ライフサイエンスコーパス: cytopathicity

1 rough active virus replication and resulting cytopathicity.

2 om entering G(2)/M also did not reduce HIV-1 cytopathicity.

3 somal secretion affect viral replication and cytopathicity.

4 g-pol and vpu, tat, and rev did not mitigate cytopathicity.

5 e resilience of macrophages to HIV-1-induced cytopathicity.

6 s that render macrophages sensitive to viral cytopathicity.

7 blasts, which are resistant to virus-induced cytopathicity.

8 diated clearance and/or elimination by viral cytopathicity.

9 ated in primary lymphocytes without inducing cytopathicity.

10 ght into the viral component responsible for cytopathicity.

11 sceptible as wild-type Jurkat cells to HIV-1 cytopathicity.

12 tics of viral replication in baboon PBMC and cytopathicity.

13 which has been previously implicated in HIV cytopathicity.

14 with the P2X7R in the absence of significant cytopathicity.

15 sufficient for the development of increased cytopathicity.

16 on of lysosomal proteases can modulate viral cytopathicity.

17 rticular coreceptor is associated with viral cytopathicity.

18 e viral replication kinetics and single-cell cytopathicity.

19 m induction but was not a key determinant of cytopathicity.

20 expression of bcl-2 did not prevent eventual cytopathicity.

21 at Tat also influences virus infectivity and cytopathicity.

22 sistant to both apoptosis and other types of cytopathicity after infection with La Crosse virus, reaf

23 m suggests that CD4(+) T cell-directed viral cytopathicity alone cannot explain the course of disease

24 ignated mycolactone was isolated that causes cytopathicity and cell cycle arrest in cultured L929 mur

25 from T cells in terms of decreased to absent cytopathicity and for active accumulation of new progeny

26 ies, implicating M as a primary regulator of cytopathicity and host transcriptional suppression.IMPOR

27 al RNA (sfRNA), a noncoding RNA that induces cytopathicity and pathogenesis.

28 hila, despite lacking both contact-dependent cytopathicity and regulated sodium sensitivity.

29 but not Fas or TRAIL receptors, inhibits the cytopathicity and replication of human CMV by a nonapopt

30 ion and nsP2 or nsP3 genes to further reduce cytopathicity and to become capable of persisting in cel

31 p between virus-mediated CD4(+) T-lymphocyte cytopathicity and viral coreceptor preference among vari

32 s (e.g., coreceptor usage, cell tropism, and cytopathicity) and is a major target of antiviral immune

33 hesis of viral nucleic acids and viral mRNA, cytopathicity, and release of progeny virions were asses

34 e molecular events that underlie Ebola virus cytopathicity are poorly understood.

35 re prepared and evaluated using a whole cell cytopathicity assay (XTT).

36 due to intrinsic differences in the in vivo cytopathicities between the two viruses.

37 ese results suggest that the primary mode of cytopathicity by laboratory-adapted molecular clones of

38 Cytopathicity by virion-delivered mutant Vpr protein cor

39 ersistent infection contrasts with the rapid cytopathicity caused by FV in vitro, suggesting a host d

40 roteins derived from MV strains with reduced cytopathicities confirm that the strength of H and F gly

41 mounting evidence suggests that direct viral cytopathicity contributes to this loss.

42 The cytopathicity defect of the mutants to the U937 cells wa

43 d self-association but dispensable for HIV-1 cytopathicity due to residual cell proliferation blockad

44 and a shared cellular link to infection and cytopathicity for distantly related lentiviruses that ca

45 However, the molecular mechanism of viral cytopathicity has not been satisfactorily elucidated.

46 t that HHV-6 may protect DC from HIV-induced cytopathicity in AIDS patients.

47 hibits rapid replication kinetics and marked cytopathicity in both human and chimpanzee peripheral bl

48 is involved in paracrine-mediated C. parvum cytopathicity in cholangiocytes, we also tested the pote

49 irus type 1 (HIV-1) evolves toward increased cytopathicity in conjunction with disease progression in

50 dence of coreceptor-independent increases in cytopathicity in isolates obtained either before corecep

51 nsible for a higher replication capacity and cytopathicity in primary CD4(+) T-cell cultures.

52 We studied the replication and cytopathicity in SCID-hu mice of R5 human immunodeficien

53 assays indicated that 4 inhibits HIV-induced cytopathicity in T lymphocytes with an EC50 of 28 muM, w

54 that viral replication can be uncoupled from cytopathicity in vitro and in vivo.

55 st relationships and potential mechanisms of cytopathicity in vivo in simian immunodeficiency virus (

56 properties also contributes to accelerating cytopathicity in vivo, we used human lymphoid tissue exp

57 that HIV-1 does not evolve toward increased cytopathicity independently of changes in coreceptor uti

58 -2 strains revealed similar, high degrees of cytopathicity induced by both HIV types.

59 tion, and the data suggest that direct viral cytopathicity is a major factor.

60 By contrast, if viral cytopathicity is high relative to the replication rate o

61 If the viral cytopathicity is low relative to the rate of viral repli

62 udies demonstrate that primary HIV-1-induced cytopathicity is separable from syncytium formation and

63 line-94, a determinant of measles virus (MV) cytopathicity, is predicted to lie in a cylindrical cavi

64 conferred its rapid replication kinetics and cytopathicity mapped to the capsid- and nucleocapsid-enc

65 human lymphoid tissue explants to assay the cytopathicity of a panel of primary HIV-1 isolates deriv

66 Instead, the cytopathicity of all HIV-1 isolates was determined solel

67 (gp41C) is implicated in the replication and cytopathicity of HIV-1 [1].

68 igated the impact of coreceptor usage on the cytopathicity of HIV-2 and compared its pathogenic poten

69 toplasmic tail influence the replication and cytopathicity of SIVMne variants that evolve in the host

70 n previously shown to be responsible for the cytopathicity of Spl574, S82F.

71 t alter the in vitro replication kinetics or cytopathicity of the mutant viruses in T-cell lines.

72 of the two types of component depend on the cytopathicity of the virus relative to its rate of repli

73 ts severely depleted CD4(+) T cells, whereas cytopathicity of the virus that used CCR5 only in lympho

74 the efficiency of primary infection and the cytopathicity of virus for infected CD4-positive T cells

75 l envelope, might influence viral-associated cytopathicity or apoptosis [6].

76 transduction may influence viral-associated cytopathicity or apoptosis.

77 s CCR3, CCR8, BOB, and Bonzo did not augment cytopathicity or diminish sensitivity toward CXCR4 antag

78 th deletions, rather than being required for cytopathicity, play a role in protecting cells from CPE.

79 age plasma membrane paralleled virus-induced cytopathicity, podosome formation, and cellular fusion.

80 ein replicates efficiently, has an increased cytopathicity, possesses a greater infectivity per parti

81 hesis", argues that viral attributes such as cytopathicity, replicability, syncytiality, cell tropism

82 This cytopathicity resembles that of Spl574 MLV, a novel vari

83 not characterized by an intrinsically lower cytopathicity than HIV-1 strains.

84 c mutants had a similar phenotype of reduced cytopathicity to the U937 cells, showed a 100-fold incre

85 that use CXCR4 or CCR5 exclusively; and (c) cytopathicity toward the general CD4(+) T cell populatio

86 Mutations in the hel genes led to reduced cytopathicity towards U937 cells, although the mutant st

87 IL-4 inhibited virus entry, replication, and cytopathicity under these conditions.

88 rs of cells and induced comparable levels of cytopathicity, viral production was considerably higher

89 We also found that HIV-1 cytopathicity was undiminished by the absence of nef.

90 The effect of Vpr on cytopathicity was unrelated to reported activities of Vp

91 molecular determinants of measles virus (MV) cytopathicity, we have characterized mutant viruses exhi

92 tion and host immunologic defense against FV cytopathicity, we quantified FV in tissues of healthy rh

93 V-1 clone resulted in a marked impairment of cytopathicity without affecting viral replication effici