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1 strongly associated with protection against HIV disease progression.
2 urs in HIV(+) patients and may contribute to HIV disease progression.
3 alleles that have been associated with slow HIV disease progression.
4 r this virus is a marker or a determinant of HIV disease progression.
5 in CD8 lymphocyte function that accompanies HIV disease progression.
6 tially participate in the pathophysiology of HIV disease progression.
7 tegrity, and are associated with accelerated HIV disease progression.
8 ects and lower d(N)/d(S) in those with rapid HIV disease progression.
9 or (nef) has been positively correlated with HIV disease progression.
10 8 months is strongly associated with risk of HIV disease progression.
11 immunization strategies aimed at preventing HIV disease progression.
12 the identification of viral determinants of HIV disease progression.
13 n suggested a link between GSH depletion and HIV disease progression.
14 ine environment, which may be altered during HIV disease progression.
15 s experienced, the greater the risk of early HIV disease progression.
16 s associated with an increased rate of early HIV disease progression.
17 no adverse effects on hemoglobin decrease or HIV disease progression.
18 s system damage, but also risk of more rapid HIV disease progression.
19 (HIV) burdens have each been correlated with HIV disease progression.
20 eductions in cytotoxic lymphocytes influence HIV disease progression.
21 herapies utilizing this cytokine for slowing HIV disease progression.
22 -controllers (NC) who are at higher risk for HIV disease progression.
23 and cardiometabolic factors and longitudinal HIV disease progression.
24 iated T cell dysfunction and correlates with HIV disease progression.
25 immunization strategies aimed at preventing HIV disease progression.
26 ality risk in women with HIV, independent of HIV disease progression.
27 , many of which are implicated in more rapid HIV disease progression.
28 ociated with increased T-cell activation and HIV disease progression.
29 with higher levels of immune activation and HIV disease progression.
30 nd immune activation, which is implicated in HIV disease progression.
31 ) and substance abuse is known to accelerate HIV disease progression.
32 sis, sTim-3 may represent a new correlate of HIV disease progression.
33 absolute CD4 counts and therefore a lack of HIV disease progression.
34 Thus, plasma sTim-3 shedding correlated with HIV disease progression.
35 during pathogenic SIV infection may prevent HIV disease progression.
36 ylori infection with favorable parameters of HIV disease progression.
37 ociated with increased immune activation and HIV disease progression.
38 bout the effect of hepatitis co-infection on HIV disease progression.
39 se alleles appear equally protective against HIV disease progression.
40 1 patients, has been suggested to accelerate HIV disease progression.
41 are the HLA alleles most protective against HIV disease progression.
42 generalized immune activation and accelerate HIV disease progression.
43 ciated CD4(+) T-cell decline, a predictor of HIV disease progression.
44 GF-basic) cytokines that have been linked to HIV disease progression.
45 or the striking age-dependent differences in HIV disease progression.
46 ial examining the effect of multivitamins on HIV disease progression.
47 tract dysfunction may influence the rate of HIV disease progression.
48 reduce the risk of HIV infection and/or slow HIV disease progression.
49 healthcare, GO does not play a major role in HIV disease progression.
50 immunodeficiency virus (HIV) load and slower HIV disease progression.
51 ne activation might be of benefit in slowing HIV disease progression.
52 n suggested to underlie important aspects of HIV disease progression.
53 ter breastfeeding cessation affects maternal HIV disease progression.
54 ric deworming of adults with HIV in delaying HIV disease progression.
55 sensitivity responses in healthy persons and HIV disease progression.
56 flicting reports regarding effects of HCV on HIV disease progression.
57 IV) infection and are highly correlated with HIV disease progression.
58 AART) when estimating the effect of HAART on HIV disease progression.
59 , they suggest HIV-Tat as a key regulator of HIV disease progression.
60 ed with better pregnancy outcomes and slowed HIV disease progression.
61 that stress and depression have an impact on HIV disease progression.
62 f pregnancy on human immunodeficiency virus (HIV) disease progression.
63 nd accelerated human immunodeficiency virus (HIV) disease progression.
64 of accelerated human immunodeficiency virus (HIV) disease progression.
65 mic failure in human immunodeficiency virus (HIV) disease progression.
66 mechanisms of human immunodeficiency virus (HIV) disease progression.
67 ce the rate of human immunodeficiency virus (HIV) disease progression.
69 al response serves as an immune correlate of HIV disease progression and a potential qualifying facto
70 antigen specific CD4 T cell activation with HIV disease progression and AIDS-related central nervous
71 te antigen (HLA) alleles have been linked to HIV disease progression and attributed to differences in
72 cy virus (HIV), but its long-term effects on HIV disease progression and comorbidities are unknown.
73 could be a target for interventions to slow HIV disease progression and extend the time before use o
75 L2 genotypes are independent determinants of HIV disease progression and heterozygosity for MBL2 codi
79 thy, all of which are key factors that drive HIV disease progression and non-HIV comorbidities; howev
81 ne treatment experience demonstrated reduced HIV disease progression and reduced mortality with PI tr
83 iretroviral therapy (ART) adherence predicts HIV disease progression and survival, but its effect on
86 y aims to identify the mucosal correlates of HIV disease progression and to determine the molecular c
89 nts and reduce human immunodeficiency virus (HIV) disease progression and mortality among individuals
90 ed as an appropriate surrogate end point for HIV disease progression, and it is currently used as the
92 ve at reducing infectious disease morbidity, HIV disease progression, and poor pregnancy outcomes in
93 ship between the number of circulating IPCs, HIV disease progression, and the occurrence of HIV-relat
95 oire diversity changes in whole blood during HIV disease progression are primarily the result of chan
96 t predictor of human immunodeficiency virus (HIV) disease progression are needed for individuals init
97 nvolved in the increased HIV replication and HIV disease progression associated with multiple opportu
98 oral triple therapy is effective at halting HIV disease progression, but can have toxic effects and
99 rts to be associated with protection against HIV disease progression, but studies have been limited b
100 and B*57 are often associated with a delayed HIV disease progression, but the exact correlates that p
101 unodeficiency virus (HIV) RNA level predicts HIV disease progression, but the extent to which it expl
102 re focus on HLA-B*14, which protects against HIV disease progression, but the immunodominant HLA-B*14
103 function, measured by sj/beta-TREC ratio, in HIV disease progression by analyzing a large number of p
104 Variability in human immunodeficiency virus (HIV) disease progression cannot be fully predicted by CD
106 or more in the treatment group had a reduced HIV disease progression compared with those in the place
107 oms among women with HIV are associated with HIV disease progression, controlling for clinical, subst
108 ns who have stable CD4+ T-cell counts and no HIV disease progression despite years of HIV infection -
109 levels were conducted along with markers of HIV disease progression, epithelial gut damage, bacteria
110 REG3alpha plasma levels were compared with HIV disease progression, epithelial gut damage, microbia
111 stemic immune responses could play a role in HIV disease progression, especially in the early stages
112 n follow-up, 15 months), and there were 2374 HIV disease progression events and 453 observed deaths (
115 we examined potential correlates of delayed HIV disease progression in 51 HIV-1-infected African chi
116 fect of empiric deworming in the delaying of HIV disease progression in adults with HIV in an area wh
117 Alternative approaches are needed to delay HIV disease progression in areas where co-infections are
119 cted tissues and could potentially influence HIV disease progression in coinfected individuals throug
120 e potential contribution of viral factors to HIV disease progression in eight infants selected from a
123 A3G's contribution to the protection against HIV disease progression in humans, we quantified hA3G mR
125 pecific CTL contribute to protection against HIV disease progression in infected individuals with B*3
126 n plasma cytokine expression and the rate of HIV disease progression in South African women who seroc
128 ith higher T-cell immune activation and with HIV disease progression in treated and untreated individ
129 enotype has been associated with the rate of HIV disease progression in untreated patients, little is
131 sibly IGF-I) are associated with the rate of HIV disease progression in women and, more broadly, that
133 cceleration of human immunodeficiency virus (HIV) disease progression in women who have a pregnancy w
136 e of the major structural gene gagIMPORTANCE HIV disease progression is known to differ between indiv
137 ment of TB, the effect of underlying LTBI on HIV disease progression is less well characterized, in p
138 , the HLA-B*14-associated protection against HIV disease progression is significantly greater for HLA
139 , if infection ensues, that slow the rate of HIV disease progression is still incomplete and will req
141 determinant of human immunodeficiency virus (HIV) disease progression, is the result of a complex int
142 the morbidity and mortality associated with HIV disease progression, it has also provided new avenue
143 surements have been central to understanding HIV disease progression, making important clinical decis
144 aboratory markers currently used to evaluate HIV disease progression may be associated with subsequen
145 rks offer further support to the notion that HIV disease progression may be dependent on complex inte
146 d effector memory subsets and correlate with HIV disease progression, measured by viral load, CD4 per
149 the HLA-B locus has the strongest impact on HIV disease progression of any polymorphisms within the
151 Similar effects were noted for late-stage HIV disease progression on information processing speed
153 supplements did not result in a decrease in HIV disease progression or death but may have resulted i
156 n during and after pregnancy did not improve HIV disease progression or pregnancy outcomes, but may i
157 onths) showed a significantly higher risk of HIV-disease progression or death in patients receiving z
159 s that may contribute to the pathogenesis of HIV disease progression, pathways that might not be a di
161 iation of these discrete HLA supertypes with HIV disease progression rates in a population of HIV-inf
163 macrophages in human immunodeficiency virus (HIV) disease progression remains incompletely defined.
164 ated with slow human immunodeficiency virus (HIV) disease progression, supporting the important role
165 ee virus in BALF was a stronger predictor of HIV disease progression than was lymphocytic alveolitis.
166 Given their utility as surrogate markers of HIV disease progression, this suggests limited evidence
167 the pre-ART era, wasting was associated with HIV disease progression to acquired immunodeficiency syn
168 infection and human immunodeficiency virus (HIV) disease progression, two studies were done among a
170 deficiency virus (HIV) type 1 RNA levels and HIV disease progression was assessed in a cohort of 109
172 on of CCR5) in human immunodeficiency virus (HIV) disease progression was studied in 132 white HIV ty