ライフサイエンスコーパス: acyclovir

1 methyl group (present in the antiherpes drug acyclovir).

2 phosphorylated form of the anti-herpes drug acyclovir.

3 ervous system infections, and is superior to acyclovir.

4 r evaluation of determinants of responses to acyclovir.

5 % of adults with varicella were treated with acyclovir.

6 variant V75I under the selective pressure of acyclovir.

7 e events were attributable to treatment with acyclovir.

8 of antiherpetic nucleoside prodrugs such as acyclovir.

9 acilitate escape from the antiviral compound acyclovir.

10 ore prolonged serum concentrations than oral acyclovir.

11 ion would explain the clinical resistance to acyclovir.

12 human enzyme that activates valacyclovir to acyclovir.

13 state and is a target for the antiviral drug acyclovir.

14 ate, and time to appropriate deescalation of acyclovir.

15 of patients from both groups were prescribed acyclovir.

16 stration of oral valacyclovir or intravenous acyclovir.

17 laxoSmithKline clinical documents related to acyclovir.

18 nt resistant to nucleoside analogues such as acyclovir.

19 From 2002, most infants received high-dose acyclovir.

20 brospinal fluid and treated with intravenous acyclovir.

21 treatment with the antiviral drug of choice, acyclovir.

22 in all 12 patients empirically treated with acyclovir.

23 previously reported outcomes for intravenous acyclovir.

24 ts receiving long-term prophylactic systemic acyclovir.

25 d 43 in the placebo group (hazard ratio with acyclovir, 0.92, 95% confidence interval [CI], 0.60 to 1

26 usly daily from day -8 to day -2), high-dose acyclovir (2 g, 3 times daily) after transplantation, an

27 clovir (38/110 patients, 35%) than with oral acyclovir (20/109 patients, 18%) (P =0.009).

28 V-1 were randomly assigned in a 1:1 ratio to acyclovir 400 mg orally twice daily or placebo, and were

29 Within a randomized trial of daily acyclovir 400 mg twice daily in African HIV-1 serodiscor

30 andomized, placebo-controlled trial of 5-day acyclovir (400 mg 3 times daily) was conducted among men

31 These data show no evidence that acyclovir (400 mg twice daily) as HSV suppressive therap

32 ntrolled trial of suppressive treatment with acyclovir (400 mg twice daily).

33 in a placebo-controlled trial of twice-daily acyclovir (400 mg) for the prevention of HIV acquisition

34 rticipants were randomly assigned to receive acyclovir (400 participants) or placebo (421 participant

35 n to be superior to an oral dosage of 800 mg acyclovir 5 times per day for 7 days in immunocompetent

36 risk for VZV reactivation were randomized to acyclovir 800 mg twice daily or placebo given from 1 to

37 er oral ganciclovir (1 g every 8 hr) or oral acyclovir (800 mg every 6 hr) from day 15 to day 100 aft

38 Acyclovir, a common antiherpetic drug, was shown to dire

39 Acyclovir, a nucleoside analog, is thought to be specifi

40 e review and analysis is to demonstrate that acyclovir (ACV) 3% ophthalmic ointment is superior to id

41 The oxidation of the antiviral drug acyclovir (ACV) and its main biotransformation product c

42 Ganciclovir (GCV) and acyclovir (ACV) are guanine nucleoside analogues that in

43 g latency can be achieved in the presence of acyclovir (ACV) for 7 days followed by 5 days of ACV was

44 The effect that long-term use of suppressive acyclovir (ACV) has on both overall herpes simplex virus

45 ly, it has been reported that phosphorylated acyclovir (ACV) inhibits human immunodeficiency virus ty

46 The low toxicity of acyclovir (ACV) is mainly due to the fact that human nuc

47 Anti-herpes simplex virus (HSV) drug acyclovir (ACV) is phosphorylated by the viral thymidine

48 man immunodeficiency virus (HIV) activity of acyclovir (ACV) phosphate prodrugs, we herein report the

49 Long-term acyclovir (ACV) prophylaxis, recommended to prevent recu

50 HSV) gene thymidine kinase (TK) gene lead to acyclovir (ACV) resistance.

51 m that of acyclic nucleoside analogs such as acyclovir (ACV) that is based primarily on MBV's ability

52 Despite the proven efficacy of acyclovir (ACV) therapy, herpes simplex encephalitis (HS

53 ed 129S6 mice with HSV1, followed by delayed Acyclovir (ACV) treatment as often occurs in the clinica

54 1) explain most cases of virus resistance to acyclovir (ACV) treatment.

55 n reported, frequently showing resistance to acyclovir (ACV) treatment.

56 man brains, and treatment with the antiviral acyclovir (ACV) was reported to block the accumulation o

57 Acyclovir (ACV), a highly specific anti-herpetic drug, a

58 On investigating the effects of four CTNAs-acyclovir (ACV), cytarabine (Ara-C), zidovudine (AZT) an

59 nificantly less common among women receiving acyclovir (adjusted OR, 0.13; 95% CI, .04-.41).

60 01) and 85.4% for acyclovir and 90.8% for no acyclovir (adjusted P=0.10).

61 ith 75.7% among patients who did not receive acyclovir (adjusted P=0.50).

62 in a randomized placebo-controlled trial of acyclovir administered at a dosage of 400 mg twice daily

63 Acyclovir administered at a dosage of 400 mg twice daily

64 ral therapy (n = 22 [52.4%]), or intravenous acyclovir alone (n = 3 [7.1%]).

65 Acyclovir also improved healing by a median of 3 days (P

66 alacyclovir is the 5'-valyl ester prodrug of acyclovir, an effective anti-herpetic drug.

67 men with HSV-2 ulcers (54 of whom were given acyclovir and 64 of whom were given placebo).

68 for no prednisolone (P<0.001) and 85.4% for acyclovir and 90.8% for no acyclovir (adjusted P=0.10).

69 r regimen of IV ganciclovir followed by oral acyclovir and almost completely eliminates CMV disease a

70 ction includes pharmaceutical drugs, such as acyclovir and docosonal, which are efficacious but maint

71 ropriate bromomethyl ethers gave the acyclic acyclovir and ganciclovir analogues.

72 Acyclovir and ganciclovir are both effective for univers

73 Both acyclovir and ganciclovir statistically significantly pr

74 d ICP0 E3 ligase inhibitors.IMPORTANCE Since acyclovir and its derivatives were launched for herpesvi

75 The most widely utilized antiherpes drugs, acyclovir and its derivatives, have serious limitations,

76 In contrast, removal of acyclovir and lamivudine was mainly attributable to slow

77 eversion of this patient's HSV-2 isolates to acyclovir and penciclovir sensitivity, although resistan

78 and TDF was 10- and 7-fold more potent than acyclovir and penciclovir, respectively, and TAF was als

79 patient have been confirmed as resistant to acyclovir and penciclovir.

80 ths, there was little difference between the acyclovir and placebo arms for cervico-vaginal HIV-1 RNA

81 Mean follow-up for the acyclovir and placebo groups was 1.52 and 1.62 years, re

82 erved 68 HSV-2 seroconversions, 40 and 28 in acyclovir and placebo groups, respectively (HSV-2 incide

83 e IRR after beginning ART was similar in the acyclovir and placebo groups.

84 .30) or CD4 cell counts (P =.85) between the acyclovir and placebo recipients.

85 cal incompatibilities that occur upon mixing acyclovir and vancomycin during management of acute meni

86 d not exhibit meaningful differences between acyclovir and WAY-150138 treatments when analyzed by in

87 sions that were refractory to treatment with acyclovir and which subsequently disseminated.

88 several clones associated with resistance to acyclovir and/or foscavir were identified.

89 yclovir and RR, 0.05 [95% CI, 0.03-0.10] for acyclovir) and PCR (RR, 0.18 [95% CI, 0.12-0.26] for val

90 A total of 309 men received acyclovir, and 306 received placebo; 63% were HIV-1 posi

91 eplication in a manner distinct from that of acyclovir, and an acyclovir-resistant VZV isolate was as

92 st dosing, and also received hydrocortisone, acyclovir, and Bactrim or equivalent prophylaxis.

93 1V in HSV-1 induced resistance to foscarnet, acyclovir, and ganciclovir (3-, 14-, and 3-fold increase

94 th genital HSV-2 received oral valacyclovir, acyclovir, and matching placebo in random order for 7-we

95 nfections employ nucleoside analogs, such as Acyclovir, and target the viral DNA polymerase, essentia

96 toward valacyclovir, the 5'-glycyl ester of acyclovir, and the 5'-valyl ester of zidovudine (AZT), w

97 ntivirals (stavudine, tenofovir, lamivudine, acyclovir, and zidovudine) was analyzed with three-dimen

98 However, both antiviral activities of acyclovir are dependent on phosphorylation by the nucleo

99 gen, and although nucleoside analogs such as acyclovir are highly effective in controlling HSV-1 or -

100 eplication is not complete, valacyclovir and acyclovir are highly effective in suppressing the freque

101 ene with uracil, 5-fluorouracil, tegafur, or acyclovir are reported.

102 detected by PCR between the valacyclovir and acyclovir arms.

103 replication complex of the polymerase and of Acyclovir as a DNA chain terminator.

104 The data support acyclovir as an inhibitor of HIV-1 replication in herpes

105 lled trial of suppressive therapy for HSV-2 (acyclovir at a dose of 400 mg orally twice daily) in cou

106 eive 10 days of treatment with prednisolone, acyclovir, both agents, or placebo.

107 when cells were infected in the presence of acyclovir but not following infection with UV-inactivate

108 y 20-fold more potent inhibitors of VZV than acyclovir but were approximately 6-fold less potent than

109 ith a potency at least comparable to that of acyclovir by blocking viral attachment and penetration i

110 uggest that equivalent plasma drug levels of acyclovir can be achieved after administration of oral v

111 d its main biotransformation product carboxy-acyclovir (carboxy-ACV) by ozone was investigated.

112 yclovir and RR, 0.20 [95% CI, 0.15-0.28] for acyclovir), compared with placebo.

113 idicolin and resistant to both foscarnet and acyclovir, compared to the wild-type KOS strain.

114 herpes zoster occurred among those assigned acyclovir, compared with 69 cases among those assigned p

115 The ferrocene-acyclovir conjugate Fc-5 featured the highest apparent b

116 act containing cream was superior to that of acyclovir cream.

117 HEDS II showed that oral acyclovir decreased the recurrence of any type of herpes

118 IV-1-infected persons with daily suppressive acyclovir did not decrease risk of HSV-2 transmission to

119 Notably, acyclovir did not eliminate HSV-2-induced HIV-1 reactiva

120 gle round HIV infectivity assay to show that acyclovir directly inhibits HIV infection with an IC50 o

121 The mean time from specimen collection to acyclovir discontinuation was 17.1 h shorter in the post

122 ease after reactivation and of resistance to acyclovir during an infection caused by this virus.

123 is important because EBV can be treated with acyclovir early in the active viral phase.

124 In conclusion, acyclovir effectively and safely prevents VZV disease du

125 e removal of five antiviral drugs (abacavir, acyclovir, emtricitabine, lamivudine and zidovudine) via

126 ircumcision, bacterial vaginosis, and use of acyclovir) explained 46% of variation in set point.

127 they received suppressive therapy with oral acyclovir for 6 months.

128 on in the clinical and virologic efficacy of acyclovir for HSV suppression warrants further evaluatio

129 benefit of topical corticosteroids and oral acyclovir for stromal keratitis.

130 In an international trial of acyclovir for suppression of HSV type 2 to prevent human

131 tudies have recently investigated the use of acyclovir for treatment of patients coinfected with HSV

132 antiherpes drugs, ganciclovir (for HCMV) and acyclovir (for HSV-1 and VZV).

133 , we examined 3 sequential cohorts receiving acyclovir from day of transplantation until engraftment

134 tomatitis and was treated alternatively with acyclovir, ganciclovir, and foscavir.

135 association of individual antiviral agents (acyclovir, ganciclovir, and valganciclovir) with outcome

136 There is no evidence of a benefit of acyclovir given alone or an additional benefit of acyclo

137 per 100 person-years (27 participants in the acyclovir group and 28 in the placebo group), and there

138 ithin couples by viral sequencing: 41 in the acyclovir group and 43 in the placebo group (hazard rati

139 eive prednisolone (P<0.001) and 71.2% in the acyclovir group as compared with 75.7% among patients wh

140 e was a trend toward more neutropenia in the acyclovir group than in the placebo group (P=0.09).

141 The odds ratio comparing the acyclovir group with the placebo group on the gold-stand

142 on the incidence of HIV (rate ratio for the acyclovir group, 1.08; 95% confidence interval, 0.64 to

143 d one case of CMV hepatitis developed in the acyclovir group.

144 isition (HIV Prevention Trials Network 039), acyclovir had a smaller effect on the frequency of genit

145 Persons receiving suppressive acyclovir had fewer GUD episodes, but the IRR after begi

146 Acyclovir had little impact on (1) detection of cervicov

147 f 16 patients (37%) receiving long-term oral acyclovir had recurrent HSV, at least one case of which

148 last decade, increased dose and duration of acyclovir has been advised to prevent disease progressio

149 proved ulcer healing--61% of those receiving acyclovir healed by day 7, compared with 42% of those re

150 Acyclovir improved ulcer healing--61% of those receiving

151 e studies compared the efficacy of CMX001 to acyclovir in BALB/c mice inoculated intranasally with HS

152 ovir given alone or an additional benefit of acyclovir in combination with prednisolone.

153 The target of acyclovir in HIV-infected cells is validated as HIV reve

154 Systemic availability of acyclovir in humans is three to five times higher when a

155 o-controlled trial of HSV-2 suppression with acyclovir in Rakai, Uganda.

156 o-controlled trial of HSV-2 suppression with acyclovir in Rakai, Uganda.

157 ed, and valacyclovir became the successor of acyclovir in the treatment of HSV and VZV infections.

158 Although the role of acyclovir in treating HSV encephalitis is clear, the rol

159 than samples obtained from mice treated with acyclovir, including 5 different regions of the brain.

160 Despite widespread use of acyclovir, infection with acyclovir-resistant herpes sim

161 The antiviral drug acyclovir is a guanosine nucleoside analog that potently

162 chondrial toxicity is relatively low because acyclovir is activated only in infected cells by the pro

163 Here, we showed that acyclovir is an inhibitor of HIV-1 replication in CD4(+)

164 Oral acyclovir is effective, but the dosage must be adjusted

165 Once incorporated, acyclovir is removed with a half-life of approximately 1

166 Acyclovir is safe and well tolerated as a treatment in p

167 by fatty acylation, or if a nonpeptide drug, acyclovir, is esterified with valine to enhance bioavail

168 headings (MESH) "Keratitis, Herpetic/" AND "Acyclovir/" limiting by the key words "topical" OR "oint

169 Topical antibiotics, oral acyclovir, low-dose topical steroids and systemic steroi

170 confirm previous reports that resistance to acyclovir may develop during prophylactic therapy in an

171 Recent in vitro studies suggest that acyclovir may directly inhibit HIV-1 replication and can

172 Although acyclovir may prove a useful lead for development of new

173 Antivirals like acyclovir might have a role in the prevention of recurre

174 irally encoded enzyme to phosphorylate it to acyclovir monophosphate.

175 tants raises a cautionary note to the use of acyclovir monotherapy in patients coinfected with HSV an

176 The efficacy of valacyclovir and acyclovir on genital herpes simplex virus (HSV) shedding

177 Attenuating effects of acyclovir on HIV disease progression observed in recent

178 Effect of acyclovir on HIV-1 disease progression was defined by a

179 We investigated the effect of acyclovir on HIV-1 progression.

180 HSV-2 seronegative to estimate the effect of acyclovir on risk of HSV-2 transmission.

181 o group), and there was no overall effect of acyclovir on the incidence of HIV (rate ratio for the ac

182 herpes simplex virus (HSV) replication than acyclovir or cidofovir.

183 3 participants with ocular HSV to receipt of acyclovir or placebo for prevention of ocular HSV recurr

184 amples of genital secretions while receiving acyclovir or placebo, each for 10 weeks.

185 1-serodiscordant couples to daily receipt of acyclovir or placebo.

186 herpes simplex virus reactivation (n = 932); acyclovir or valacyclovir 1 year (n = 1117); or acyclovi

187 e in vivo studies suggest that standard-dose acyclovir or valacyclovir does not select for HIV-1 resi

188 ya, Peru, and the United States taking daily acyclovir or valacyclovir for between 8 weeks and 24 mon

189 Additionally, acyclovir phosphates were detected by reverse-phase-high

190 ed thymidine phosphorylation 10-20-fold, and acyclovir phosphorylation >100-fold.

191 schedule of 2 g of valacyclovir TID reaches acyclovir plasma levels similar to those achieved with i

192 d, double-blind, placebo-controlled trial of acyclovir plus antibacterials and were monitored for 28

193 sodium current increases were unaffected by acyclovir pre-treatment but were abolished by exposure t

194 g-term prednisone treatment and intermittent acyclovir prophylaxis at suboptimal doses and persisted

195 No consensus exists on whether acyclovir prophylaxis should be given for varicella-zost

196 Daily acyclovir prophylaxis significantly reduced herpes zoste

197 To our knowledge, the acyclovir ProTides described here represent the first ex

198 Acyclovir ProTides represent a new class of antivirals t

199 Acyclovir ProTides retained activity against acyclovir-r

200 Acyclovir ProTides suppressed both HIV-1 and HSV-2 at me

201 We developed acyclovir ProTides, monophosphorylated acyclovir with th

202 Acyclovir reduced risk of HIV-1 disease progression by 1

203 Suppression with acyclovir reduced the mean plasma concentration of HIV-1

204 Acyclovir reduces the incidence of GUD but does not prev

205 er twice daily treatment with 400 mg of oral acyclovir reduces the incidence of herpes zoster in a ra

206 cations for the prevalence and prevention of acyclovir resistance in patients with herpes simplex ker

207 A common mutation conferring acyclovir resistance in patients with herpes simplex vir

208 ing multiple episodes of recurrent bilateral acyclovir resistant herpes simplex keratitis in an immun

209 idine kinase (TK) was previously found in an acyclovir-resistant clinical isolate.

210 idine kinase (TK) was previously found in an acyclovir-resistant clinical isolate.

211 sisted, possibly because of the evolution of acyclovir-resistant EBV.

212 Many acyclovir-resistant herpes simplex virus isolates from p

213 Many acyclovir-resistant herpes simplex virus mutants from cl

214 widespread use of acyclovir, infection with acyclovir-resistant herpes simplex virus type 2 (HSV-2)

215 tation was complicated by the development of acyclovir-resistant herpes simplex virus viremia, primar

216 C value for TFT and GCV combined against the acyclovir-resistant HSV-1 strain was 0.84, indicating no

217 maintained potent antiviral activity against acyclovir-resistant HSV-1 strains.

218 in lesion formation in mice infected with an acyclovir-resistant HSV-1, without noticeable adverse ef

219 Among immunocompetent women, the finding of acyclovir-resistant HSV-2 isolates likely represents tra

220 Acyclovir ProTides retained activity against acyclovir-resistant HSV-2.

221 eminated HSV infection, and lung tissue grew acyclovir-resistant HSV-2.

222 t VZV early-passage clinical isolates and an acyclovir-resistant isolate.

223 isolates were obtained before and after the acyclovir-resistant isolates from 5 women were detected.

224 Most acyclovir-resistant isolates have mutations in the thymi

225 Infections caused by acyclovir-resistant isolates of herpes simplex virus (HS

226 Acyclovir-sensitive and acyclovir-resistant isolates were detected in samples co

227 f the women was receiving acyclovir when the acyclovir-resistant isolates were detected.

228 The acyclovir-resistant isolates were transient, because acy

229 d the frequency and clinical significance of acyclovir-resistant isolates, we evaluated the in vitro

230 IC(50) values of TFT and GCV against the acyclovir-resistant strain were 15.40 +/- 3.17 and 93.00

231 ty against 12 strains of HSV-1 (including an acyclovir-resistant strain) was measured by plaque-formi

232 nner distinct from that of acyclovir, and an acyclovir-resistant VZV isolate was as sensitive to the

233 licity of infection (MOI) in the presence of acyclovir results in a quiescent infection resembling la

234 Acyclovir-sensitive and acyclovir-resistant isolates wer

235 nd plaque formation following infection with acyclovir-sensitive and resistant clinical isolates.

236 r-resistant isolates were transient, because acyclovir-sensitive isolates were obtained before and af

237 itive to the effects of JNK inhibition as an acyclovir-sensitive VZV isolate in neurons.

238 esistant isolates, we evaluated the in vitro acyclovir sensitivities of sequential isolates from 34 i

239 In vitro acyclovir sensitivity testing was performed using the dy

240 After she initially responded to intravenous acyclovir, she was switched to oral valacyclovir.

241 Acyclovir significantly reduced both GUD and HSV-2 shedd

242 Acyclovir significantly reduced VZV infections at 1 year

243 reverse transcriptase reported from in vitro acyclovir studies were not observed.

244 infants were randomly assigned to immediate acyclovir suppression (300 mg per square meter of body-s

245 In conclusion, acyclovir suppression during HIV-1 seroconversion and th

246 We evaluated whether acyclovir suppression during human immunodeficiency viru

247 nvolvement who had been randomly assigned to acyclovir suppression had significantly higher mean Bayl

248 Acyclovir suppressive therapy (400 mg twice daily) reduc

249 TFT and GCV are synergistic against acyclovir-susceptible HSV-1 at concentrations significan

250 ulting in 50% inhibition of PFUs (IC(50)) of acyclovir-susceptible HSV-1 strains ranged from 3.07 +/-

251 For acyclovir-susceptible HSV-1 strains, TFT and GCV combine

252 (10:1) were 10 times more potent against all acyclovir-susceptible HSV-1 strains.

253 say; isolates for which the concentration of acyclovir that inhibited cytopathic effect by 50% (EC50)

254 ing a regimen of 14 to 21 days of parenteral acyclovir, the infants were randomly assigned to immedia

255 Daily acyclovir therapy did not reduce the risk of transmissio

256 time to result reporting and the duration of acyclovir therapy for children with signs and symptoms o

257 s similar to those achieved with intravenous acyclovir therapy given to immunocompromised patients (1

258 in a placebo-controlled trial of suppressive acyclovir therapy to prevent HIV transmission, 349 of wh

259 The median duration of acyclovir therapy was also significantly reduced in the

260 around times and the duration of unnecessary acyclovir therapy.

261 st and side effects of prolonged intravenous acyclovir therapy; in contrast, immunocompromised patien

262 wth spurt that caused the baseline dosage of acyclovir to become subtherapeutic.

263 Addition of acyclovir to syndromic management will improve healing o

264 zyme, we compared the kinetic parameters for acyclovir to those governing incorporation of dGTP.

265 e only death from CMV disease occurred in an acyclovir-treated patient with CMV pneumonia.

266 tion of the ME panel reduced the duration of acyclovir treatment from an average of 66 h (standard de

267 Acyclovir treatment in patients coinfected with HSV and

268 Acyclovir treatment of 129 mice beginning on day 4 p.i.

269 , and animals could be protected from HSE by acyclovir treatment provided 4 d after ocular infection.

270 In contrast to acyclovir, treatment of cells during latency for 24 h wi

271 ve examined the kinetics of incorporation of acyclovir triphosphate by the herpes simplex virus-1 DNA

272 we examined the incorporation and removal of acyclovir triphosphate by the human mitochondrial DNA po

273 (10 s(-1)) afford efficient incorporation of acyclovir triphosphate by the Pol-UL42 enzyme.

274 Biochemical analyses demonstrate that acyclovir triphosphate is a chain terminator substrate f

275 Recently, acyclovir triphosphate was shown to be a direct inhibito

276 factor of approximately 50 favors dGTP over acyclovir triphosphate, mostly due to a faster maximum r

277 not controlled by high-dose prophylaxis with acyclovir, valacyclovir, and famciclovir.

278 oral corticosteroids alone, the addition of acyclovir, valacyclovir, or famcyclovir to oral corticos

279 clovir or valacyclovir 1 year (n = 1117); or acyclovir/valacyclovir for at least 1 year or longer if

280 In conclusion, acyclovir/valacyclovir prophylaxis given for 1 year led

281 rogression by 16%; 284 participants assigned acyclovir versus 324 assigned placebo reached the primar

282 duced HIV-1 ulcer shedding on day 7 (24% for acyclovir vs 37% for placebo; P= .05).

283 Intravenous acyclovir was given for the duration of all RI.

284 Resistance to acyclovir was observed in a patient with a prolonged ini

285 Acyclovir was utilized to stop residual acute-phase viru

286 Acyclovir was well tolerated.

287 lgrastim, sulfamethoxazole/trimethoprim, and acyclovir were administered prophylactically.

288 nt of HSV infections the aminoacyl esters of acyclovir were designed, and valacyclovir became the suc

289 Both oral ganciclovir and oral acyclovir were generally well tolerated.

290 At day 7, women receiving acyclovir were less likely to have detectable lesional H

291 No serious adverse events related to acyclovir were observed.

292 None of the women was receiving acyclovir when the acyclovir-resistant isolates were det

293 yed to block production of infectious virus: acyclovir, which inhibits viral DNA synthesis, and WAY-1

294 Acyclovir, which prevents lytic viral replication but no

295 %) with rejected specimens were treated with acyclovir, which suggests a low clinical concern for HSV

296 It is uncertain whether episodic acyclovir will enhance ulcer healing if delivered at pri

297 loped acyclovir ProTides, monophosphorylated acyclovir with the phosphate group masked by lipophilic

298 loaded separately with either vancomycin or acyclovir, with high entrapment efficiency (ca. 46-56%),

299 of HHV-6 by FA-ME led to discontinuation of acyclovir within 12.0 h in all 12 patients empirically t

300 ared with 8 of 109 patients (7.3%) receiving acyclovir within the first year after transplantation (P