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1                                              HGV clearance occurs after many acute infections but unc
2                                              HGV did not worsen the course of concurrent HCV infectio
3                                              HGV had little impact on alanine aminotransferase, aspar
4                                              HGV infection appears to be extremely common in these pa
5                                              HGV infection does not appear to have a role in mixed cr
6                                              HGV infection is not associated with hepatic inflammatio
7                                              HGV infection was present before transplantation in 13%
8                                              HGV RNA and anti-E2 were mutually exclusive except in 9
9                                              HGV RNA is not causally related to non-A-E fulminant hep
10                                              HGV RNA levels are suppressed by IFN but not by zidovudi
11                                              HGV RNA levels were measured by branched DNA signal ampl
12                                              HGV RNA levels were not correlated with the severity of
13                                              HGV RNA was also measured before and after liver transpl
14                                              HGV RNA was detected at the most recent visit in 38 (15.
15                                              HGV RNA was detected by polymerase chain reaction (PCR)
16                                              HGV RNA was detected by reverse transcription polymerase
17                                              HGV RNA was detected in 30 (17.3%) plasma units, 2 of wh
18                                              HGV RNA was detected in 4 of 45 patients with a diagnosi
19                                              HGV RNA was detected in 9 (31%) of 29 short-term IDUs, a
20                                              HGV RNA was measured using a research-based branched DNA
21                                              HGV RNA was present in 1 of 28 patients with non-A-E hep
22                                              HGV RNA-positive patients (HGV-infected and HGV-hepatiti
23                                              HGV was associated with acute and chronic hepatitis.
24                                              HGV was common in a group of volunteer blood donors, and
25                                              HGV was detected by reverse transcriptase-polymerase cha
26                                              HGV was detected in 29 of 60 (48%) patients.
27                                              HGV was present in serum of 14 of the 36 patients (38.8%
28                                              HGV-positive IDUs were younger and had fewer years of dr
29                                              HGV-RNA was absent from all 20 liver specimens, includin
30                                           3) HGV RNA becomes undetectable in about one third of recip
31                                There were 35 HGV infections among the 357 transfusion recipients; onl
32                                        All 6 HGV-infected patients were negative for the presence of
33  Compared with HGV-negative patients, the 60 HGV-positive patients (46%), including 22 who were posit
34                                For 31 (82%), HGV RNA was also found at all prior visits occurring a m
35  of 29 short-term IDUs, and 5 (56%) of the 9 HGV infections cleared.
36 s in which a transfusion recipient had acute HGV infection after transfusion and samples from all don
37 d; of the remaining 13 patients, 3 had acute HGV infection, and 10 were infected with unidentified ag
38                                     Although HGV coinfection is frequent in patients with end-stage H
39                                     Although HGV RNA was demonstrable in the majority (67%) of patien
40                                     Although HGV RNA was significantly associated with hepatitis C, p
41  serum levels of liver-related enzymes among HGV RNA-positive and -negative participants (P > .20).
42 as developed to detect covariant sites among HGV/GBV-C sequences of different genotypes.
43 ervations indicate that a larger study of an HGV population is required to more clearly define the re
44 ; the levels of alanine aminotransferase and HGV RNA were not well correlated.
45 percent) and those with both hepatitis C and HGV infection (61 percent).
46 7 percent of those with both hepatitis C and HGV infection.
47 eron response was similar in both groups and HGV was not associated with outcome following therapy.
48 ers from the 5' non-coding region of HCV and HGV by a nested polymerase chain reaction (PCR).
49 arly define the relationship between HCV and HGV coinfection and their response to antiviral therapy.
50                         The combined HCV and HGV infections were no more severe than HCV infections a
51                                Serum HCV and HGV RNA were detected by reverse transcription-polymeras
52        Serum samples were tested for HCV and HGV RNA; HCV RNA was quantitated by branched DNA assay,
53                  In coinfected sera, HCV and HGV were quantitated by competitive RT-PCR assays.
54  HGV RNA-positive patients (HGV-infected and HGV-hepatitis C virus [HCV]-coinfected) developed light-
55 rvival were similar between HGV-positive and HGV-negative patients.
56 in human populations, and homologues such as HGV/GBV-CCPZ and GBV-A are found in a variety of differe
57 nths, only 5% treated with zidovudine became HGV RNA negative, compared with 95% who received IFN-alp
58 ins the reported lack of association between HGV infection and liver pathology encountered in many cl
59                       No association between HGV RNA positivity and HCC risk was observed in either H
60                   No causal relation between HGV and hepatitis has been established.
61 tment clinical features were similar between HGV RNA-positive and -negative patients.
62 ient and graft survival were similar between HGV-positive and HGV-negative patients.
63                                         Both HGV-positive and -negative groups had similar survival,
64 ted using branched DNA (bDNA) assay for both HGV and HCV in the liver explants and pretransplant seru
65 ially reduced or eliminated contamination by HGV RNA sequences.
66  donors, and 230 donors of blood received by HGV-infected patients were tested for HGV RNA by qualita
67 te counts, and 12-year AIDS-free survival by HGV positivity (viremia [RNA] or anti-E2 antibodies).
68 sociated with hepatitis in humans, and GBV-C/HGV coinfection is common in patients chronically infect
69                                        GBV-C/HGV infection also had no significant impact on the post
70    To determine the clinical impact of GBV-C/HGV infection in such patients and the effect of interfe
71                       We conclude that GBV-C/HGV infection is very common in LT recipients, but that
72                                        GBV-C/HGV infection was not related to the number of blood pro
73 namese were tested for the presence of GBV-C/HGV RNA by the reverse transcription polymerase chain re
74 n-alpha and ribavirin therapy on serum GBV-C/HGV RNA levels, GBV-C/HGV RNA was detected and quantitat
75                                        GBV-C/HGV RNA was commonly detected in post-LT patients compar
76 therapy on serum GBV-C/HGV RNA levels, GBV-C/HGV RNA was detected and quantitated in serum samples fr
77 t usually transient reduction in serum GBV-C/HGV RNA, and ribavirin had, at most, a modest antiviral
78 y: 10 patients were positive for serum GBV-C/HGV RNA.
79 lence of GB virus-C/hepatitis G virus (GBV-C/HGV) infection in liver transplant recipients transplant
80          GB virus C/hepatitis G virus (GBV-C/HGV) is a newly described virus associated with hepatiti
81       GB virus C or hepatitis G virus (GBV-C/HGV), a novel Flavivirus, is detected in 1.5% of US bloo
82 stologic features of the patients with GBV-C/HGV-HCV coinfection compared with those with HCV infecti
83                              To characterize HGV particle types, we evaluated plasma from chronically
84                                  Chronically HGV-infected individuals contained antibody to the HGV c
85              Plasma samples from chronically HGV-infected individuals and controls were assessed by a
86 regions of the United States had circulating HGV RNA.
87  We investigated the presence of circulating HGV in 36 patients with well-documented non-A-E fulminan
88 d immunoassay to determine if they contained HGV antibody specific for a conserved region in the codi
89                                 First, could HGV coinfection play any role in the response of HCV to
90                Patients with past or current HGV infection have higher CD4+ lymphocyte counts and bet
91  assay for HGV-RNA, we were unable to detect HGV-RNA within the livers of patients with cryptogenic c
92 t one third of recipients who had detectable HGV RNA in the first month after OLT.
93 ed blood donors (1.4 percent) had detectable HGV RNA.
94  was found to be most efficient in detecting HGV and was subsequently used to test 162 HCV-positive a
95 tion and its association with liver disease, HGV RNA was assessed in the most recent serum sample for
96        Among non-renumerated UK blood donors HGV infection (detected by PCR) was more common than HCV
97 d and shared common parenteral risk factors; HGV did not appear to cause hepatitis or to worsen the c
98 nd a commercially available RT-PCR assay for HGV or GBV-C gave concordant results for 96% of the pati
99 cription-polymerase chain reaction assay for HGV-RNA, we were unable to detect HGV-RNA within the liv
100 s drug abuse was the leading risk factor for HGV transmission, followed by blood transfusion, snortin
101 ards models, risk for AIDS was 40% lower for HGV-positive patients independent of age, HIV and HCV vi
102 opism, but this pattern was not observed for HGV.
103 ted concentrates, 13 (14%) were positive for HGV compared with 79 (83%) who were positive for HCV.
104 these 25 positive patients were positive for HGV or GBV-C by the commercial RT-PCR assay.
105 t significantly different) were positive for HGV RNA in serum.
106 ut 75 percent were persistently positive for HGV RNA, as were 87 percent of those with both hepatitis
107 one of 6 patients with EMC were positive for HGV RNA, for an overall prevalence of 3.0% in mixed cryo
108 ts (46%), including 22 who were positive for HGV RNA, had higher CD4+ lymphocyte counts (difference,
109 of the control populations were positive for HGV.
110 erum samples were recoded and reanalyzed for HGV RNA using different primer sets to assess the validi
111                                Retesting for HGV RNA with different primers was positive in all but 1
112 iver is not the primary replication site for HGV, at least in a significant proportion of patients.
113 iver is not the primary replication site for HGV, at least in the population of HCV/HGV-coinfected pa
114  of hepatitis G virus (HGV), were tested for HGV or GB virus C (GBV-C) RNA.
115 rom 96 hemodialysis patients were tested for HGV or GBV-C RNA, 25 patients (26%) were positive by the
116 ved by HGV-infected patients were tested for HGV RNA by qualitative and quantitative polymerase-chain
117 d after liver transplantation was tested for HGV RNA by reverse transcriptase (RT)-PCR using primers
118                Serum samples were tested for HGV RNA by the polymerase chain reaction.
119 NA was significantly higher for HCV than for HGV (median 129 and 0.3 respectively, P < .01).
120 iver were consistently higher than those for HGV RNA (median 1.13 x 10(8) and 360,000 Eq/g respective
121 hosis by analyzing archival liver tissue for HGV-RNA in patients undergoing orthotopic liver transpla
122 IDUs) and in prior specimens for those found HGV RNA-positive.
123             The significance of hepatitis G (HGV) infection in liver transplant recipients is not kno
124 etected up to a 9% incidence of hepatitis G (HGV)-RNA in patients with acute and chronic liver diseas
125  There was no difference between the groups (HGV+ vs. HGV-) when baseline alanine aminotransferase (A
126                      Initially, 66 (37%) had HGV RNA.
127 ailable in the first postoperative month had HGV infection.
128                              Similar to HCV, HGV particles included an extremely-low-density virion p
129 ed with hepatitis C, patients with mixed HCV-HGV infections did not demonstrate a more severe course
130 e for HGV, at least in the population of HCV/HGV-coinfected patients.
131 ples from 30 transplant recipients: Group I, HGV/HCV coinfection (n = 10); group II, HCV infection al
132 II, HCV infection alone, (n = 8); group III, HGV alone (n = 12).
133 m this surveillance study does not implicate HGV as an etiologic agent of non-A-E hepatitis.
134 e two groups (38% in HGV-positive and 22% in HGV-negative patients).
135 ficantly different in the two groups (38% in HGV-positive and 22% in HGV-negative patients).
136                                   Changes in HGV-RNA levels were evaluated before, during, and after
137       There was no significant difference in HGV positivity between patients treated before the intro
138                   There was no difference in HGV positivity rates between those with normal AST level
139 al therapy appeared to induce a reduction in HGV-RNA load in five of nine patients coinfected with HC
140        Although hepatitis G virus infection (HGV) is usually asymptomatic, it has been associated wit
141 in 9 donors (1.5%); 8 of 9 subsequently lost HGV RNA but anti-E2 persisted.
142                                         Mean HGV RNA levels were 9.8 (+/-4.2) (viral molecular equiva
143 ipients persistently infected with HGV, mean HGV RNA titers increase after OLT.
144 c recipients who continue to have measurable HGV RNA, three have unexplained hepatitis histologically
145 following liver transplantation, we measured HGV RNA by polymerase chain reaction in pre and posttran
146 detectable in the first postoperative month, HGV RNA fell to undetectable levels at the most recent f
147                                         Most HGV infections were not associated with hepatitis.
148 centrated in cryoglobulins, and HCV, but not HGV, correlated with cryoglobulinemia in a longitudinal
149             In coinfected sera, HCV, but not HGV, was concentrated in cryoglobulins, and HCV, but not
150 ined, although prevalences as high as 43% of HGV infections in type II cryoglobulinemia have also bee
151  significantly higher rate of acquisition of HGV infection following transplantation (53%, P < .001)
152 ble with the high rate of sequence change of HGV/GBV-C over short observation periods.
153 t- and long-term rates of sequence change of HGV/GBV-C violates the assumptions of the "molecular clo
154 terogeneity consistent with the existence of HGV genetic groups or types.
155         Clinical and biochemical features of HGV-positive and HCV-positive patients and patients with
156                               The finding of HGV RNA in serum from these patients is likely related t
157  inoculated with approximately 10(4.7) GE of HGV had late appearance (week 7 pi) of viremia.
158  inoculated with approximately 10(6.7) GE of HGV had viremia at week 1 pi.
159 proximately 10(8) genome equivalents (GE) of HGV.
160 nces (8,500 bases) of different genotypes of HGV/GBV-C showed an excess of invariant synonymous sites
161 rs, clinical significance, and the impact of HGV on coexistent hepatitis C virus (HCV).
162 ed the prevalence of persistent infection of HGV and HCV in patients exposed to non-virus-inactivated
163 ay explain the reported lack of influence of HGV coinfection on the course of chronic hepatitis C.
164  liver disease and examined the influence of HGV coinfection on the outcome of liver transplantation.
165 m = 500,000 vs. 200,000 Eq/mL) and levels of HGV RNA in liver and serum were similar in patients with
166                                      NS4A of HGV was demonstrated to be a cofactor for NS3-mediated p
167 re is no association between the presence of HGV coinfection and the severity of liver disease post-t
168              We searched for the presence of HGV RNA and HCV RNA sequences in liver and serum samples
169  was no relationship between the presence of HGV RNA and the presence of posttransplantation liver di
170                              The presence of HGV RNA in prediagnostic serum was not associated with t
171                            The prevalence of HGV co-infection was 21% before transplantation and 22%
172                            The prevalence of HGV in a group of multitransfused patients with hematolo
173  suggest the following: 1) The prevalence of HGV infection in patients undergoing OLT for cryptogenic
174               The preoperative prevalence of HGV infection in recipients transplanted for cryptogenic
175 ents were HGV positive and the prevalence of HGV infection was similar for different HCV genotypes.
176                            The prevalence of HGV RNA was determined in samples collected before and a
177  Consequently, the biophysical properties of HGV may be very different from those of HCV.
178                       The prevalence rate of HGV RNA in transplanted controls was 64% (P < .01) with
179               The overall prevalence rate of HGV RNA in transplanted patients with chronic hepatitis
180              The median liver/serum ratio of HGV RNA was less than unity, a finding consistent with s
181 at least part of the putative core region of HGV is expressed in vivo.
182                      Inconsistent results of HGV and the risk of hepatocellular carcinoma (HCC) have
183             We sought to clarify the role of HGV as a causative agent in cryptogenic cirrhosis by ana
184 , China, was conducted to assess the role of HGV infection in HCC development.
185 ver disease of unknown cause and the role of HGV infection in posttransplantation hepatitis, we studi
186 clude that the liver is not the main site of HGV replication.
187 eled the levels of HCV RNA, but not those of HGV RNA.
188 , the pre- and postoperative viral titers of HGV, and the allograft histology in patients infected wi
189 rom all donors could be tested, at least one HGV-positive donor was identified.
190                   HGV RNA-positive patients (HGV-infected and HGV-hepatitis C virus [HCV]-coinfected)
191 ology occurs in 60% (3 of 5) of persistently HGV-infected cryptogenic recipients.
192 f pretransplantation and posttransplantation HGV infection was 24% and 28%, respectively.
193 sitively correlated with posttransplantation HGV infection (P < 0.001).
194 18 months after disease onset, have remained HGV RNA-positive but have become HCV RNA-negative.
195                                        Serum HGV RNA and hepatitis B surface antigen (HBsAg) were ass
196                                        Serum HGV RNA was determined by reverse transcriptase-polymera
197                                        Serum HGV titer increased steadily until it plateaued at 10(6)
198 ents with HCV infection had detectable serum HGV-RNA.
199 trol subjects (3.2%) were positive for serum HGV RNA.
200           In two patients, the fall in serum HGV-RNA correlated with biochemical response, independen
201  coinfected population have changes in serum HGV-RNA induced by interferon.
202 cantly associated with the presence of serum HGV RNA (P <.02).
203                              Negative-strand HGV RNA was detected in three of four bone marrow sample
204                                  In summary, HGV and HCV infections were frequently associated and sh
205                  This study does not support HGV as a primary hepatotropic virus.
206                         It is concluded that HGV infection plays no role in HCC development in this h
207                     These data indicate that HGV has a nucleocapsid and that at least part of the put
208 ing infected with HGV alone, suggesting that HGV is not the main etiologic agent of non-A-E hepatitis
209 had fewer years of drug use, suggesting that HGV RNA had previously been cleared.
210 fference between the particle types was that HGV was consistently more stable in cesium chloride than
211                                          The HGV nucleotide and protein sequences obtained in this st
212                                          The HGV sequences obtained from one patient showed no change
213  on 10-fold serial dilutions of RNA from the HGV reference strain, the last positive dilution was 10(
214  no significant variations were found in the HGV nucleotide and derived amino acid sequences over tim
215 s based on the 5'-untranslated region of the HGV genome.
216 T)-PCR using primers to the 5' region of the HGV genome.
217 ion using primers from the NS5 region of the HGV genome.
218 ions from 6 known full-size sequences of the HGV genomes demonstrated notable discrete heterogeneity
219 nt core protein at the amino terminus of the HGV polyprotein.
220 nt primer sets to assess the validity of the HGV RNA assay.
221 livers were negative for the presence of the HGV RNA minus strand and only six were positive for the
222 tients were negative for the presence of the HGV RNA minus strand in the liver when tested with a str
223 fected individuals contained antibody to the HGV core protein peptide, whereas no binding to a hepati
224 udy hepatitis G virus (HGV), antibody to the HGV envelope protein (anti-E2), risk factors, clinical s
225     Competitive inhibition of binding to the HGV peptide confirmed the specificity of the assay.
226                               After therapy, HGV RNA levels returned to baseline in most subjects.
227                                        Thus, HGV infection is common among HIV-infected homosexual ma
228                                        Thus, HGV is frequently found in transplantation patients co-i
229 rom archival paraffin-embedded liver tissue; HGV sequences were amplified by nested reverse transcrip
230               This lends further evidence to HGV infection not being a cause of cryptogenic cirrhosis
231 rences utilized during in vitro translation, HGV appears to have a truncated or absent core protein a
232                          Pre-transplantation HGV infection was positively correlated with posttranspl
233                                          Two HGV proteases similar to nonstructural proteins NS2 and
234    In serial specimens obtained from the two HGV-infected patients, no significant variations were fo
235 hat all but two positive patients had unique HGV or GBV-C sequences.
236                           Hepatitis G virus (HGV or GB-C virus) is a newly described virus that is cl
237     It is unclear whether hepatitis G virus (HGV) can lead to chronic liver disease and cirrhosis.
238 o tested positive for the hepatitis G virus (HGV) did not have a significantly increased risk of CLD,
239 om a 2.6-kb region of the hepatitis G virus (HGV) genome at nucleotide positions 5829 to 8421 were de
240 examine the prevalence of hepatitis G virus (HGV) in end-stage liver disease of unknown cause and the
241 e pathogenic role for the hepatitis G virus (HGV) in patients with cryptogenic fulminant hepatitis (n
242               The role of hepatitis G virus (HGV) in transfusion-associated infection and its relatio
243 ntrast to HCV, a role for hepatitis G virus (HGV) in type II cryoglobulinemia has not been defined, a
244 assess the persistence of hepatitis G virus (HGV) infection and its association with liver disease, H
245 athogenic implications of hepatitis G virus (HGV) infection are still unclear.
246               The role of hepatitis G virus (HGV) infection in acute non-A-E hepatitis was investigat
247 ermined the prevalence of hepatitis G virus (HGV) infection in end-stage hepatitis C virus (HCV)-rela
248 he health consequences of hepatitis G virus (HGV) infection in humans remain to be determined.
249 lence and consequences of hepatitis G virus (HGV) infection were determined in 180 patients with huma
250                           Hepatitis G virus (HGV) is a newly described RNA virus that is parenterally
251                           Hepatitis G virus (HGV) is a newly described virus that has been implicated
252                           Hepatitis G virus (HGV) is prevalent in patients with chronic liver disease
253                           Hepatitis G virus (HGV) is transmissible by blood transfusion, but its role
254   The recently discovered hepatitis G virus (HGV) or GB virus C (GBV-C) is widely distributed in huma
255 f the recently discovered hepatitis G virus (HGV) remain unknown.
256 n of the newly discovered hepatitis G virus (HGV) to the cause and clinical course of acute and chron
257                           Hepatitis G virus (HGV) was transmitted to 2 chimpanzees by inoculation wit
258                           Hepatitis G virus (HGV), a positive sense RNA virus, is distantly related t
259            Infection with hepatitis G virus (HGV), also known as GB virus C, is prevalent but is not
260 alyses were used to study hepatitis G virus (HGV), antibody to the HGV envelope protein (anti-E2), ri
261 gest that TTV, similar to hepatitis G virus (HGV), may be an example of a human virus with no clear d
262 ecently identified virus, hepatitis G virus (HGV), shows considerable homology to hepatitis C virus (
263  An RNA virus, designated hepatitis G virus (HGV), was identified from the plasma of a patient with c
264 rom a reference strain of hepatitis G virus (HGV), were tested for HGV or GB virus C (GBV-C) RNA.
265 s no difference between the groups (HGV+ vs. HGV-) when baseline alanine aminotransferase (ALT) value
266 onors with confirmed HCV infection, 12% were HGV RNA-positive and 44% were anti-E2-positive (total ex
267 nts, 16 of whom were HGV-positive and 9 were HGV-negative.
268              Forty-one (25.3%) patients were HGV positive and the prevalence of HGV infection was sim
269 a bone marrow transplantation procedure were HGV positive compared with 9 of 27 (33%) treated with co
270 ity-acquired non-A, non-B hepatitis who were HGV RNA positive.
271 on hepatitis in 25 patients, 16 of whom were HGV-positive and 9 were HGV-negative.
272               We sought to determine whether HGV was hepatotropic and to determine whether coinfectio
273 n 4 of the 11 cryptogenic recipients in whom HGV RNA was detectable in the first postoperative month,
274 ic and to determine whether coinfection with HGV and hepatitis C virus (HCV) influenced the level of
275 here is a low prevalence of coinfection with HGV in patients with mixed cryoglobulinemia and HCV infe
276                             Coinfection with HGV occurs in 10% to 20% of HCV-infected subjects.
277                                Compared with HGV-negative patients, the 60 HGV-positive patients (46%
278 howed high frequencies of contamination with HGV (16 of 17 factor VIII batches positive; six of six f
279 gamma-glutamyl transpeptidase in donors with HGV infection alone or those coinfected with HCV.
280 fusion recipients; only 3 had hepatitis with HGV as the sole viral marker.
281 patient was confirmed as being infected with HGV alone, suggesting that HGV is not the main etiologic
282 llograft histology in patients infected with HGV who underwent OLT for cryptogenic cirrhosis.
283  2) In recipients persistently infected with HGV, mean HGV RNA titers increase after OLT.
284  tested (10 percent) were also infected with HGV.
285                               Infection with HGV is common in end-stage HCV-infected patients present
286                               Infection with HGV may affect the risk for AIDS in HIV-infected persons
287                    Persistent infection with HGV was common, but it did not lead to chronic disease a
288        The three patients infected only with HGV had mild hepatitis (mean peak alanine aminotransfera
289 acute illness were similar for patients with HGV alone and those with hepatitis A, B, or C with or wi
290  did not develop in any of the patients with HGV alone, but 75 percent were persistently positive for
291 iver and serum were similar in patients with HGV infection alone compared to those with HGV/HCV coinf
292 ificantly lower in the control patients with HGV infection alone following transplantation than in pa
293  higher in liver biopsies from patients with HGV infection than in those without HGV infection (2 [ra
294                          Three patients with HGV-HCV coinfection, tested within 18 months after disea
295 s with HCV infection alone versus those with HGV/HCV coinfection (median; liver = 1.15 x 10(7) vs. 1.
296 h HGV infection alone compared to those with HGV/HCV coinfection (median; liver = 1.2 x 10(6) vs. 4.0
297  patients infected with HCV with and without HGV infection.
298 t survival between patients with and without HGV infection.
299 se with hepatitis A, B, or C with or without HGV infection.
300 nts with HGV infection than in those without HGV infection (2 [range, 0-14] and 1 [range, 0-3]; P = .

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