ライフサイエンスコーパス: AIDS virus

1 tion, they are persistent reservoirs for the AIDS virus.

2 ell responses can control replication of the AIDS virus.

3 successfully control the replication of the AIDS virus.

4 luence the outcome of exposure to HIV-1, the AIDS virus.

5 straints on the CTL-TCR interaction with the AIDS virus.

6 a sanctuary and a reservoir for replicating AIDS viruses.

7 man primates following challenge with simian AIDS viruses.

8 ry lymphoid tissues, are readily infected by AIDS viruses and are a major source of persistent virus

9 Although replication-competent AIDS viruses attenuated for pathogenicity by selective g

10 he findings suggest that vaccination against AIDS virus can alter patterns of immune responses to the

11 Therefore, these findings suggest that AIDS viruses can evade virus-specific CTL responses thro

12 se progression following a highly pathogenic AIDS virus challenge.

13 ient magnitude to protect against pathogenic AIDS virus challenges.

14 ted Th1 or Th17/Th22 responses after malaria/AIDS-virus coinfection correlate with distinct outcomes

15 ose to 20% of the patients infected with the AIDS virus develops neurological deficit; eventhough HIV

16 udy demonstrates for the first time that the AIDS virus differentially impacts two distinct subsets o

17 e tissue and organ distribution of a primate AIDS virus during HAART.

18 er elucidate the potential and scope of anti-AIDS virus effector CD4 T-cell function.

19 ly influence CD8+ T cell-mediated control of AIDS viruses; however, the potential to modulate the rep

20 The human AIDS viruses human immunodeficiency virus type 1 (HIV-1)

21 The AIDS virus, human immunodeficiency virus type 1 (HIV-1),

22 the contrary, speculation continues that the AIDS virus, human immunodeficiency virus type 1 (HIV-1),

23 discovered and is the predominant variant of AIDS virus in most countries outside of sub-Saharan Afri

24 a measure of control over replication of the AIDS virus in the complete absence of neutralizing antib

25 However, evidence of protection against AIDS viruses in animal models and control of HIV in huma

26 esponses are critical for the containment of AIDS viruses in humans and Asian nonhuman primates.

27 d Mycobacterium can impact remarkably on the AIDS virus-induced disease.

28 provide in vivo evidence that coinfection of AIDS virus-infected individuals with an avirulent mycoba

29 ly account for the follicular hyperplasia in AIDS virus-infected individuals.

30 , mediate short-term reduction of viremia in AIDS virus-infected individuals.

31 influence rates of disease progression among AIDS virus-infected individuals.

32 It is possible, therefore, that while AIDS virus-infected macrophages constitute only a small

33 of both CD4(+) and CD8(+) T cell turnover in AIDS virus infection and have important implications for

34 e results support the notions that a chronic AIDS virus infection can induce clonal expansion, in add

35 The establishment of AIDS virus infection in an individual is essentially a r

36 ism underlying the enhanced pathogenicity of AIDS virus infection in the coinfected individuals.

37 o determine the extent to which a coincident AIDS virus infection might compromise immune responses o

38 on the mechanisms of protective immunity to AIDS virus infection represents a major obstacle to the

39 3 repertoire of primate B cells during acute AIDS virus infection, contrary to predictions of the gp1

40 accine efficacy and biological outcome in an AIDS virus infection.

41 CD4(+) T-lymphocyte dysfunction following an AIDS virus infection.

42 th of the CTL response that evolves after an AIDS virus infection.

43 t MAIT cells are systemically depleted in an AIDS virus infection.

44 as not been prospectively assessed during an AIDS virus infection.

45 e advantageous for the host in containing an AIDS virus infection.

46 AIDS virus infections are rarely controlled by cell-medi

47 pite recent advances in the understanding of AIDS virus pathogenesis, which cell subsets support HIV

48 ppress residual viral replication.IMPORTANCE AIDS virus persistence in individuals under effective dr

49 gents can improve the clinical outcome of an AIDS virus-related tuberculosis-like disease.

50 were employed to explore the pathogenesis of AIDS virus-related tuberculosis.

51 t their importance in the immune response to AIDS viruses remains unknown.

52 itor cells can retain the ability to inhibit AIDS virus replication after T-cell differentiation and

53 itor cells can retain the ability to inhibit AIDS virus replication following T-cell differentiation

54 Natural containment of AIDS virus replication in Mamu-B*08-positive macaques ma

55 e observed role of CTL in the containment of AIDS virus replication suggests that an effective HIV va

56 y not be sufficient to substantially contain AIDS virus replication.

57 e immunogenicity does not predict control of AIDS virus replication.

58 ence for the importance of CTL in containing AIDS virus replication.

59 ective virus-specific CD8 T cells into these AIDS virus sanctuaries and potentially suppress residual

60 Animals were challenged with a pathogenic AIDS virus (SHIV89.6P).

61 is associated with control of the pathogenic AIDS virus SIVmac239.

62 Vaccines designed to elicit AIDS virus-specific CD8+ T cells should engender broad r

63 against a cryptic epitope suggests that the AIDS virus-specific cellular immune response is likely f

64 bservations suggest that characterization of AIDS virus-specific CTL activity by sampling of cells in

65 sus monkey model to explore the induction of AIDS virus-specific CTL responses by DNA vaccination.

66 virus Ankara (MVA) as a vector for eliciting AIDS virus-specific cytotoxic T lymphocytes (CTL) was ex

67 ne whether IL-15 can induce the expansion of AIDS virus-specific pre-CTL to mature CTL.

68 levant vaccine vector - can be used to prime AIDS virus-specific T-cell responses in heterologous pri

69 ol replication of a pathogenic, heterologous AIDS virus, suggesting that T-cell-based vaccines may ha

70 on that recognizes a dominant epitope of the AIDS virus, the CD8(+) T cells recognizing the tetrameri

71 The ability of an AIDS virus to escape from immune containment by selectiv

72 e is an excellent model to examine candidate AIDS virus vaccines.

73 he presence of env trimers on the surface of AIDS virus virions, albeit at numbers much lower than ge

74 ermining the in vivo replicative capacity of AIDS viruses, we have examined the replication kinetics