ライフサイエンスコーパス: foscarnet

1 istant to the broad-spectrum antiviral agent foscarnet.

2 ir, systemic cidofovir analog, and localized foscarnet.

3 (26%) of 39 at some time before switching to foscarnet.

4 loped rapidly in all 3 patients treated with foscarnet.

5 ion and selection with either ganciclovir or foscarnet.

6 usceptibility to cidofovir, ganciclovir, and foscarnet.

7 es showed reduced susceptibility (4-fold) to foscarnet.

8 that were resistant to both ganciclovir and foscarnet.

9 Pol conferred resistance to ganciclovir and foscarnet.

10 ganciclovir alone or ganciclovir followed by foscarnet.

11 icity associated with other options, such as foscarnet.

12 olates that are resistant to ganciclovir and foscarnet.

13 All isolates were susceptible to foscarnet.

14 acyclovir but susceptible to ganciclovir and foscarnet.

15 CV) and a second during later treatment with foscarnet.

16 h of these isolates are sensitive to GCV and foscarnet.

17 clovir (23.1%) and the second-line agent was foscarnet (73.1% and 84.6%).

18 the W780V mutation was slightly resistant to foscarnet (a 1.9-fold increase in the EC50) and suscepti

19 utation W781V in HSV-1 induced resistance to foscarnet, acyclovir, and ganciclovir (3-, 14-, and 3-fo

20 The apparent inhibition constant values of foscarnet against mutant UL30 and UL54 DNA polymerases w

21 ble complexes were formed in the presence of foscarnet (an analog of pyrophosphate), the dNTP complem

22 s, since it is blocked by UV irradiation and foscarnet, an inhibitor of viral DNA-polymerase.

23 eptible to aphidicolin and resistant to both foscarnet and acyclovir, compared to the wild-type KOS s

24 I (V781I) were associated with resistance to foscarnet and adefovir.

25 and a 3-5-fold increased resistance to both foscarnet and cidofovir, compared with the wild-type CMV

26 CMV resistance to foscarnet and ganciclovir was detected after only 6 and

27 hich were shown by marker transfer to confer foscarnet and multidrug resistance, respectively.

28 gesting that the combination of intravitreal foscarnet and systemic antiviral therapy may have greate

29 Both foscarnet and the hydrazone inhibit RNase H cleavage and

30 HCMV and especially HSV-1 susceptibility to foscarnet and the possible contribution of other residue

31 ompounds, including the polymerase inhibitor foscarnet and the putative RNase H inhibitor 4-chlorophe

32 despite intravenous ganciclovir followed by foscarnet and then cidofovir.

33 r PBMCs during administration of intravenous foscarnet and/or ganciclovir.

34 <6-fold) but were sensitive to cidofovir and foscarnet, and 7 showed moderately reduced susceptibilit

35 Antiviral susceptibilities to ganciclovir, foscarnet, and cidofovir and sequencing of UL97 and DNA

36 ction is challenging, and salvage therapies, foscarnet, and cidofovir, have significant toxicities.

37 om the patient was resistant to ganciclovir, foscarnet, and cidofovir.

38 r treating CMV: ganciclovir, valganciclovir, foscarnet, and cidofovir.

39 cluding intravenous ganciclovir, intravenous foscarnet, and intravenous cidofovir, is effective.

40 iptase enzyme inhibitors AZT, ddI, 3TC, d4T, foscarnet, and nevirapine, as well as the protease inhib

41 Combining AZT, foscarnet, and/or arabinofuranyl-guanosine with ddG did

42 involved ganciclovir as first-line agent and foscarnet as second-line agent.

43 Phosphonoformic acid (PFA, foscarnet) belongs to a class of antiviral drugs that in

44 Acyclovir, foscarnet, cidofovir, and PMEA reduced the number of cel

45 ganciclovir dose escalation, ganciclovir and foscarnet combination, and adjunct therapy such as CMV-s

46 The ability to form a specific foscarnet complex might explain the inhibitory propertie

47 RT is located upstream in the foscarnet complex, relative to the +1 complex, and downs

48 solved completely with the application of 1% foscarnet cream.

49 drothymidine (d4T), or phosphonoformic acid (foscarnet) did not cause reproducible telomere shortenin

50 Among 44 patients treated with foscarnet, drug resistance increased the risk of retinit

51 7 of 8 patients who received ganciclovir or foscarnet for > or =7 days, compared with 0% (0 of 4) in

52 rus (CMV) retinitis received ganciclovir and foscarnet for 20 and 5 months, respectively, with eviden

53 ailable antiherpesvirus drugs, cidofovir and foscarnet, had no effect on the transcription of these v

54 her antiherpes drugs such as ganciclovir and foscarnet is warranted.

55 Phosphonoformate (foscarnet) is a pyrophosphate (PP(i)) analogue and a pot

56 Lipid-derivatized foscarnet liposome formulations may be a useful long-act

57 The adjunctive use of intravitreal foscarnet may be more effective than systemic therapy al

58 in the laboratory, including ganciclovir and foscarnet, no clinical trials have assessed their benefi

59 the different profiles of susceptibility to foscarnet of the HSV-1 and HCMV mutants could be related

60 ) and 9 required therapy with ganciclovir or foscarnet (only 1 post-CTL infusion).

61 Older age at BMT (P <.001), use of foscarnet (P =.003), and receipt of iopamidol (P =.073)

62 presence or absence of ganciclovir (GCV) or foscarnet (PFA), were cocultured with CMV-seropositive o

63 ast, the presence of the pyrophosphate mimic foscarnet (phosphonoformate), and also the presence of G

64 ctly decreasing the binding and retention of foscarnet, PP(i), and ATP.

65 , the RB69 enzyme is relatively resistant to foscarnet, requiring the mutation V478W in helix N to pr

66 The incidence of foscarnet resistance after 6, 9, and 12 months of therap

67 us containing V809 showed 6.3-fold increased foscarnet resistance and 2.6-fold increased ganciclovir

68 nically significant viral genetic marker for foscarnet resistance and decreased susceptibility to gan

69 se enzymes and was inversely correlated with foscarnet resistance and directly correlated with AZT re

70 These mutations may confer foscarnet resistance and reduce primer unblocking by ind

71 partial responses, and in vitro evidence of foscarnet resistance developed rapidly in all 3 patients

72 ral mutations that conferred ganciclovir and foscarnet resistance had evolved sequentially.

73 ing activity for HIV-1 RT containing various foscarnet resistance mutations (K65R, W88G, W88S, E89K,

74 crystal structures of HIV-1 RT, many of the foscarnet resistance mutations affect residues that do n

75 Nine isolates had foscarnet resistance mutations, including V787L and E756

76 inical significance of cytomegalovirus (CMV) foscarnet resistance was studied in patients with acquir

77 lovir (GCV) and cidofovir resistance but not foscarnet resistance when incorporated into laboratory s

78 ecognized functional domains, each conferred foscarnet resistance.

79 n unusually high incidence of acyclovir- and foscarnet-resistant herpes simplex virus (HSV) infection

80 nt in nonsevere patients for whom the use of foscarnet should be avoided.

81 s the modest effect of the W780V mutation on foscarnet susceptibility.

82 conferred slightly decreased ganciclovir and foscarnet susceptibility.

83 n of CMV disease occurred after switching to foscarnet therapy.

84 ively to characterize those who had received foscarnet treatment for ganciclovir-resistant or refract

85 ropoxymethyl]guanine) (IC50 = 2.7-4 microM), foscarnet (trisodium phosphonoformate hexahydrate) (IC50

86 [RR], 0.56; 95% CI, 0.22-1.44; P = .23) and foscarnet use (RR, 0.40; 95% CI, 0.051-3.10; P = .38) we

87 Median duration of foscarnet was 32 days.

88 Antiviral treatment with ganciclovir or foscarnet was associated with improved outcome compared

89 The antiviral drug foscarnet was associated with the largest increase in th

90 s of T2294, and its plating efficiency under foscarnet was increased approximately 30-fold over that

91 pectrum antiviral phosphonoformic acid (PFA, foscarnet) was shown to freeze the pre-translocational s

92 781V mutation in HSV-1 induced resistance to foscarnet, whereas the W780V mutation in HCMV slightly d