ライフサイエンスコーパス: antiretroviral agent

1 linical outcomes following treatment with an antiretroviral agent.

2 types associated with drug resistance to any antiretroviral agent.

3 t immunosuppressive agent, or PMPA, a potent antiretroviral agent.

4 y significant changes in the exposure of any antiretroviral agents.

5 HIV-1 viral load declined in the absence of antiretroviral agents.

6 uld make the zinc finger an ideal target for antiretroviral agents.

7 nceptional exposure to dolutegravir or other antiretroviral agents.

8 V-1 viral load, and qualitative detection of antiretroviral agents.

9 metabolism between statins and commonly used antiretroviral agents.

10 d to support its use as one of the preferred antiretroviral agents.

11 challenging despite continued development of antiretroviral agents.

12 ted PBMCs, inhibiting de novo infection with antiretroviral agents.

13 new class of immune-stimulating long-acting antiretroviral agents.

14 (HIV-1) infection in combination with other antiretroviral agents.

15 ne receptor 5 antagonists are a new class of antiretroviral agents.

16 gn of new DIS selective ligands as potential antiretroviral agents.

17 to the drug regimen or suboptimal levels of antiretroviral agents.

18 erfamily, confers resistance to purine-based antiretroviral agents.

19 ssed to AIDS and has never been treated with antiretroviral agents.

20 health services and limited or no access to antiretroviral agents.

21 were treated with multidrug combinations of antiretroviral agents.

22 proach to the design of anti-inflamatory and antiretroviral agents.

23 presents an attractive target for developing antiretroviral agents.

24 nate analog, is one of a new class of potent antiretroviral agents.

25 exists, there will be a need for more potent antiretroviral agents.

26 should be studied in combination with other antiretroviral agents and in persons with more advanced

27 timated by inhibiting virion production with antiretroviral agents and modelling the resulting declin

28 V-1 infection persist despite treatment with antiretroviral agents and represent the main barrier to

29 ug-drug interactions (DDIs) between these LA antiretroviral agents and rifampicin using physiological

30 The availability of an increasing number of antiretroviral agents and the rapid evolution of new inf

31 ce is critical for developing more effective antiretroviral agents and therapies.

32 serves as a prototype for this new class of antiretroviral agents and validates gp120 as a viable ta

33 s a single entity (in combination with other antiretroviral agents) and as a fixed-dose combination (

34 s, review the interaction data with DAAs and antiretroviral agents, and identify the knowledge gaps i

35 The efficacy of antiretroviral agents approved for the treatment of HIV-

36 Furthermore, several antiretroviral agents are active against HBV infection,

37 A wide variety of antiretroviral agents are available through private phar

38 Long-acting injectable antiretroviral agents are being developed for HIV-1 prev

39 Long-term safety data for antiretroviral agents are not yet available.

40 he most recent preclinical advances in novel antiretroviral agents are reviewed and promising new app

41 ic inflammation, immune activation, and some antiretroviral agents, are not taken into account in the

42 Several antiretroviral agents (ARVs) are associated with chronic

43 inhibitor, given with one or two nucleoside antiretroviral agents, as compared with the safety and e

44 re realistic with the development and use of antiretroviral agents, as well as studies on the role of

45 Antiretroviral agents associated with fewer metabolic ef

46 Stavudine is a promising antiretroviral agent, but its clinical efficacy has not

47 integration system is a promising target for antiretroviral agents, but to date no clinically useful

48 Since the efficacy of antiretroviral agents can be impacted by interactions be

49 estoration of anti-mycobacterial immunity by antiretroviral agents can improve the clinical outcome o

50 Currently available antiretroviral agents can suppress viral replication and

51 HIV RNA load is warranted or when preferred antiretroviral agents cannot be used.

52 to 700 cells/mm(3); 48% receiving prescribed antiretroviral agents), comprising 43 asymptomatic indiv

53 ment regimens in the United States contain 3 antiretroviral agents, costing >$30 000/person/year.

54 rase (IN) inhibitors are the newest class of antiretroviral agents developed for the treatment of HIV

55 ger, longitudinal cohorts.IMPORTANCE Several antiretroviral agents do not efficiently enter the CNS,

56 om the US Food and Drug Administration of an antiretroviral agent for adults and the first publicatio

57 aternal transmission and may be an effective antiretroviral agent for treatment.

58 nhibitors (ALLINIs) are a promising class of antiretroviral agents for clinical development.

59 Long-acting antiretroviral agents for preexposure prophylaxis (PrEP)

60 ses, including HIV-1, and the application of antiretroviral agents for prevention holds great promise

61 Maturation inhibitors are a new class of antiretroviral agents for treatment of HIV-1.

62 irst-line therapy could be reconsidered when antiretroviral agents from other classes become availabl

63 1 (HIV-1) infection, treatment with a single antiretroviral agent has limited efficacy.

64 Combination therapy with three antiretroviral agents has been integral to successful HI

65 Preexposure prophylaxis with antiretroviral agents has been shown to reduce the trans

66 Treatment of HIV disease with antiretroviral agents has changed considerably.

67 ad after initiation of treatment with potent antiretroviral agents has provided substantial insight i

68 IV-1) and the infected host by administering antiretroviral agents has revealed the rapid turnover of

69 val and health in PWH, several commonly used antiretroviral agents have been associated with kidney i

70 Several new antiretroviral agents have been introduced into pediatri

71 lipoatrophy led to the development of newer antiretroviral agents; however, studies have demonstrate

72 known resistance-conferring genotypes to any antiretroviral agent in this cohort of 80 newly infected

73 Within the multicenter Pharmacokinetics of ANtiretroviral agents in HIV-infected pregNAnt women (PA

74 rformed (Pharmacokinetics of Newly Developed Antiretroviral Agents in HIV-Infected Pregnant Women Net

75 longside the drive for access to more robust antiretroviral agents in resource-limited settings, ther

76 Therapeutic concentrations of antiretroviral agents in seminal plasma (SP) may reduce

77 utively exposing an HIV-1 variant to various antiretroviral agents including IN strand transfer inhib

78 r problem affecting the clinical efficacy of antiretroviral agents, including protease inhibitors, in

79 Antiretroviral agents, including those used in recent ye

80 The optimal penetration of antiretroviral agents into the central nervous system ma

81 Although the use of more than one antiretroviral agent is essential for effective HIV-1 tr

82 patients who have been treated with numerous antiretroviral agents, it may be impossible to achieve s

83 Potent antiretroviral agents markedly suppress HIV and have dra

84 stances, the enhanced viral suppression from antiretroviral agents may actually improve or decrease t

85 se, which suggests that early treatment with antiretroviral agents may be indicated for these infants

86 ntial interaction between anti-KS agents and antiretroviral agents needs to be kept in mind.

87 ents with HIV infection who are treated with antiretroviral agents often lose subcutaneous fat and ha

88 from the direct effects of HIV proteins and antiretroviral agents on adipocyte health, genetic facto

89 go reverse transcription, a step impaired by antiretroviral agents or by introduction of mutations in

90 Thus, following screening of many antiretroviral agents, our findings support only the pot

91 Antiretroviral agents, particularly protease inhibitors

92 Treatment with antiretroviral agents, particularly protease inhibitors,

93 The use of combination antiretroviral agents, particularly the protease inhibit

94 Unfortunately, current antiretroviral agents penetrate the lymph nodes insuffic

95 ith HIV/AIDS when treated with highly active antiretroviral agents, persons with HIV infection are th

96 Nelfinavir (NLF), an antiretroviral agent, preserves mitochondrial membranes

97 Oral antiretroviral agents provide life-saving treatments for

98 While protease inhibitors are effective antiretroviral agents, recent studies have shown that pr

99 Antiretroviral agents remain the cornerstone of HIV trea

100 Resistance to antiretroviral agents remains a leading cause of treatme

101 and drug-resistant mutant) and two types of antiretroviral agents (reverse transcriptase and proteas

102 Treatment of HIV-infected individuals with antiretroviral agents selects for drug-resistant mutants

103 aquinavir alone or in combination with other antiretroviral agents should be investigated further.

104 The antiretroviral agent, tenofovir, formulated as a vaginal

105 ent resistance has been demonstrated for all antiretroviral agents tested; therefore, we tested for v

106 tructure of ALDOA identified raltegravir, an antiretroviral agent that targets HIV integrase, as a ph

107 translocation inhibitors (NRTTIs) are potent antiretroviral agents that block HIV replication.

108 Treatment for HIV has relied on the use of antiretroviral agents that can be subject to the develop

109 protease inhibitors are a promising class of antiretroviral agents that compromise enzymatic function

110 itors (ALLINIs) are a promising new class of antiretroviral agents that disrupt proper viral maturati

111 ernative to the daily administration of oral antiretroviral agents that has recently shown promise as

112 oviral exposure, the toxicity profile of the antiretroviral agent, the toxicity of the chemotherapy,

113 Despite the large number of approved antiretroviral agents, the number of sequential treatmen

114 rocess of discovering the next generation of antiretroviral agents, this study presents a highly sens

115 Motivated by the ability of combinations of antiretroviral agents to sustain viral suppression in HI

116 ate potency of drugs or suboptimal levels of antiretroviral agents, viral resistance, and other facto

117 leukoencephalopathy who are treated with the antiretroviral agents we used, nor does high-dose antire

118 Trough plasma concentrations of measured antiretroviral agents were all above minimum effective c

119 When antiretroviral agents were coadministered, the 10 U dose

120 ear proof of concept for PRO 140 as a potent antiretroviral agent with extended activity after a sing

121 hough information regarding the use of newer antiretroviral agents with chemotherapy is limited, the

122 Antiretroviral agents with long-acting properties have p

123 IV-1 therapy underscores the need to develop antiretroviral agents with new mechanisms of action.

124 Antiretroviral agents with novel mechanisms and dosing i

125 IDS (RH = 0.83, 95% CI: 0.7, 0.9) and use of antiretroviral agents with protease inhibitors before AI

126 le approaches involve topical application of antiretroviral agents with specific activity against HIV

127 n neonatal clinical pharmacology research on antiretroviral agents with the goal of stimulating resea

128 te that FIs constitute an expanding class of antiretroviral agents with the potential to be sequenced

129 Further, treatment with the antiretroviral agent zidovudine either significantly red