The KLEAN study of fosamprenavir-ritonavir versus lopinavir-ritonavir, each in combination with abacavir-lamivudine, for initial treatment of HIV infection over 48 weeks: a randomised non-inferiority trial

Eron, Joseph J.; Yéni, Patrick; Gathe, Joseph; Estrada, Vicente; DeJesus, Edwin; Staszewski, Schlomo; Lackey, Philip; Katlama, Christine; Young, Benjamin; Yau, Linda; Sutherland-Phillips, Denise; Wannamaker, Paul; Vavro, Cindy; Patel, Lisa; Yeo, Jane; Shaefer, Mark S.

doi:10.1016/s0140-6736(06)69155-1

Cited by 318 publications

(185 citation statements)

References 12 publications

Supporting

Mentioning

163

Contrasting

Unclassified

Order By: Relevance

“…Numerous studies of patients who fail PI have not identified mutations in the protease gene associated with resistance (2)(3)(4)(5). In a systematic review of failure of first-line antiretroviral therapy, persons failing PI-containing regimens had the least accumulation of drug resistance mutations, both within the protease gene and, to a lesser extent, in the reverse transcriptase gene (6).…”

Section: Knowledge Gapmentioning

confidence: 99%

Lack of protease inhibitor resistance following treatment failure — too good to be true?

Bartlett¹

2013

J. Clin. Invest.

View full text Add to dashboard Cite

A 29-year-old man with recently diagnosed HIV infection and a CD4 cell count of 225/mm 3 began treatment with atazanavir (300 mg), ritonavir (100 mg), emtricitabine (200 mg), and tenofovir (300 mg) daily. For 18 months, he was treatment adherent and his plasma HIV RNA level was below the limit of detection. He then began a relationship with a new partner, who introduced him to methamphetamines. His medication adherence became erratic, and he missed appointments in clinic. Eventually. he was hospitalized for rehabilitation, and he resumed taking his medications on schedule. Following his discharge, he was found to have a plasma HIV RNA level of 11,400 copies/ml. Genotypic resistance testing revealed only an M184V mutation associated with emtricitabine resistance. A decision regarding his next treatment regimen needs to be made.

show abstract

Section: Knowledge Gapmentioning

confidence: 99%

Lack of protease inhibitor resistance following treatment failure — too good to be true?

Bartlett¹

2013

J. Clin. Invest.

View full text Add to dashboard Cite

show abstract

“…For instance, the presence of K65R or L74V (J. Eron, Jr. et al, 2006;Gallant et al, 2006;Moyle et al, 2005) point mutations ( Figure 2 and Table 2) in addition to the M184V is sufficient for high level resistance to ddI and ABC , particularly in patients with non-subtype B clades (Harrigan et al, 2000;Lanier et al, 2004a;Svarovskaia et al, 2007;M. A. Winters et al, 1997 .…”

Section: Point Mutations Associated With Resistance To Nrtismentioning

confidence: 99%

Point Mutations Associated with HIV-1 Drug Resistance, Evasion of the Immune Response and AIDS Pathogenesis

Khati¹,

Millroy²

2012

Point Mutation

View full text Add to dashboard Cite

“…PIs can be effective components of initial, second-line, and salvage antiretroviral regimens, although elevated blood cholesterol and triglyceride levels, also known as dyslipidemias, can be a problem with some PIs and may develop within weeks to months of starting PI-based therapy (56,61,66,70). Although certain PI-based regimens increase the risk of insulin resistance and diabetes (3,23,46,48), this is unlikely to be a class-wide PI effect and, in certain cases, may have more to do with a regimen's NRTI backbone (6,9,12,28,45,47,69). There is often a higher genetic barrier to resistance to protease inhibitors than to either NNRTIs or integrase inhibitors, and multiple mutations are typically required for protease inhibitors to lose substantial antiviral activity, although exceptions exist (e.g., saquinavir and nelfinavir).…”

Section: Available Antiretroviral Classes and Drugsmentioning

confidence: 99%

Antiretroviral Therapy in the Clinic

Tsibris

Hirsch

2010

J Virol

View full text Add to dashboard Cite

Currently, over 25 antiretroviral drugs and several fixed-dose drug combinations are available in most developed countries. Individual agents target many of the critical steps in the HIV replication cycle-entry, reverse transcription, integration, and proteolytic processing. Newer regimens offer greater convenience and less toxicity than ones previously used, and emerging data suggest that antiretroviral therapy should be initiated earlier during the natural history of HIV infection than was previously recommended (54). Randomized comparative testing has demonstrated superior clinical, immunologic, and virologic outcomes with certain drug combinations, although the use of certain otherwise effective antiretroviral regimens may sometimes be limited by co-morbid illnesses and toxicities. This review focuses on the translation of insights gleaned from both bench and clinical research into the day-to-day care of HIV-infected patients. We discuss the practical issues of how to choose an antiretroviral regimen, when to start therapy, how to monitor the clinical response, and how to adjust therapy for treatment failure or drug-associated toxicities.

show abstract

The KLEAN study of fosamprenavir-ritonavir versus lopinavir-ritonavir, each in combination with abacavir-lamivudine, for initial treatment of HIV infection over 48 weeks: a randomised non-inferiority trial

Cited by 318 publications

References 12 publications

Lack of protease inhibitor resistance following treatment failure — too good to be true?

Lack of protease inhibitor resistance following treatment failure — too good to be true?

Point Mutations Associated with HIV-1 Drug Resistance, Evasion of the Immune Response and AIDS Pathogenesis

Antiretroviral Therapy in the Clinic

Contact Info

Product

Resources

About