, Hazuda, D. J., additional, and Margolis, D. M., additional

Published
2012
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27. Risk of End‐Stage Renal Disease in HIV‐Positive Potential Live Kidney Donors

Author

Muzaale, A. D., Althoff, K. N., Sperati, C. J., Abraham, A. G., Kucirka, L. M., Massie, A. B., Kitahata, M. M., Horberg, M. A., Justice, A. C., Fischer, M. J., Silverberg, M. J., Butt, A. A., Boswell, S. L., Rachlis, A. R., Mayor, A. M., Gill, M. J., Eron, J. J., Napravnik, S., Drozd, D. R., Martin, J. N., Bosch, R. J., Durand, C. M., Locke, J. E., Moore, R. D., Lucas, G. M., and Segev, D. L.

Abstract

New federal regulations allow HIV‐positive individuals to be live kidney donors; however, potential candidacy for donation is poorly understood given the increased risk of end‐stage renal disease (ESRD) associated with HIV infection. To better understand this risk, we compared the incidence of ESRDamong 41 968 HIV‐positive participants of North America AIDSCohort Collaboration on Research and Design followed for a median of 5 years with the incidence of ESRDamong comparable HIV‐negative participants of National Health and Nutrition Examination IIIfollowed for a median of 14 years. We used risk associations from multivariable Cox proportional hazards regression to derive cumulative incidence estimates for selected HIV‐positive scenarios (no history of diabetes, hypertension, AIDS, or hepatitis C viruscoinfection) and compared these estimates with those from similarly selected HIV‐negative scenarios. For 40‐year‐old HIV‐positive individuals with health characteristics that were similar to those of age‐matched kidney donors, viral load <400 copies/mL, and CD4+count ≥500 cells/μL, the 9‐year cumulative incidence of ESRDwas higher than that of their HIV‐negative peers, yet still low: 2.5 versus 1.1 per 10 000 among white women, 3.0 versus 1.3 per 10 000 among white men, 13.2 versus 3.6 per 10 000 among black women, and 15.8 versus 4.4 per 10 000 among black men. HIV‐positive individuals with no comorbidities and well‐controlled disease may be considered low‐risk kidney donor candidates. This North American study demonstrates that HIV‐positive individuals with no comorbidities and well‐controlled disease may be considered low‐risk live kidney donor candidates. See Steiner's editorial on page 1701.

Published
2017
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40. Second-line treatment in the Malawi antiretroviral programme: high early mortality, but good outcomes in survivors, despite extensive drug resistance at baseline.

Author

Hosseinipour, M. C., Kumwenda, J. J., Weigel, R., Brown, L. B., Mzinganjira, D., Mhango, B., Eron, J. J., Phiri, S., and van Oosterhout, J. J.

Subjects
ANTIRETROVIRAL agents, DRUG resistance, HIV-positive persons, HIV infections, DISEASE complications
Abstract

Objectives The Malawi antiretroviral therapy (ART) programme uses the public health approach to identify ART failure. Advanced disease progression may occur before switching to second-line ART. We report outcomes for patients evaluated and initiated on second-line treatment in Malawi. Methods Patients meeting Malawi immunological or clinical criteria for ART failure in two large urban ART clinics were evaluated for virological failure (viral load >400 HIV-1 RNA copies/mL) and, if failure was confirmed, initiated on second-line ART (zidovudine/lamivudine/tenofovir/lopinavir/ritonavir). Patients were seen monthly and laboratory evaluations were performed quarterly and as needed. We performed logistic regression modelling to identify factors associated with mortality, mortality or new HIV illnesses, and virological suppression at 12 months. Results Of the 109 patients with confirmed virological failure, five patients died prior to initiation, three declined switching and 101 patients initiated second-line treatment. Over 12 months, 10 additional patients died, 34 patients experienced 45 HIV-related events, and 19 patients experienced grade 3 or 4 toxicities. Among survivors, 85.2% had HIV-1 RNA<400 copies/mL at 12 months. While power to distinguish differences was limited, response rates were similar regardless of baseline resistance level. The median CD4 count increase was 142 cells/μL. World Health Organization clinical failure at baseline [odds ratio (OR) 3.47; 95% confidence interval (CI) 1.14–10.59] and body mass index <18.5 (OR 4.43; 95% CI 1.15–17.12) were risk factors for death. Baseline CD4 count <50 cells/μL was associated with increased risk for death or morbidity at 12 months (OR 2.57; 95% CI 1.01–6.52). Conclusions Second-line treatment in Malawi was associated with substantial mortality, morbidity and toxicity but, among survivors, virological outcomes were favourable. [ABSTRACT FROM AUTHOR]

Published
2010
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42. Correlation between self-reported adherence to highly active antiretroviral therapy (HAART) and virologic outcome.

Author

DeMasi, Ralph, Graham, Neil, Tolson, Jerry, Pham, Sissi, Capuano, George, Fisher, Robin, Shaefer, Mark, Pakes, Gary, Sawyerr, Gosford, Eron, Joseph, DeMasi, R A, Graham, N M, Tolson, J M, Pham, S V, Capuano, G A, Fisher, R L, Shaefer, M S, Pakes, G E, Sawyerr, G A, and Eron, J J Jr

Abstract

The Patient Medication Adherence Questionnaire Version 1.0 (PMAQ-V1.0) is a patient-reported adherence instrument to assess medication-taking behaviors and identify barriers to adherence with antiretroviral therapy. To assess the correlation between adherence and virologic outcome, the PMAQ-V1.0 was administered to 194 antiretroviral-experienced adults with HIV infection enrolled in a 16-week evaluation of protease inhibitor-containing regimens featuring a lamivudine/zidovudine combination tablet. At baseline, plasma HIV-1 RNA levels were less than 10,000 copies/mL and CD4(+)-cell counts were equal to or greater than 300 x 10(6)/L; patients had been receiving a conventional regimen of lamivudine + zidovudine (separately) plus a protease inhibitor for at least 10 weeks immediately prior to the study. Forty-eight percent of patients who reported missing at least one dose of a nucleoside reverse-transcriptase inhibitor (NRTI) during the study had detectable plasma HIV-1 RNA, compared with 26% of patients who reported no missed doses (P = .002). Patients who missed at least one dose of an NRTI or protease inhibitor were 2.5 times more likely to have quantifiable HIV-1 RNA than those who reported no missed doses. Patients who reported fewer barriers and more motivators to adherence had better virologic outcomes (P = .001). Several dimensions of the PMAQ-V1.0 did not function as well as hypothesized. In this study, self-reported adherence derived from the PMAQ-V1.0 predicted virologic outcomes, but further refinement of the dimensions appears warranted. [ABSTRACT FROM AUTHOR]

Published
2001
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43. Hyper-excretion of Human Immunodeficiency Virus Type 1 RNA in Saliva.

Author

Shugars, D. C., Patton, L. L., Freel, S. A., Gray, L. R., Vollmer, R. T., Eron, J. J., and Fiscus, S. A.

Subjects
HIV, SALIVA, VIRAL load, BLOOD plasma, ANTIRETROVIRAL agents, RNA
Abstract

Anatomical compartments (e.g., the reproductive tract) are reservoirs of human immunodeficiency virus type-I (HIV-1) and potential sites of residual infection in patients receiving anti-retroviral therapy (ART). Viral hyper-excretion relative to blood is a hallmark of reservoirs. To determine whether hyper-excretion can occur in the oral cavity, we compared viral loads in blood plasma and saliva of 67 adults. Salivary viral hyper-excretion was defined as a four-fold or higher viral load in saliva than in plasma. HIV-1 RNA was detected in 79% of plasma samples, in 44% of unfiltered saliva samples, in 16% of filtered saliva samples, and in 59% of saliva-derived cell pellets. Compared with non-hyper-excretors (n =62), hyper-excretors (n =5) had elevated levels of viral RNA in unfiltered saliva and saliva-derived cells, HIV-associated periodontal disease, gingival inflammation, and no combination ART. Morphological characterization of cell pellets identified lymphocytes as a likely HIV-1 source. These collective findings are consistent with an oral HIV-1 reservoir in selected individuals. [ABSTRACT FROM AUTHOR]

Published
2001
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46. Randomised trial of MNrgp120 HIV-1 vaccine in symptomless HIV-1 infection.

Author

Eron, J J Jr, Ashby, M A, Giordano, M F, Chernow, M, Reiter, W M, Deeks, S G, Lavelle, J P, Conant, M A, Yangco, B G, Pate, P G, Torres, R A, Mitsuyasu, R T, and Twaddell, T

Abstract

Background: Most individuals infected with HIV-1 show disease progression despite both cellular and humoral immune responses. We investigated whether immunisation of patients who had symptomless HIV-1 infection with an envelope subcomponent vaccine (MNrgp120) to augment immune response can slow progression of HIV-1 disease.Methods: In a randomised, double-blind, placebo-controlled trial, carried out in university infectious disease clinics and community infectious disease practices, we enrolled 573 HIV-infected patients with CD4 counts above 600 cells/microL (0.6 x 10(9)/L). Patients received 600 micrograms vaccine or placebo by intramuscular injection monthly for 6 months then every alternate month throughout the study. The primary endpoint was the rate of decline in CD4 count; secondary endpoints were HIV-1 RNA concentrations in plasma and minor clinical events associated with HIV. Analysis was by intention to treat.Findings: At baseline, the study participants had a mean CD4 count of 775 cells/microL (SD 172) and 89% of participants had detectable HIV RNA (> 200 copies/mL). These RNA-positive individuals had a median viral load of 9250 copies/mL (IQR 2670-26960). Analysis after 15 months of follow-up of the 568 subjects who had at least one CD4 count done after randomisation showed no difference between the 287 vaccine recipients and 281 placebo recipients in rate of decline of CD4 count (yearly decrease 53.8 [SE 7.6] vs 42.3 [7.6] cells/microL; ratio of mean gradients 1.27 [95% CI 0.63-2.55]) or in plasma HIV-1 RNA concentrations (p > or = 0.63). The study was designed with power to detect a vaccine-induced reduction in rate of decline in CD4 count of 60%; these results exclude with 95% confidence a reduction of 40% or more. More vaccine-treated patients than placebo recipients showed a 50% decrease in CD4 count (11 vs 5; relative risk 2.15 [95% CI 0.76-6.12], p = 0.13). The frequencies of HIV-related minor clinical events were similar in the two groups. Pain at the injection site was the only adverse event that occurred more frequently in vaccine-treated group.Interpretation: Postinfection immunisation of symptom-free HIV-infected patients with MNrgp120 vaccine did not alter HIV-1 disease progression as measured by immunological, virological, and clinical endpoints over a 15-month period. [ABSTRACT FROM AUTHOR]

Published
1996
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47. Simultaneous vs sequential initiation of therapy with indinavir, zidovudine, and lamivudine for HIV-1 infection: 100-week follow-up.

Author

Gulick, Roy M., Mellors, John W., Havlir, Diane, Eron, Joseph J., Gonzalez, Charles, McMahon, Deborah, Jonas, Leslie, Meibohm, Anne, Holder, Daniel, Schleif, William A., Condra, Jon H., Emini, Emilio A., Isaacs, Robin, Chodakewitz, Jeffrey A., Richman, Douglas D., Gulick, R M, Mellors, J W, Havlir, D, Eron, J J, and Gonzalez, C

Subjects
HIV infections, AZIDOTHYMIDINE, DRUG therapy
Abstract

Context: Combination antiretroviral therapy can markedly suppress human immunodeficiency virus (HIV) replication but the duration of HIV suppression varies among patients.Objective: To compare the antiretroviral effect of a 3-drug regimen started simultaneously or sequentially in patients with HIV infection.Design: A multicenter, randomized, double-blind study, modified after at least 24 weeks of blinded therapy to provide open-label 3-drug therapy with follow-up through 100 weeks.Setting: Four clinical research unitsPatients: Ninety-seven patients with HIV infection who had taken zidovudine for at least 6 months with serum HIV RNA level of at least 20000 copies/mL and CD4 cell count of 0.05 to 0.40 x 10(9)/L.Interventions: Patients were initially randomized to receive 1 of 3 antiretroviral regimens: indinavir, 800 mg every 8 hours; zidovudine, 200 mg every 8 hours and lamivudine, 150 mg every 12 hours; or all 3 drugs. After at least 24 weeks of blinded therapy, all patients received open-label 3-drug therapy.Main Outcome Measures: Antiretroviral activity was assessed by changes in HIV RNA level and CD4 cell count from baseline. Data through 100 weeks were summarized.Results: Simultaneous initiation of indinavir, zidovudine, and lamivudine suppressed HIV RNA in 78% (25/32) of contributing patients to less than 500 copies/mL and increased CD4 cell count to a median of 0.209 x 10(9)/L above baseline at 100 weeks. When these 3 drugs were initiated sequentially, only 30% to 45% of contributing patients (10 of 33 in the zidovudine-lamivudine group and 13 of 29 in the indinavir group, respectively) had a sustained reduction in HIV RNA to less than 500 copies/mL, and median CD4 cell count increased to 0.101 to 0.163 x 10(9)/L above baseline at 100 weeks.Conclusions: A 3-drug combination of indinavir, zidovudine, and lamivudine started simultaneously has durable antiretroviral activity for at least 2 years. Sequential initiation of the same 3 drugs is much less effective. [ABSTRACT FROM AUTHOR]

Published
1998
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48. Association of CD4 cell depletion and elevated blood and seminal plasma human immunodeficiency virus type 1 (HIV-1) RNA concentrations with genital ulcer disease in HIV-1-infected men in Malawi.

Author

Dyer, John R., Eron, Joseph J., Hoffman, Irving F., Kazembe, Peter, Vernazza, Pietro L., Nkata, Eniffa, Daly, Celine Costello, Fiscus,, Susan A., Cohen, Myron S., Dyer, J R, Eron, J J, Hoffman, I F, Kazembe, P, Vernazza, P L, Nkata, E, Costello Daly, C, Fiscus, S A, and Cohen, M S

Abstract

CD4 cell counts and blood plasma and seminal plasma human immunodeficiency virus type 1 (HIV-1) concentrations were compared in HIV-1 RNA-seropositive men with urethritis and with or without genital ulcer disease (GUD). GUD was associated with lower CD4 cell counts (median, 258 vs. 348/μL) and increased blood plasma HIV-1 RNA (median, 240 × 103 vs. 79.4 × 103 copies/ mL). Men with nongonococcal urethritis and GUD shed significantly greater quantities of HIV-1 in semen (median, 195 × 103 vs. 4.0 × 103 copies/mL) than men with nongonococcal urethritis without GUD. These levels decreased ∽4-fold following antibiotic therapy. The results indicate an association between GUD and increased blood HIV-1 RNA levels. Increased HIV-1 in semen was demonstrated in some men with GUD; such an increase could lead to increased transmission, thus complicating interpretation of the role of the genital ulcer itself in the infectiousness of HIV. Reasons for increased HIV RNA in semen in men with GUD remain to be determined. [ABSTRACT FROM PUBLISHER]

Published
1998
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