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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 , the secondary lymphoid tissues targeted by AIDS viruses.
7 a sanctuary and a reservoir for replicating AIDS viruses.
8 man primates following challenge with simian AIDS viruses.
9 ry lymphoid tissues, are readily infected by AIDS viruses and are a major source of persistent virus
11 he findings suggest that vaccination against AIDS virus can alter patterns of immune responses to the
15 ted Th1 or Th17/Th22 responses after malaria/AIDS-virus coinfection correlate with distinct outcomes
16 ose to 20% of the patients infected with the AIDS virus develops neurological deficit; eventhough HIV
17 udy demonstrates for the first time that the AIDS virus differentially impacts two distinct subsets o
20 ly influence CD8+ T cell-mediated control of AIDS viruses; however, the potential to modulate the rep
23 the contrary, speculation continues that the AIDS virus, human immunodeficiency virus type 1 (HIV-1),
24 discovered and is the predominant variant of AIDS virus in most countries outside of sub-Saharan Afri
25 a measure of control over replication of the AIDS virus in the complete absence of neutralizing antib
29 provide in vivo evidence that coinfection of AIDS virus-infected individuals with an avirulent mycoba
34 of both CD4(+) and CD8(+) T cell turnover in AIDS virus infection and have important implications for
35 e results support the notions that a chronic AIDS virus infection can induce clonal expansion, in add
38 o determine the extent to which a coincident AIDS virus infection might compromise immune responses o
39 on the mechanisms of protective immunity to AIDS virus infection represents a major obstacle to the
40 3 repertoire of primate B cells during acute AIDS virus infection, contrary to predictions of the gp1
48 iated immunity in vivo In the rhesus macaque AIDS virus model, infusing simian immunodeficiency virus
49 pite recent advances in the understanding of AIDS virus pathogenesis, which cell subsets support HIV
50 ppress residual viral replication.IMPORTANCE AIDS virus persistence in individuals under effective dr
54 itor cells can retain the ability to inhibit AIDS virus replication after T-cell differentiation and
55 the small intestine, a site of intense early AIDS virus replication and pathology in rhesus macaques.
56 itor cells can retain the ability to inhibit AIDS virus replication following T-cell differentiation
58 e observed role of CTL in the containment of AIDS virus replication suggests that an effective HIV va
62 ective virus-specific CD8 T cells into these AIDS virus sanctuaries and potentially suppress residual
66 against a cryptic epitope suggests that the AIDS virus-specific cellular immune response is likely f
67 bservations suggest that characterization of AIDS virus-specific CTL activity by sampling of cells in
68 sus monkey model to explore the induction of AIDS virus-specific CTL responses by DNA vaccination.
69 virus Ankara (MVA) as a vector for eliciting AIDS virus-specific cytotoxic T lymphocytes (CTL) was ex
71 levant vaccine vector - can be used to prime AIDS virus-specific T-cell responses in heterologous pri
72 ol replication of a pathogenic, heterologous AIDS virus, suggesting that T-cell-based vaccines may ha
73 on that recognizes a dominant epitope of the AIDS virus, the CD8(+) T cells recognizing the tetrameri
76 he presence of env trimers on the surface of AIDS virus virions, albeit at numbers much lower than ge
77 ermining the in vivo replicative capacity of AIDS viruses, we have examined the replication kinetics
78 37.6 million people are living with the HIV/AIDS virus worldwide, placing HIV/AIDS among the ten lea