ライフサイエンスコーパス: acyclovir

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

2 ervous system infections, and is superior to acyclovir.

3 r evaluation of determinants of responses to acyclovir.

4 of patients from both groups were prescribed acyclovir.

5 % of adults with varicella were treated with acyclovir.

6 stration of oral valacyclovir or intravenous acyclovir.

7 variant V75I under the selective pressure of acyclovir.

8 e events were attributable to treatment with acyclovir.

9 of antiherpetic nucleoside prodrugs such as acyclovir.

10 acilitate escape from the antiviral compound acyclovir.

11 ore prolonged serum concentrations than oral acyclovir.

12 ion would explain the clinical resistance to acyclovir.

13 human enzyme that activates valacyclovir to acyclovir.

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

15 owed by the rapid and complete conversion to acyclovir.

16 t approaches that achieved by a high dose of acyclovir.

17 4 cell count was 48% lower when treated with acyclovir.

18 ailability compared with orally administered acyclovir.

19 laxoSmithKline clinical documents related to acyclovir.

20 nt resistant to nucleoside analogues such as acyclovir.

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

22 brospinal fluid and treated with intravenous acyclovir.

23 treatment with the antiviral drug of choice, acyclovir.

24 previously reported outcomes for intravenous acyclovir.

25 ts receiving long-term prophylactic systemic acyclovir.

26 phosphorylated form of the anti-herpes drug acyclovir.

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

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

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

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

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

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

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

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

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

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

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

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

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

40 y profiles of valacyclovir (</=1000 mg/day), acyclovir (800 mg/day), and placebo were similar.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 ipeptide prodrug of the antiviral nucleoside acyclovir (ACV), val-val-ACV (VVACV), was evaluated in v

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

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

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

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

64 Acyclovir administered at a dosage of 400 mg twice daily

65 acy and safety of oral ganciclovir with oral acyclovir after induction with intravenous (IV) ganciclo

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

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

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

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

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

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

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

73 Acyclovir and ganciclovir are both effective for univers

74 Both acyclovir and ganciclovir statistically significantly pr

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 patient have been confirmed as resistant to acyclovir and penciclovir.

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

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

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

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

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

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

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

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

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

88 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

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

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

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

92 1V in HSV-1 induced resistance to foscarnet, acyclovir, and ganciclovir (3-, 14-, and 3-fold increase

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

94 ection, 18 (5.2%) had pneumonia treated with acyclovir, and none died.

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 An unusually high incidence of acyclovir- and foscarnet-resistant herpes simplex virus

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

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

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

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 Valacyclovir enhances acyclovir bioavailability compared with orally administe

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

171 irally encoded enzyme to phosphorylate it to acyclovir monophosphate.

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

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

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

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

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

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

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

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

180 3 participants with ocular HSV to receipt of acyclovir or placebo for prevention of ocular HSV recurr

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

182 1-serodiscordant couples to daily receipt of acyclovir or placebo.

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

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

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

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

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

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

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

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

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

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

193 Daily acyclovir prophylaxis significantly reduced herpes zoste

194 ter stem-cell transplantation (SCT), despite acyclovir prophylaxis.

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

196 Acyclovir ProTides represent a new class of antivirals t

197 Acyclovir ProTides retained activity against acyclovir-r

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

199 We developed acyclovir ProTides, monophosphorylated acyclovir with th

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

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

202 Acyclovir reduces the incidence of GUD but does not prev

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

204 sceral infection (9.8% vs. 2.2%; P=.001) and acyclovir resistance (5.8% vs. 1.8%; P=.03) were more co

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

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

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

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

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

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

211 Many acyclovir-resistant herpes simplex virus isolates from p

212 Many acyclovir-resistant herpes simplex virus mutants from cl

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

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

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

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

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

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

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

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

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

222 Most acyclovir-resistant isolates have mutations in the thymi

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

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

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

226 The acyclovir-resistant isolates were transient, because acy

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

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

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

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

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

232 Acyclovir-sensitive and acyclovir-resistant isolates wer

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

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

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

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

237 In vitro acyclovir sensitivity testing was performed using the dy

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

239 Acyclovir significantly reduced both GUD and HSV-2 shedd

240 Acyclovir significantly reduced VZV infections at 1 year

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

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

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

244 We evaluated whether acyclovir suppression during human immunodeficiency viru

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

246 Acyclovir suppressive therapy (400 mg twice daily) reduc

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

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

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

250 (10:1) were 10 times more potent against all acyclovir-susceptible HSV-1 strains.

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

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

253 Daily acyclovir therapy did not reduce the risk of transmissio

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

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

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

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

258 around times and the duration of unnecessary acyclovir therapy.

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

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

261 Addition of acyclovir to syndromic management will improve healing o

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

263 reated, non-ISS oligonucleotide-treated, and acyclovir-treated animals also were monitored.

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

265 Acyclovir treatment in patients coinfected with HSV and

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

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

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

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

270 (10 s(-1)) afford efficient incorporation of acyclovir triphosphate by the Pol-UL42 enzyme.

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

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

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

274 Cytotoxicity of VVACV in comparison with val-acyclovir (VACV), ACV, and TFT was evaluated in cellular

275 h the intention of extending the benefits of acyclovir, valacyclovir is now being explored in a numbe

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

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

278 Controlled trials suggest that acyclovir/valacyclovir can provide significant clinical

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 ng, and after HSV suppression with high-dose acyclovir was measured to determine whether HSV suppress

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

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 -1 and HSV-2 disease and more effective than acyclovir when the treatment frequency per day was reduc

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

295 Acyclovir, which prevents lytic viral replication but no

296 %) with rejected specimens were treated with acyclovir, which suggests a low clinical concern for HSV

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

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

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

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