ライフサイエンスコーパス: foscarnet

1 icity associated with other options, such as foscarnet.

2 istant to the broad-spectrum antiviral agent foscarnet.

3 ir, systemic cidofovir analog, and localized foscarnet.

4 loped rapidly in all 3 patients treated with foscarnet.

5 (26%) of 39 at some time before switching to foscarnet.

6 ion and selection with either ganciclovir or foscarnet.

7 usceptibility to cidofovir, ganciclovir, and foscarnet.

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

9 that were resistant to both ganciclovir and foscarnet.

10 Pol conferred resistance to ganciclovir and foscarnet.

11 ganciclovir alone or ganciclovir followed by 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 ociated with less acute kidney injury versus foscarnet (8.5% vs 21.3%) and neutropenia versus valganc

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

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

21 and the Q727R isolate additionally exhibited foscarnet/adefovir resistance.

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

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

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

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

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

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

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

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

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

31 Both foscarnet and the hydrazone inhibit RNase H cleavage and

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

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

34 despite intravenous ganciclovir followed by foscarnet and then cidofovir.

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

36 <6-fold) but were sensitive to cidofovir and foscarnet, and 7 showed moderately reduced susceptibilit

37 rir, intravitreal and systemic injections of foscarnet, and anti-Cytomegalovirus human immunoglobulin

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

39 al effective concentrations for ganciclovir, foscarnet, and cidofovir were 8.6-, 3.4- and 2.9-fold hi

40 rred high, triple resistance to ganciclovir, foscarnet, and cidofovir, and A543V had 10-fold reduced

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

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

43 ansplant patients included (val)ganciclovir, foscarnet, and cidofovir.

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

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

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

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

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

49 nt 1 developed resistance to ganciclovir and foscarnet because of 2 DP mutations (V715M and V781I), p

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

51 ) to available antivirals ([val]ganciclovir, foscarnet, cidofovir) are associated with higher mortali

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

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

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

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

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

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

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

59 7 of 8 patients who received ganciclovir or foscarnet for > or =7 days, compared with 0% (0 of 4) in

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

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

62 ed; 2 achieved virological suppression after foscarnet induction with a sustained suppression at Week

63 ed salvage regimen (with or without a 4-week foscarnet induction) in individuals harboring multidrug-

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

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

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

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

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

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

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

71 testing revealed resistance to ganciclovir, foscarnet, or cidofovir in 56% of patients receiving mar

72 ed therapy (IAT; valganciclovir/ganciclovir, foscarnet, or cidofovir) for 8 weeks, with 12 weeks of f

73 n was reversed by pretreatment of cells with Foscarnet, or p38 inhibitor.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

91 ecognized functional domains, each conferred foscarnet resistance.

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

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

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

95 conferred slightly decreased ganciclovir and foscarnet susceptibility.

96 Foscarnet therapy led to CMV DNAemia clearance and disea

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

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

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

100 [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

101 Median duration of foscarnet was 32 days.

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

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

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

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

106 781V mutation in HSV-1 induced resistance to foscarnet, whereas the W780V mutation in HCMV slightly d