ライフサイエンスコーパス: minus-strand

1 and with C-to-T editing of the proviral DNA minus strand.

2 osphorylated P23/nsP3 and reduced amounts of minus strands.

3 icted to be more stable on plus strands than minus strands.

4 sP3 and lost selectively the ability to make minus strands.

5 ished that HCV dsRNA contained genome-length minus strands.

6 The West Nile virus minus-strand 3' terminal stem loop (SL) RNA was previous

7 of APOBEC3F and -3G dictates the retroviral minus strand 5'-TC and 5'-CC dinucleotide hypermutation

8 The minus strand and ambisense segmented RNA viruses include

9 rus (MHV) RNA at the 3' end of both plus and minus strands and modulate MHV RNA synthesis.

10 like all organisms, involves synthesis of a minus-strand and a plus-strand of nucleic acid.

11 on reversibly affected an early step in both minus-strand and plus-strand RNA synthesis, although inh

12 ts and variants of the promoter template for minus-strand and subgenomic RNA initiation, we found tha

13 At this point, the 3' end of the minus strand becomes the template via the second templat

14 , an RC DNA species with a covalently closed minus strand but an open plus strand (closed minus-stran

15 hesis by SIN2V produced 250% of wt levels of minus strands but accumulated only 110% of wt levels (0.

16 312 to Ser) made phosphorylated P23/nsP3 and minus strands but failed to increase plus-strand synthes

17 e that H5 functions to suppress synthesis of minus strands by sequestering the 3' terminus from the R

18 cells by deaminating dC to dU in the first (minus)-strand cDNA replication intermediate.

19 ing C-->U, with 3'-->5' polarity, on nascent minus-strand cDNA.

20 f the plus strand in RC DNA, suggesting that minus-strand closing can occur before plus-strand proces

21 hairpin overlapping the 5' end of DR1 in the minus strand contributes to the regulation of primer tra

22 estering a host-coded tRNA for initiation of minus (-) strand DNA synthesis is central to the reverse

23 rimer-binding site controlling initiation of minus strand DNA synthesis in retroviruses and retrotran

24 APOBEC3G deaminates deoxycytidines in minus strand DNA to deoxyuridines, resulting in G to A h

25 in situ priming by making the 3' end of the minus-strand DNA a poor template for initiation.

26 A cytidine deaminase that targets retroviral minus-strand DNA and has potent antiviral activity again

27 ide which represents the 5' end of the viral minus-strand DNA and is covalently attached to the RT.

28 to copy through the DNA-RNA junction of the minus-strand DNA and the tRNA because of its bent confor

29 he cis-acting sequences for the synthesis of minus-strand DNA are present near the 5' and 3' ends of

30 ntial decrease in the accumulation of longer minus-strand DNA by A3G, compared to the shorter minus-s

31 example, mutations within the 3' end of the minus-strand DNA can lead to increased levels of in situ

32 echanism involves deaminating dC residues in minus-strand DNA during reverse transcription, resulting

33 equences that contribute to the synthesis of minus-strand DNA for human hepatitis B virus (HBV).

34 redundancy (5'r and 3'r) on the ends of the minus-strand DNA has been shown to be important, but not

35 hepadnaviruses is important for synthesis of minus-strand DNA in both DHBV and HHBV but not in HBV.

36 The 3' end of the minus-strand DNA makes important contributions to both o

37 otein covalently linked to the 5' end of the minus-strand DNA occurs inside the capsid in the cytopla

38 Synthesis of minus-strand DNA of human hepatitis B virus (HBV) can be

39 as been shown to form near the 3' end of the minus-strand DNA overlapping the direct repeat 1 in avih

40 the recombination events taking place during minus-strand DNA synthesis and plus-strand DNA synthesis

41 ploidy and preferential recombination during minus-strand DNA synthesis are discussed.

42 al and that most recombinations occur during minus-strand DNA synthesis catalyzed by viral reverse tr

43 riptase inhibitors influence the kinetics of minus-strand DNA synthesis differently, providing insigh

44 or the first time the ex vivo rates of HIV-1 minus-strand DNA synthesis in 293T and human primary CD4

45 iring between phi and epsilon contributes to minus-strand DNA synthesis is not known, but a simple sp

46 identified a cis-acting element involved in minus-strand DNA synthesis that lies within a 27-nucleot

47 The efficiency of minus-strand DNA synthesis was defined as the amount of

48 nditions in which little or no inhibition of minus-strand DNA synthesis was observed.

49 During and after minus-strand DNA synthesis, human immunodeficiency virus

50 During minus-strand DNA synthesis, RNase H degrades viral RNA s

51 At the completion of minus-strand DNA synthesis, the final RNase H cleavage g

52 At the completion of minus-strand DNA synthesis, the final RNase H cleavage g

53 Although much is known about minus-strand DNA synthesis, the mechanism(s) by which th

54 5' half of epsilon contributes to efficient minus-strand DNA synthesis.

55 degradation of genomic RNA fragments during minus-strand DNA synthesis.

56 hesis and to remove the tRNA primer used for minus-strand DNA synthesis.

57 sure encapsidated pregenomic RNA (pgRNA) and minus-strand DNA synthesized in cell culture.

58 d DNA synthesis was defined as the amount of minus-strand DNA synthesized per encapsidation event.

59 hout an appreciable decrease in the level of minus-strand DNA synthesized, indicating that most of th

60 ynthesis at one of two distinct sites on the minus-strand DNA template, resulting in two different en

61 Most variants of DHBV synthesized minus-strand DNA to 50 to 100% of the wild-type (WT) lev

62 For HHBV, most variants synthesized minus-strand DNA to less than 50% the WT level.

63 nd of the plus strand from the 5' end of the minus-strand DNA to the 3' end, where further elongation

64 e nascent plus strand from the 5' end of the minus-strand DNA to the 3' end, where further elongation

65 ation as a result of cytidine deamination of minus-strand DNA transcripts.

66 We also determined the rates of minus-strand DNA transfer ( approximately 4 min), plus-s

67 These data demonstrate that minus-strand DNA transfer is homology driven and a minim

68 The molecular nature of minus-strand DNA transfer was characterized in 63 provir

69 of the homology lengths on the efficiency of minus-strand DNA transfer.

70 define the effects of R homology lengths on minus-strand DNA transfer.

71 ength is required for accurate and efficient minus-strand DNA transfer.

72 2 (DR2) located near the opposite end of the minus-strand DNA, a process called primer translocation.

73 s-strand DNA by A3G, compared to the shorter minus-strand DNA, and suggest that A3G exerts its inhibi

74 e transcribed by the viral polymerase into a minus-strand DNA, followed by synthesis of the plus-stra

75 erences in their mechanisms for synthesizing minus-strand DNA, more so than for other steps in replic

76 ar the 5' end, the middle, and the 3' end of minus-strand DNA, respectively.

77 of deaminating cytosines to uracils on viral minus-strand DNA, resulting in disruption of the viral l

78 least partly by C-to-U deamination of viral minus-strand DNA, resulting in G-to-A hypermutation.

79 e to deoxyuridine in newly synthesized viral minus-strand DNA, thereby inducing G-to-A hypermutation.

80 esis, the template switch, and elongation of minus-strand DNA.

81 eotides that is 100 nucleotides 3' of DR2 on minus-strand DNA.

82 r sequences are at, or near, the ends of the minus-strand DNA.

83 DHBV does not contribute to the synthesis of minus-strand DNA.

84 ptor site (DR2) near the opposite end of the minus-strand DNA.

85 padnaviruses that contribute to synthesis of minus-strand DNA.

86 d from DR2 are extended to the 5' end of the minus-strand DNA.

87 e, phi, that contributes to the synthesis of minus-strand DNA.

88 mic RNA (pgRNA) involved in the synthesis of minus-strand DNA.

89 mega) are necessary for the synthesis of HBV minus-strand DNA.

90 s with phi to contribute to the synthesis of minus-strand DNA.

91 lon and phi, contributes to the synthesis of minus-strand DNA.

92 sequence called DR1 during the synthesis of minus-strand DNA.

93 scontiguous portions of viral or host RNA or minus-strand DNA.

94 switch and/or the initiation of synthesis of minus-strand DNA.

95 he polymerase and the 5' phosphoryl group of minus-strand DNA.

96 ated that the result of C to U conversion in minus-stranded DNA of human immunodeficiency virus type

97 and transcribe asymmetric levels of plus and minus strands during replication of plus-sense RNA virus

98 and transcribe asymmetric levels of plus and minus strands during RNA replication.

99 1 His374 and wild-type nsP4 Arg183 made more minus strands during the early period of infection and b

100 if1-hairpin (M1H), a replication enhancer on minus strands, forms a plus-strand hairpin flanked by CA

101 evidence of template strand switching, from minus-strand genome DNA to palindromic strand DNA, durin

102 site on the accumulation of BMV RNA3 genomic minus-strand, genomic plus-strand, and subgenomic RNAs i

103 satRNA of Cucumber mosaic virus is caused by minus-strand induction of the programmed cell death path

104 we found that a specificity determinant for minus-strand initiation could function at variable dista

105 silencer element (RSE), and the 3'-terminal minus-strand initiation promoter (gPR).

106 h of which are similar to the hairpin of the minus-strand initiation promoter, can function as a prom

107 the viral RNA comprising part of the minimal minus-strand initiation promoter.

108 3'CCA of the tRNA-like sequence (TLS) affect minus-strand initiation unless repaired.

109 re abundant plus-strand RNA progeny than the minus-strand intermediate, a hallmark of replication of

110 First, the minus strand is synthesized by the viral replicase compl

111 nstructs expressing RNA1 and RNA2 suppressed minus-strand levels but increased plus-strand RNA accumu

112 olymerases was unaffected when corrected for minus-strand numbers, although 26S mRNA synthesis was en

113 nd with the transcription start sites on the minus strand of another distinct group of genes; togethe

114 rimer extension assay maps the 5' end of the minus strand of DP-rcDNA at the authentic end of virion

115 aminate deoxycytidine to deoxyuridine on the minus strand of nascent reverse transcripts.

116 equal proportions on the plus strand and the minus strand of the host genome.

117 ual transcripts are derived from the plus or minus strands of chromosomes.

118 m the 3'-terminal sequences of both plus and minus strands of the HCV RNA genome.

119 duct, likely by premature termination at the minus-strand oligo(U) tract.

120 rnal promotion from the full-length template minus strand or by transcription from the minus-stranded

121 e contributes to the efficient initiation of minus strands or the formation of its replicase and that

122 Their minus-strand origin is disrupted by a large cassette tha

123 ad a complex rearrangement that restored the minus-strand origin while retaining tetracycline resista

124 s, one with a contaminant having a wild-type minus-strand origin.

125 d by assembling oligonucleotides of plus and minus strand polarity.

126 of nsP4 for the formation or activity of the minus-strand polymerase.

127 transcription because of the position of the minus strand primer downstream of the LTR.

128 RNase H cleavages that remove the plus- and minus-strand primers; these ends can be joined to form t

129 optimal structure of the 3' component of the minus-strand promoter is the wild-type 3' CSE followed a

130 like other satellite RNAs, both the plus and minus strands proved to be equally infectious.

131 r the observed approximately 6:1 plus-strand/minus-strand ratio in vesicular-membrane structures, and

132 ed the copy number of TMEV genomes, plus- to minus-strand ratios, and full-length species in the spin

133 minus strand but an open plus strand (closed minus-strand RC DNA [cM-RC DNA]) was detected by this ap

134 the nsP4 Arg183 residue itself is needed for minus-strand replicase assembly or function in the mosqu

135 in P123 or P23 components of the short-lived minus-strand replicase, and upon polyprotein cleavage, m

136 a hairpin ribozyme (Rz3'X) targeting the HCV minus-strand replication intermediate at position 40 wit

137 old-more plus-stranded progeny RNAs than the minus-stranded replication intermediate.

138 emplate specificity, since a mutated repRNA, minus-stranded repRNA, or a heterologous viral RNA could

139 tes deoxycytidine to deoxyuridine on nascent minus-strand retroviral cDNA, leading to hyper-deoxyguan

140 ncapsidated cellular protein that deaminates minus-strand reverse transcript cytosines to uracils.

141 originates as a replication intermediate of minus-strand ribozyme replication and thus contains all

142 y simple process that involves complementary minus-strand RNA [(-)RNA] synthesis and subsequent (+)RN

143 these predicted structures were required for minus-strand RNA accumulation, including a conserved hex

144 nts throughout the 3' NTR were important for minus-strand RNA accumulation.

145 nt for plus-strand RNA accumulation than for minus-strand RNA accumulation.

146 is transferred to the 3' end of plus- and/or minus-strand RNA and serves as primer for production of

147 +5, and +7 template nucleotides accumulated minus-strand RNA at levels similar to the the wild-type

148 -UA-5' is required at the 3' terminus of the minus-strand RNA for initiation of plus-strand genomic R

149 ntaining precursor at the 3' end of plus- or minus-strand RNA for production of full-length RNA.

150 irectly interact with the 3' terminus of the minus-strand RNA for the initiation of the plus-strand g

151 (ii) the observed 10:1 asymmetry of plus- to minus-strand RNA levels can be explained by a higher-aff

152 ped with other sequence required for optimal minus-strand RNA levels.

153 se-containing replication complexes with HCV minus-strand RNA over HCV plus-strand RNA in order to in

154 ine genome stability, translation, plus- and minus-strand RNA replication, and scaffolding of viral r

155 ition of the minimal promoters for plus- and minus-strand RNA syntheses.

156 dings of this study with regard to efficient minus-strand RNA synthesis are the following: (i) the wi

157 es of PV RNA are essential for initiation of minus-strand RNA synthesis at its 3' end.

158 A portion of the promoter for BMV minus-strand RNA synthesis could substitute for the subg

159 assumed to constitute the core promoter for minus-strand RNA synthesis during genome replication; ho

160 Among these, nsp10 plays a critical role in minus-strand RNA synthesis in a related coronavirus, mur

161 of eEF1A binding to the 3' SL RNA increased minus-strand RNA synthesis in transfected cells, which r

162 inding to the 3' SL RNA also decreased viral minus-strand RNA synthesis in transfected cells.

163 Minus-strand RNA synthesis in vitro requires a structure

164 nucleotides of the 3' CSE severely inhibits minus-strand RNA synthesis, (iv) templates possessing no

165 re-sensitive mutants showed reduction in the minus-strand RNA synthesis, a function that has not yet

166 ntained the tRNA-like structures that direct minus-strand RNA synthesis, three were within the 3' reg

167 ch model states that AMV coat protein blocks minus-strand RNA synthesis, while another report states

168 protein is not, by definition, inhibitory to minus-strand RNA synthesis.

169 role of these elements in the initiation of minus-strand RNA synthesis.

170 cts plus-strand RNA accumulation rather than minus-strand RNA synthesis.

171 U nucleotides in comparison to templates for minus-strand RNA synthesis.

172 irus type 14 (HRV-14) is essential for viral minus-strand RNA synthesis.

173 binding the viral polymerase NS5 to initiate minus-strand RNA synthesis.

174 that contains the core promoter for genomic minus-strand RNA synthesis.

175 nome and its complement in the 3' end of the minus-strand RNA synthesized during virus replication se

176 sis, three were within the 3' region of each minus-strand RNA that contained the core promoter for ge

177 In addition, no minus-strand RNA was produced from the EMCV chimeric tem

178 ing region), the amount of replicon-specific minus-strand RNA was uniform; however, the accumulation

179 tion of SL3 was required for accumulation of minus-strand RNA, whereas SL1 and SL2 formation were les

180 gpU, VPgpUpU, and VPg-poly(U), the 5' end of minus-strand RNA.

181 he presence of a replication enhancer on the minus-stranded RNA of tombusviruses.

182 eplicase, and (iv) the ratio of plus- versus minus-stranded RNA replication products.

183 in the BMV replicase in vitro reaction, the minus-strand RNA3 template generated the sgRNA3a product

184 acity to bind to the 3'-ends of HCV plus and minus strand RNAs.

185 in complex with the 5' consensus sequence of minus-strand rotavirus RNA.

186 able of de novo initiation on both plus- and minus-strand satC and satD templates, which are small pa

187 We propose that minus strand segmented viruses replicating in the cytopl

188 en reading frames, which produced additional minus-strand sgRNAs corresponding to the 3'-terminal mRN

189 te minus strand or by transcription from the minus-stranded sgRNAs.

190 bound specifically to the West Nile virus 3' minus-strand stem-loop [WNV3'(-)SL] RNA (37) and colocal

191 Retrovirus minus strand strong stop transfer (minus strand transfer

192 Minus strand strong stop transfer is obligatory for comp

193 Quantitative real-time PCRs for minus-strand strong stop DNA and complete viral cDNA syn

194 MAD-4 for 1 h prior to infection reduced HIV minus-strand strong stop DNA and HIV cDNA by 4- to 20-fo

195 resulted in a threefold increase in both HIV minus-strand strong stop DNA and HIV cDNA over the first

196 had little or no effect on the formation of minus-strand strong-stop cDNA but caused a significant r

197 t regions at the 3'-ends of acceptor RNA and minus-strand strong-stop DNA ((-) SSDNA).

198 DNA") at the 3'-end of the newly synthesized minus-strand strong-stop DNA ((-) SSDNA).

199 strates derived from the 3' end of the HIV-1 minus-strand strong-stop DNA (-sssDNA).

200 verse transcription in infected cells and no minus-strand strong-stop DNA is detected.

201 that remained annealed to the 3' end of the minus-strand strong-stop DNA only if NC was present in t

202 Moreover, minus-strand strong-stop DNA rapidly accumulated in the

203 e tested in vitro for exogenous RT activity, minus-strand strong-stop DNA synthesis in endogenous RT

204 late minus-strand transfer, it did stimulate minus-strand strong-stop DNA synthesis.

205 the complementary "TAR DNA" generated during minus-strand strong-stop DNA synthesis.

206 RNA to the complementary region (TAR DNA) in minus-strand strong-stop DNA.

207 ry sequence located in the newly synthesized minus-strand strong-stop DNA.

208 showed that all three were able to form the minus-strand strong-stop DNA.

209 substrates derived from the 3' end of HIV-1 minus-strand strong-stop DNA.

210 e to the complementary sequence (TAR DNA) in minus-strand strong-stop DNA.

211 erse transcription prior to the formation of minus-strand strong-stop products.

212 entered target ED cells and produced early (minus-strand strong-stop) and late (Gag) viral DNA produ

213 duced amounts of early intermediates such as minus-strand, strong-stop DNA.

214 egration site sequences into plus-strand and minus-strand subpopulations, and use this to identify th

215 utants can promote template switching during minus strand synthesis more efficiently than WT HIV-1 RT

216 ansfer is obligatory for completion of HIV-1 minus strand synthesis.

217 T) cleaves the viral genome concomitant with minus strand synthesis.

218 nts, revealed that this interaction inhibits minus-strand synthesis 7-fold.

219 Minus-strand synthesis and incorporation of [3H]uridine

220 t nsP2, all showed a phenotype of continuous minus-strand synthesis and of unstable, mature replicati

221 hese results implicate nsP2 in regulation of minus-strand synthesis and suggest that different region

222 s of this function leads to continuous viral minus-strand synthesis and the production of unstable RC

223 at it may also act with the host to regulate minus-strand synthesis and the stability of the RTC.

224 t a single point mutation in nsP1 results in minus-strand synthesis at greater than wild-type levels

225 Q or mutations to independence do not modify minus-strand synthesis behavior.

226 Minus-strand synthesis by PI cells appeared normal; it w

227 Continuous minus-strand synthesis by SIN2V produced 250% of wt leve

228 l degradation of the retroviral genome after minus-strand synthesis can occur through sequence-specif

229 ing the early period of infection and before minus-strand synthesis ceased at about 4 h postinfection

230 Mutations in the template for minus-strand synthesis had only modest effects on BMV re

231 Minus-strand synthesis has restrictions that are differe

232 ggesting a general mechanism for controlling minus-strand synthesis in the genus.

233 Our recent study found minus-strand synthesis to be temperature sensitive in ve

234 Inhibiting translation caused minus-strand synthesis to stop and a loss of transcripti

235 The failure by the PI replicons to shut off minus-strand synthesis was not due to some defect in the

236 s) growth phenotype caused by a ts defect in minus-strand synthesis whose extent varied with the part

237 Instead of using a tRNA, Tf1 primes minus-strand synthesis with an 11-nucleotide RNA removed

238 10))VAV, had defects in subgenome synthesis, minus-strand synthesis, and overall levels of viral RNA

239 cis-acting sequences involved in minus-strand synthesis, including promoters, enhancers,

240 cells with wt SFV triggered the shutdown of minus-strand synthesis, which we believe is a host respo

241 crinkle virus (TCV) regulates initiation of minus-strand synthesis.

242 and synthesis was more profound than that of minus-strand synthesis.

243 present in an inoculum is required to permit minus-strand synthesis.

244 ovided insights into the pioneering round of minus-strand synthesis.

245 the template that is used for initiation of minus-strand synthesis.

246 ossibly involved in controlling the level of minus-strand synthesis.

247 sphorylation of nsP3 correlated with reduced minus-strand synthesis.

248 uble-stranded RNA in cessation of alphavirus minus-strand synthesis.

249 itution suppressed the nsP4 Ser183 defect in minus-strand synthesis.

250 P4 N-terminal mutants were defective also in minus-strand synthesis.

251 en eEF1A and the WNV 3' SL facilitates viral minus-strand synthesis.

252 identified change, N374 to H, suppressed the minus-strand synthetic defect.

253 k hepatitis B virus capsids, the ends of the minus-strand template are juxtaposed via base pairing to

254 ommon theme of switching from one end of the minus-strand template to the other end.

255 n by base pairing with each other within the minus-strand template.

256 he site of its generation, the 3' end of the minus-strand template.

257 mmetric amplification of genome RNA from the minus-strand template.

258 cient MEF, there was continuous synthesis of minus-strand templates and the formation of new replicat

259 (RdRp) preparation, we demonstrate that the minus-strand templates of tombusviruses contain a replic

260 vity was lost without the degradation of the minus-strand templates.

261 ate cRNA synthesis de novo on both plus- and minus-stranded templates, (ii). to generate replicase pr

262 vides unpaired 3'-UA-5' at the 3' end of the minus strand that can be utilized by the mutant polymera

263 V-infected cells accumulated only 40% of the minus strands that were made, cells must possess some pr

264 Unlike wild-type (wt) SIN, it caused minus strands to be made continuously and replication-tr

265 The minus strand transfer mechanism in human immunodeficienc

266 We previously proposed that HIV-1 minus strand transfer occurs by an acceptor invasion-ini

267 virus-1, which contains a 97-nt R sequence, minus strand transfer occurs through an acceptor invasio

268 in vitro were designed to test mechanisms of minus strand transfer of human immunodeficiency virus 1

269 or acceptor invasion initiation site using a minus strand transfer system in vitro, containing the 97

270 sm of human immunodeficiency virus 1 (HIV-1) minus strand transfer was examined using a genomic RNA s

271 Human immunodeficiency virus type 1 minus strand transfer was measured using a genomic donor

272 etrovirus minus strand strong stop transfer (minus strand transfer) requires reverse transcriptase-as

273 an acceptor invasion-initiated mechanism for minus strand transfer.

274 nate regions of homology was observed during minus strand transfer.

275 applied successively by HIV-1 for efficient minus strand transfer.

276 ity in an assay that measures stimulation of minus-strand transfer and inhibition of nonspecific self

277 d acceptor RNA constructs were used to assay minus-strand transfer and self-priming in vitro.

278 is reaction mimics the annealing step of the minus-strand transfer process in reverse transcription.

279 stability, is a critical determinant for the minus-strand transfer step (annealing of acceptor RNA to

280 nucleic acid rearrangements that precede the minus-strand transfer step in reverse transcription.

281 The minus-strand transfer step of HIV-1 reverse transcriptio

282 In the minus-strand transfer step of HIV-1 reverse transcriptio

283 vity of the nucleocapsid protein (NC) in the minus-strand transfer step of HIV-1 reverse transcriptio

284 ase-pair duplex, is an essential step in the minus-strand transfer step of reverse transcription.

285 TAR DNA hairpin is an essential step in the minus-strand transfer step of reverse transcription.

286 ay roles in Ty1 reverse transcription at the minus-strand transfer step.

287 In an in vitro minus-strand transfer system consisting of a (-) SSDNA m

288 s demonstrate that for efficient NC-mediated minus-strand transfer, a delicate thermodynamic balance

289 by the nucleocapsid protein (NC), including minus-strand transfer, in which the DNA transactivation

290 wed that although the drug did not stimulate minus-strand transfer, it did stimulate minus-strand str

291 During human immunodeficiency virus type 1 minus-strand transfer, the nucleocapsid protein (NC) fac

292 In minus-strand transfer, the transactivation response regi

293 ming, a dead-end reaction that competes with minus-strand transfer.

294 C in its role as a nucleic acid chaperone in minus-strand transfer.

295 s reduced; there was also a strong effect on minus-strand transfer.

296 e mechanism of NC-dependent and -independent minus-strand transfer.

297 s G to A hypermutations in newly synthesized minus strand viral cDNA at the step of reverse transcrip

298 ly resulting from C-to-U modification during minus-strand viral DNA synthesis.

299 lly induce deaminations toward the 5' end of minus-strand viral DNA, presumably because of the sequen

300 s exist in a "melted" configuration, and the minus-strand viral genome and a palindromic strand are a

301 he cytosine (C) to uracil (U) conversions in minus-stranded viral DNA.