ライフサイエンスコーパス: HHV-6B

1 HHV-6B causes exanthem subitum.

2 HHV-6B could not be reactivated under similar conditions

3 HHV-6B DNAemia was uncommon, HHV-6A DNAemia was not obse

4 HHV-6B reactivation is well established as causing limbi

5 HHV-6B transcriptome analysis revealed that the majority

6 HHV-6B-infected HPDA showed no morphological changes, in

7 Human herpesvirus 6A (HHV-6A), HHV-6B, and HHV-7 are classified as roseoloviruses and a

8 Human herpesvirus 6A (HHV-6A), HHV-6B, and HHV-7 are classified as roseoloviruses.

9 oseoloviruses human herpesvirus 6A (HHV-6A), HHV-6B, and HHV-7 comprise the Roseolovirus genus of the

10 es, human herpesvirus-6A -6B and -7 (HHV-6A, HHV-6B and HHV-7) cause acute infection, establish laten

11 osely related to the roseoloviruses, HHV-6A, HHV-6B, and HHV-7, than to another murine betaherpesviru

12 ggest that MRV is a mouse homolog of HHV-6A, HHV-6B, and HHV-7.IMPORTANCE Herein we describe the comp

13 virus (EBV), cytomegalovirus (CMV), HHV-6A, HHV-6B, and HHV-8, using quantitative polymerase chain r

14 ected with Epstein-Barr virus/HHV-4, HHV-6A, HHV-6B, HHV-7, and KSHV.

15 Human herpesvirus 6B (HHV-6B) commonly reactivates after umbilical cord blood

16 in-Barr virus (EBV) or human herpesvirus 6B (HHV-6B), with one coinfection.

17 to previous data indicating that HHV-6A and HHV-6B are distinct herpesvirus species.

18 phalitis recognizing firstly that HHV-6A and HHV-6B are separate species with differing properties, a

19 Our results demonstrate that HHV-6A and HHV-6B have differential tropisms and patterns of infect

20 HHV-6A and HHV-6B have recently been classified as two distinct vir

21 al models for human herpesvirus (HHV)-6A and HHV-6B infections has been slow.

22 leotide sequence identity between HHV-6A and HHV-6B is 90%.

23 in which differential tropism of HHV-6A and HHV-6B may be associated with different disease outcomes

24 was highly cross-reactive between HHV-6A and HHV-6B variants.

25 n herpesvirus 6 variants A and B (HHV-6A and HHV-6B) are closely related viruses that can be readily

26 the assay detects both subtypes, HHV-6A and HHV-6B, it is specific and does not cross-react with a s

27 blish latency, and in the case of HHV-6A and HHV-6B, whole virus can integrate into the host chromoso

28 Two viral variants are known: HHV-6A and HHV-6B.

29 ysis of the relationships between HHV-6A and HHV-6B.

30 genomes of human herpesvirus 6A (HHV-6A) and HHV-6B have the capacity to integrate into telomeres, th

31 lated with human herpesvirus 6A (HHV-6A) and HHV-6B, the lack of animal models has prevented studies

32 Our studies show that both HHV-6A (GS) and HHV-6B (Z-29) can infect highly purified primary fetal a

33 lambda-DNA and human herpes virus 6 type B (HHV-6B) DNA, we have used our labeling method in combina

34 In contrast, HHV-6B was associated with a nonproductive infection.

35 incidence of postnatal infection was 76% for HHV-6B, 59% for CMV, 47% for EBV, 8% for HSV-1, and 0% f

36 rames (ORFs), 9 of which are present only in HHV-6B.

37 f both CD4(+) and CD8(+) T cells, whereas in HHV-6B-infected tissue CD4(+) T cells were predominantly

38 nder similar conditions; however, the latent HHV-6B could be recovered after the cells were infected

39 liver, or bone marrow transplantation latent HHV-6B is reactivated, at times causing severe or fatal

40 CD134(+/neg-lo) cells contained little to no HHV-6B copies.

41 advances have underscored the association of HHV-6B and HHV-7 primary infection with febrile status e

42 o) cells showed 0.308 versus 0.129 copies of HHV-6B/cell (P = .0002).

43 e sequence element formed at the junction of HHV-6B genome concatemers (pac2-pac1) is necessary and s

44 lls harbor significantly increased levels of HHV-6B, suggesting that CD134 (OX40) may facilitate vira

45 Understanding the pathophysiology of HHV-6B encephalitis remains incomplete, especially regar

46 re warranted for treatment and prevention of HHV-6B encephalitis after transplantation.

47 nt of an in vitro system for reactivation of HHV-6B and HHV-7 from latency.

48 rum samples, we demonstrated reactivation of HHV-6B in 25% (4/16 recipients) of HCT recipients with d

49 re we report the complete genome sequence of HHV-6B strain Z29 [HHV-6B(Z29)], describe its genetic co

50 Only HHV-6B DNA was found in primary infection, whereas in vi

51 Reports of HHV-6A or HHV-6B encephalitis in immunocompetent older children/ad

52 tivation.IMPORTANCE Inheritance of HHV-6A or HHV-6B integrated into a telomere occurs at a low freque

53 he complete viral genome of either HHV-6A or HHV-6B is present in every nucleated cell in the body.

54 s using novel, fluorescent-labeled HHV-6A or HHV-6B reagents demonstrated strong G1/S phase inhibitio

55 ng by contacts was associated with HHV-6A or HHV-6B transmission.

56 After long-term passage, HHV-6B-infected HPDA had stable but low levels of intrac

57 ation, 4 patients had HHV-6A and 17 patients HHV-6B.

58 Encephalitis due to primary HHV-6B infection in young children is commonly reported

59 ated cleavage of plasmid DNAs containing the HHV-6B lytic-phase origin of DNA replication (oriLyt).

60 affinity to its two cognate OBP sites in the HHV-6B oriLyt.

61 Once reactivated, the HHV-6B genomes became prominent and the HHV-7 disappeare

62 As sequenced, the HHV-6B(Z29) genome is 162,114 bp long and is composed of

63 This is in contrast to the HHV-6B OBP (OBP(H6B)), which binds with similar affinity

64 ncy of lymphoproliferative response (78%) to HHV-6B was demonstrated in MS patients.

65 Most healthy controls (71%) proliferated to HHV-6B lysate, and fewer (33%) responded to the HHV-6A l

66 oproliferative responses to HHV-6A (U1102)-, HHV-6B (Z29)-, and HHV-7 (H7SB)-infected cell lysates in

67 entional PCR and sequence analysis; all were HHV-6B.

68 o disease has been linked to HHV-6A, whereas HHV-6B may cause encephalitis.

69 Primary infection with HHV-6B occurs in nearly all children and was first linke

70 mplete genome sequence of HHV-6B strain Z29 [HHV-6B(Z29)], describe its genetic content, and present