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1                                              HHV-6B causes exanthem subitum.
2                                              HHV-6B could not be reactivated under similar conditions
3                                              HHV-6B detection was low level (median peak, 435 copies
4                                              HHV-6B DNAemia was uncommon, HHV-6A DNAemia was not obse
5                                              HHV-6B reactivation is well established as causing limbi
6                                              HHV-6B transcriptome analysis revealed that the majority
7                                              HHV-6B U20 trafficked slowly through the secretory syste
8                                              HHV-6B-infected HPDA showed no morphological changes, in
9               Human herpesvirus 6A (HHV-6A), HHV-6B, and HHV-7 are classified as roseoloviruses and a
10               Human herpesvirus 6A (HHV-6A), HHV-6B, and HHV-7 are classified as roseoloviruses.
11 oseoloviruses human herpesvirus 6A (HHV-6A), HHV-6B, and HHV-7 comprise the Roseolovirus genus of the
12 es, human herpesvirus-6A -6B and -7 (HHV-6A, HHV-6B and HHV-7) cause acute infection, establish laten
13 osely related to the roseoloviruses, HHV-6A, HHV-6B, and HHV-7, than to another murine betaherpesviru
14 ggest that MRV is a mouse homolog of HHV-6A, HHV-6B, and HHV-7.IMPORTANCE Herein we describe the comp
15  virus (EBV), cytomegalovirus (CMV), HHV-6A, HHV-6B, and HHV-8, using quantitative polymerase chain r
16 ected with Epstein-Barr virus/HHV-4, HHV-6A, HHV-6B, HHV-7, and KSHV.
17  virus [EBV], human herpesvirus 6A [HHV-6A], HHV-6B, herpes simplex virus 1 [HSV-1], HSV-2, JC virus
18                        Human herpesvirus 6B (HHV-6B) belongs to the beta-herpesvirus subfamily of the
19                        Human herpesvirus 6B (HHV-6B) commonly reactivates after umbilical cord blood
20                        Human herpesvirus 6B (HHV-6B) DNA is frequently detected in bronchoalveolar la
21                        Human herpesvirus 6B (HHV-6B) DNA is frequently detected in human samples.
22                        Human herpesvirus 6B (HHV-6B) frequently reactivates after allogeneic hematopo
23  immunopathogenesis of human herpesvirus 6B (HHV-6B) has prevented its acceptance as a pulmonary path
24  adenovirus (HAdV) and human herpesvirus 6B (HHV-6B) in 23 of 31 and 16 of 23, respectively, of the c
25 s during the course of human Herpesvirus 6B (HHV-6B) infection, we made use of large-scale RNA sequen
26 se of RNA-seq to study human Herpesvirus 6B (HHV-6B) infection.
27  recipients.IMPORTANCE Human herpesvirus 6B (HHV-6B) is a DNA virus that infects most children within
28                        Human herpesvirus 6B (HHV-6B) reactivation and disease are increasingly report
29 in-Barr virus (EBV) or human herpesvirus 6B (HHV-6B), with one coinfection.
30                                Additionally, HHV-6B can integrate into germ line chromosomes, resulti
31 cidofovir has high in vitro activity against HHV-6B and other DNA viruses, but its in vivo activity f
32          Finally, we show transmission of an HHV-6B strain from an iciHHV-6B mother to her non-iciHHV
33          Second, we retrospectively analyzed HHV-6B detection in the blood and/or cerebrospinal fluid
34  to previous data indicating that HHV-6A and HHV-6B are distinct herpesvirus species.
35 phalitis recognizing firstly that HHV-6A and HHV-6B are separate species with differing properties, a
36  genome imaging of the integrated HHV-6A and HHV-6B genomes using whole-genome optical site mapping t
37      Our results demonstrate that HHV-6A and HHV-6B have differential tropisms and patterns of infect
38                                   HHV-6A and HHV-6B have recently been classified as two distinct vir
39 al models for human herpesvirus (HHV)-6A and HHV-6B infections has been slow.
40 t on the genetic structure of the HHV-6A and HHV-6B integration locus, demonstrating the utility of o
41 leotide sequence identity between HHV-6A and HHV-6B is 90%.
42  in which differential tropism of HHV-6A and HHV-6B may be associated with different disease outcomes
43 was highly cross-reactive between HHV-6A and HHV-6B variants.
44 n herpesvirus 6 variants A and B (HHV-6A and HHV-6B) are closely related viruses that can be readily
45      Human herpesvirus 6A and 6B (HHV-6A and HHV-6B) are closely related viruses that infect most hum
46    Human herpesviruses 6A and 6B (HHV-6A and HHV-6B) are human viruses capable of chromosomal integra
47  the assay detects both subtypes, HHV-6A and HHV-6B, it is specific and does not cross-react with a s
48 blish latency, and in the case of HHV-6A and HHV-6B, whole virus can integrate into the host chromoso
49 were probed for PCR reactivity to HHV-6A and HHV-6B.
50     Two viral variants are known: HHV-6A and HHV-6B.
51 ysis of the relationships between HHV-6A and HHV-6B.
52 genomes of human herpesvirus 6A (HHV-6A) and HHV-6B have the capacity to integrate into telomeres, th
53 lated with human herpesvirus 6A (HHV-6A) and HHV-6B, the lack of animal models has prevented studies
54   Our studies show that both HHV-6A (GS) and HHV-6B (Z-29) can infect highly purified primary fetal a
55  complexes reflecting both HAdV-mediated and HHV-6B-mediated replication.
56  respiratory failure, and the effect of anti-HHV-6B antivirals on these outcomes.
57  lambda-DNA and human herpes virus 6 type B (HHV-6B) DNA, we have used our labeling method in combina
58 products aided by HAdV and, in severe cases, HHV-6B may have triggered immune-mediated hepatic diseas
59 -blood samples from patients with concurrent HHV-6B viremia.
60                                 In contrast, HHV-6B was associated with a nonproductive infection.
61                                  We detected HHV-6B(+) BALF from 147 of 553 (27%) individuals.
62 ect viral DNA is the mainstay for diagnosing HHV-6B infection, the characteristics of HHV-6B infectio
63 ssociated neurotoxicity syndrome, diagnosing HHV-6B encephalitis is challenging.
64             Diagnostic assays distinguishing HHV-6B reactivation from latency are limited.
65 ll, the data expand the number of documented HHV-6B CD4 T-cell antigens from approximately 11 to 60.
66                                 We establish HHV-6B DNA viral load thresholds in BALF that are highly
67 incidence of postnatal infection was 76% for HHV-6B, 59% for CMV, 47% for EBV, 8% for HSV-1, and 0% f
68 er DNA viruses, but its in vivo activity for HHV-6B has not been demonstrated.
69                          A RT-qPCR assay for HHV-6B U38 may be useful to identify lytic HHV-6B infect
70                           We tested BALF for HHV-6B DNA using polymerase chain reaction in allogeneic
71  HCT, we test blood and BAL fluid (BALF) for HHV-6B DNA and mRNA transcripts associated with lytic in
72 t the study of intravenous brincidofovir for HHV-6B prophylaxis.
73  remained associated with a lower hazard for HHV-6B plasma detection (hazard ratio, 0.40; 95% confide
74                         We tested plasma for HHV-6B through week 6 post-HCT.
75 immunocompromised patients who have frequent HHV-6B reactivation.
76 ected in 37% of BALs, 49% of which also have HHV-6B mRNA detection.
77        Compared to other beta-herpesviruses, HHV-6B exhibits high similarity in capsid structure but
78                         These data implicate HHV-6B as a pulmonary pathogen after allogeneic HCT.
79   180 "VLambda"-shaped CATCs are observed in HHV-6B, distinguishing from the 255 "Lambda"-shaped dime
80 rames (ORFs), 9 of which are present only in HHV-6B.
81 ATC's binding to triplexes Ta, Tc, and Tf in HHV-6B.
82 f both CD4(+) and CD8(+) T cells, whereas in HHV-6B-infected tissue CD4(+) T cells were predominantly
83                     After primary infection, HHV-6B persists as a chronic, latent infection in many c
84 B testing for up to 12 weeks after infusion, HHV-6B reactivation occurred in 8 of 89 participants; 3
85 ects with inherited chromosomally integrated HHV-6B or latent infection with HHV-6B, and (iv) HHV-6B
86 uals with inherited chromosomally integrated HHV-6B.
87              Our results offer insights into HHV-6B capsid assembly and the roles of its tegument pro
88 6B or latent infection with HHV-6B, and (iv) HHV-6B Z29 infected SupT1 CD4(+) T cells.
89 cells from 18 healthy donors with each known HHV-6B protein.
90 nder similar conditions; however, the latent HHV-6B could be recovered after the cells were infected
91 liver, or bone marrow transplantation latent HHV-6B is reactivated, at times causing severe or fatal
92 r HHV-6B U38 may be useful to identify lytic HHV-6B infection in nonplasma samples and samples from i
93  had an approximately 1 log(10) lower median HHV-6B BALF viral load, as well as a lower risk of overa
94 cussed on HHV-6B-specific reads matching new HHV-6B transcripts.
95               Differential expression of new HHV-6B transcripts were observed in all samples analyzed
96            The presence of many of these new HHV-6B transcripts were confirmed by RT-PCR and Sanger s
97                                           No HHV-6B U38 transcripts were detected by RNA-seq or rever
98 CD134(+/neg-lo) cells contained little to no HHV-6B copies.
99 advances have underscored the association of HHV-6B and HHV-7 primary infection with febrile status e
100 azards models to evaluate the association of HHV-6B(+) BALF with overall mortality, death from respir
101 ing HHV-6B infection, the characteristics of HHV-6B infection complicate efforts to distinguish betwe
102 o) cells showed 0.308 versus 0.129 copies of HHV-6B/cell (P = .0002).
103 me (ORF) reported in the annotated genome of HHV-6B Z29 strain.
104                  The cumulative incidence of HHV-6B plasma detection through day 42 post-HCT was sign
105 uded, resulting in a cumulative incidence of HHV-6B reactivation of 6% (95% confidence interval [CI],
106 e sequence element formed at the junction of HHV-6B genome concatemers (pac2-pac1) is necessary and s
107 lls harbor significantly increased levels of HHV-6B, suggesting that CD134 (OX40) may facilitate vira
108 ence assessing the incidence and outcomes of HHV-6B after CARTx.
109 erapy should consider this expanded panel of HHV-6B antigens.IMPORTANCE Human herpesvirus 6 is highly
110         Understanding the pathophysiology of HHV-6B encephalitis remains incomplete, especially regar
111 sholds in BALF that are highly predictive of HHV-6B mRNA detection and associated with increased risk
112 re warranted for treatment and prevention of HHV-6B encephalitis after transplantation.
113 nt of an in vitro system for reactivation of HHV-6B and HHV-7 from latency.
114 rum samples, we demonstrated reactivation of HHV-6B in 25% (4/16 recipients) of HCT recipients with d
115       Our results indicate that selection of HHV-6B ORFs for immunotherapy should consider this expan
116 re we report the complete genome sequence of HHV-6B strain Z29 [HHV-6B(Z29)], describe its genetic co
117 actions, here we report atomic structures of HHV-6B capsid and capsid-associated tegument complex (CA
118  HCT to study the effect of brincidofovir on HHV-6B reactivation.
119               The initial search focussed on HHV-6B-specific reads matching new HHV-6B transcripts.
120  correlate our work with previous studies on HHV-6B.
121                                         Only HHV-6B DNA was found in primary infection, whereas in vi
122 HV-6B viral polymerase gene U38 was the only HHV-6B transcript detected in all next-generation RNA se
123                         Reports of HHV-6A or HHV-6B encephalitis in immunocompetent older children/ad
124  individuals inherit the genome of HHV-6A or HHV-6B in the germline, and viral genomes are therefore
125 tivation.IMPORTANCE Inheritance of HHV-6A or HHV-6B integrated into a telomere occurs at a low freque
126 he complete viral genome of either HHV-6A or HHV-6B is present in every nucleated cell in the body.
127 s using novel, fluorescent-labeled HHV-6A or HHV-6B reagents demonstrated strong G1/S phase inhibitio
128 ng by contacts was associated with HHV-6A or HHV-6B transmission.
129                      Among 116 participants, HHV-6B DNA is detected in 37% of BALs, 49% of which also
130                     After long-term passage, HHV-6B-infected HPDA had stable but low levels of intrac
131 ation, 4 patients had HHV-6A and 17 patients HHV-6B.
132 d studies of antiviral treatments to prevent HHV-6B reactivation.
133                  Encephalitis due to primary HHV-6B infection in young children is commonly reported
134 agnostic, proteome-wide approach, we queried HHV-6B-specific CD4 T cells from 18 healthy donors with
135 onclusion, brincidofovir prophylaxis reduced HHV-6B reactivation after allogeneic HCT in a post hoc a
136 el reverse transcription-PCR assay targeting HHV-6B U38, which identified U38 mRNA in all tested whol
137 tent viral reactivation and demonstrate that HHV-6B can become reactivated in cultures of human CD4(+
138                    Our data demonstrate that HHV-6B reactivation and disease are infrequent after CAR
139             These data provide evidence that HHV-6B detection in BALF is associated with higher morta
140                                          The HHV-6B viral polymerase gene U38 was the only HHV-6B tra
141 of large-scale RNA sequencing to analyze the HHV-6B transcriptome during productive infection of huma
142 , we used RNA sequencing to characterize the HHV-6B gene expression profile in multiple sample types,
143 A sequencing to characterize and compare the HHV-6B transcriptome in multiple sample types, including
144 ated cleavage of plasmid DNAs containing the HHV-6B lytic-phase origin of DNA replication (oriLyt).
145 affinity to its two cognate OBP sites in the HHV-6B oriLyt.
146   We demonstrated substantial overlap in the HHV-6B transcriptome observed in in vivo and in vitro sa
147 ead sequencing mapped the integration of the HHV-6B genome to a locus on chromosome 22q.
148   We exploited a hypervariable region of the HHV-6B genome to investigate the relationship between ac
149 ates the diversity and the complexity of the HHV-6B transcriptome.IMPORTANCERNA sequencing (RNA-seq)
150  have led us to propose a new version of the HHV-6B Z29 GenBank annotated file, without changing ORF
151                        Once reactivated, the HHV-6B genomes became prominent and the HHV-7 disappeare
152                            As sequenced, the HHV-6B(Z29) genome is 162,114 bp long and is composed of
153                   This is in contrast to the HHV-6B OBP (OBP(H6B)), which binds with similar affinity
154 ncy of lymphoproliferative response (78%) to HHV-6B was demonstrated in MS patients.
155  Most healthy controls (71%) proliferated to HHV-6B lysate, and fewer (33%) responded to the HHV-6A l
156 as impaired strategies to diagnose and treat HHV-6B-associated diseases.
157 oproliferative responses to HHV-6A (U1102)-, HHV-6B (Z29)-, and HHV-7 (H7SB)-infected cell lysates in
158    First, in a prospective study with weekly HHV-6B testing for up to 12 weeks after infusion, HHV-6B
159 entional PCR and sequence analysis; all were HHV-6B.
160 o disease has been linked to HHV-6A, whereas HHV-6B may cause encephalitis.
161                                      Whether HHV-6B is a pulmonary pathogen is unclear.
162 cts with large B cell lymphoma infected with HHV-6B, (iii) lymphoblastoid cell lines (LCLs) from subj
163                       Primary infection with HHV-6B occurs in nearly all children and was first linke
164 y integrated HHV-6B or latent infection with HHV-6B, and (iv) HHV-6B Z29 infected SupT1 CD4(+) T cell
165                            Participants with HHV-6B DNA in BALF exhibit distinct host gene expression
166 ung tissue in all three tested subjects with HHV-6B(+) BALF and sufficient tissue RNA preservation.
167  CI, 0.16-1.10), compared with subjects with HHV-6B(+) BALF not receiving antivirals.
168                                Subjects with HHV-6B(+) BALF who received antivirals within 3 days pre
169                                Subjects with HHV-6B(+) BALF, with or without copathogens, had signifi
170 % CI, 1.56-4.01) compared with subjects with HHV-6B(-) BALF.
171 transplant (HCT) recipients with and without HHV-6B plasma viremia, (ii) tumor tissue samples from su
172 in whole-blood samples from subjects without HHV-6B plasma detection or from latently infected LCLs.
173 mplete genome sequence of HHV-6B strain Z29 [HHV-6B(Z29)], describe its genetic content, and present

 
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