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1 components underlying ongoing activation in HIV infection.
2 d with bladder cancer and increased risk for HIV infection.
3 l-molecule inhibitors of LIMK for inhibiting HIV infection.
4 g unprecedented insights into the biology of HIV infection.
5 lope proteins (Envs) play a critical role in HIV infection.
6 revent disease progression, it does not cure HIV infection.
7 o optimize clinical outcomes in persons with HIV infection.
8 cells in response to TCR stimulation and/or HIV infection.
9 s one of the earliest pathological events in HIV infection.
10 with men, particularly those with coexistent HIV infection.
11 advances in the prevention and treatment of HIV infection.
12 ing host immune homeostasis with and without HIV infection.
13 PrEP over 48 weeks in U.S. women at risk for HIV infection.
14 molecules inside the target cell that fight HIV infection.
15 or differentiation as well as for productive HIV infection.
16 ed approaches to treatment and prevention of HIV infection.
17 stable correlates of protection from initial HIV infection.
18 sent during pathogenic conditions, including HIV infection.
19 terest in using antibodies to treat and cure HIV infection.
20 nfected with HIV, and 283 were controls with HIV infection.
21 se by women at substantial risk of acquiring HIV infection.
22 development of lung cancer in the setting of HIV infection.
23 hieve greater reductions in the incidence of HIV infection.
24 in ECs than in subjects with typical chronic HIV infection.
25 test (Alere HIV Combo) for the diagnosis of HIV infection.
26 or IFN-I blockade as a potential therapy for HIV infection.
27 rus replication in a murine model of chronic HIV infection.
28 ietic stem cells in conferring resistance to HIV infection.
29 as new NNRTIs for the potential treatment of HIV infection.
30 r their incorporation into the management of HIV infection.
31 s mediate long-range GJ communication during HIV infection.
32 n models to identify correlates of prevalent HIV infection.
33 mong participants without hepatitis C and/or HIV infection.
34 ident a suspected exposure did not result in HIV infection.
35 have a major contribution to host control of HIV infection.
36 e used to eliminate persistent reservoirs of HIV infection.
37 nts, and was more frequent among people with HIV infection.
38 neuropathy is a neurological complication of HIV infection.
39 SF characteristics, compared with absence of HIV infection.
40 istant variants in participants with chronic HIV infection.
41 te relationships between gender identity and HIV infection.
42 ormalities in brain structure in relation to HIV infection.
43 losis immunity at the site of disease during HIV infection.
44 min quotient (QAlb) in patients with primary HIV infection.
45 t of excess adiposity in adults with treated HIV infection.
46 cells and eradicate persistent reservoirs of HIV infection.
47 production and immune activation in chronic HIV infection.
48 ssociated with both human papillomavirus and HIV infection.
49 y place them at a particularly high risk for HIV infection.
50 It is not yet possible to cure HIV infection.
51 -dimer, and HA levels were elevated in acute HIV infection.
52 in part, on their perceived risk of incident HIV infection.
53 ion and is a central obstacle to the cure of HIV infection.
54 ctivate CD4(+) T cells, the target cells for HIV infection.
55 ongitudinal observational studies of primary HIV infection.
56 ipants were not necessarily at high risk for HIV infection.
57 ong three case-control sets of children with HIV infection.
58 learance strategies to eradicate established HIV infection.
59 (9.8) years, 97.0% were male, and 32.2% had HIV infection.
60 e-exposure prophylaxis for the prevention of HIV infection.
61 cs against CNS complications associated with HIV infection.
62 rovirals for use in therapy or prevention of HIV infection.
63 ell as the presence of disability-associated HIV infection.
64 of Gag peptides in the long-term control of HIV infection.
65 ancy to achieve the elimination of pediatric HIV infections.
66 nd to identify predictors of newly diagnosed HIV infections.
67 acquisition of human immunodeficiency virus (HIV) infection.
68 dividuals with human immunodeficiency virus (HIV) infection.
69 rue in chronic human immunodeficiency virus (HIV) infection.
70 d mortality in human immunodeficiency virus (HIV) infection.
71 patients with human immunodeficiency virus (HIV) infection.
72 lth effects of human immunodeficiency virus (HIV) infection.
73 mian (SIV) and human immunodeficiency virus (HIV) infections.
74 s than 1% reported ever being diagnosed with HIV infection (0.9%, 95% CI 0.4-2.5) and initiated antir
75 es not infected with HIV, 75 were cases with HIV infection, 1118 were controls not infected with HIV,
77 ( pound1.0 billion discounted), avert 25% of HIV infections (42% of which would be directly because o
78 ngs suggest that within the first year after HIV infection, a relatively weak neutralizing antibody r
80 or sustain disparities in the prevalence of HIV infection, alone or in conjunction with scenarios of
81 rtant to immune control of HIV.IMPORTANCE In HIV infection, although cytotoxic T lymphocytes (CTL) pl
82 for live births, the incidence of perinatal HIV infection among infants born in the United States in
83 study of the natural and treated history of HIV infection among men who have sex with men in the USA
84 he change in community burden of undiagnosed HIV infection among older children and adolescents follo
85 e strongly associated with increased risk of HIV infection among participants with disabilities but n
87 ll as psychosocial and behavioral drivers of HIV infection among transgender women compared with cisg
88 an outbreak of human immunodeficiency virus (HIV) infection among persons who inject drugs (PWID) in
90 of undiagnosed human immunodeficiency virus (HIV) infections among persons who inject drugs (PWID) wa
96 n to its direct morbidity, increases risk of HIV infection and can cause lifelong morbidity in childr
99 athia, and other anaerobes) inflammation and HIV infection and found that high-risk bacteria increase
101 than non-users, the direct impact of METH on HIV infection and its link to the development of neuroco
106 e I interferon (IFN) is induced early during HIV infection and that type I IFN-associated gene signat
107 nv identified in our work seem to facilitate HIV infection and therefore may constitute a new therape
108 be preferred to avoid missing cases of acute HIV infection and to decrease the related risks of viral
109 ence, patients present to care with advanced HIV infection and with a low CD4 cell count or re-presen
111 e collected from local youth at high risk of HIV infection and, specifically, sexual minority males o
113 mon in treated human immunodeficiency virus (HIV) infection and contribute to morbidity and mortality
115 ssues are major primary target cells for SIV/HIV infection, and massive depletion of these cells is c
116 e is highly effective against acquisition of HIV infection, and only two cases of infection with a mu
117 criteria (ie, brain metastases, minimum age, HIV infection, and organ dysfunction and prior and concu
118 b induction and maturation in the setting of HIV infection, and point to key roles for both central a
120 APOL1 renal risk variants in the context of HIV infection, antiretroviral therapy-related nephrotoxi
122 ld be sustainable in the context of vertical HIV infection as repeated testing would not be necessary
123 ralizing antibodies in the immune control of HIV infection as well as for the development of effectiv
124 t disabilities reflects a higher exposure to HIV infection as well as the presence of disability-asso
126 ns can confer protection in animal models of HIV infection at modest concentrations, inspiring effort
127 costs (in 2015 US dollars), health outcomes (HIV infections averted, change in HIV prevalence, and di
128 pheresis from a 55-year-old man with chronic HIV infection before and after allo-SCT to measure the s
130 s the abnormalities in B cells that occur in HIV infection both in the peripheral blood and lymphoid
131 line of iNKT cells is associated with age or HIV infection, both situations associated with HHV-8-rel
132 ine has identified host factors required for HIV infection but dispensable for cellular survival.
134 loss occurs in human immunodeficiency virus (HIV) infection but paradoxically is intensified by HIV-a
135 -specific CD4+ T cells in blood during early HIV infection, but little is known about responses in th
136 ceptors augments CD8 T cell functionality in HIV infection, but their influence on CD4 T cells remain
137 for preventing human immunodeficiency virus (HIV) infection, but risk compensation (RC) in men who ha
138 ong women with human immunodeficiency virus (HIV) infection, but whether the risk differs by ART regi
139 irus (HCV) and human immunodeficiency virus (HIV) infections, but the independent contributions of HC
143 We assessed predictors of newly diagnosed HIV infections by comparing newly diagnosed with HIV-neg
144 during primary human immunodeficiency virus (HIV) infection by evaluating the cerebrospinal fluid (CS
145 n the USA, we examined the effect of ageing, HIV infection (by disease stage), and their interaction
146 o reduce leukocyte mobilization during early HIV infection, can provide prolonged neuroprotection, wh
149 Nevertheless, in individuals with aTB and/or HIV infection, circulating ex vivo M. tuberculosis-speci
153 syringes, and the proportion of undiagnosed HIV infection declined from 84.3% to 15.0% (P < .001).
154 In this longitudinal study, the incidence of HIV infection declined significantly with the scale-up o
155 A total of 236 (37.5%) of the mothers had HIV infection diagnosed before pregnancy in 2002-2005 co
156 o blockade of IFN-I signaling during chronic HIV infection diminished HIV-driven immune activation, d
158 dence is markedly elevated among people with HIV infection, especially in MSM, older individuals, and
159 ents with co-infection (hepatitis B virus or HIV infection), evidence of decompensated liver disease,
160 h condomless receptive anal sex, the odds of HIV infection for transgender women were 2.2 times great
161 the course of Human Immunodeficiency Virus (HIV) infection from an almost universally fatal disease
164 ease (CHD) and human immunodeficiency virus (HIV) infection has been well recognized for many years.
169 uscript, we demonstrate that TNTs induced by HIV infection have functional GJs at the ends of their m
171 he participants' history of tuberculosis and HIV infection, hospitalizations, and social networks.
173 als, although the precise mechanisms whereby HIV infection impedes successful T cell-mediated control
174 8(+) T cells in elite controllers to inhibit HIV infection.IMPORTANCE The greater ex vivo antiviral i
175 rus-specific CD8 T cells with progression of HIV infection in humans and during chronic lymphocytic c
179 INTERPRETATION: The higher prevalence of HIV infection in people with disabilities than people wi
180 abeys or mandrills (SIVrcm/mnd-2), increased HIV infection in resting CD4 T cells, but not in macroph
181 intrahost evolutionary patterns during human HIV infection in the absence of antiretroviral therapy.
182 e associated with reduced risk of peripartum HIV infection in the historic U.S. Woman and Infant Tran
183 counted for 687 (38.0%) of infants born with HIV infection in the United States during the overall pe
186 g women detected during Fiebig stage I acute HIV infection in whom treatment was initiated immediatel
187 Furthermore, we assessed to which extent HIV infection in women is associated with maternal recto
193 Sub-Saharan Africa has decreased lately, new HIV infections in the Middle East and North Africa regio
195 be a consideration in treatment choices for HIV infection, including the choices of antiretroviral r
198 ecognized that human immunodeficiency virus (HIV) infection increases the risk of developing TB, but
205 ted partner services for index patients with HIV infections involves elicitation of information about
206 Ts) used for early infant diagnosis (EID) of HIV infection is <100%, leading some HIV-uninfected infa
212 chronic human immunodeficiency virus type 1 (HIV) infection is a key mechanism that leads to the deve
214 trol of human immunodeficiency virus type 1 (HIV) infection is typically associated with effective Ga
215 nalysis can estimate the probable country of HIV infection, it can help to inform the design of publi
216 for a functional cure or the eradication of HIV infection, it is necessary to know the sizes of the
219 , suggesting that its down-regulation during HIV infection may be part of an anti-viral host response
220 and the relationships to viral load in acute HIV infection, measurements of the latent reservoir in c
221 lb was elevated in 106 patients with primary HIV infection (median time of measurement, 91 days after
222 nalysis and the resulting data regarding how HIV infection might change the balance of commensal bact
226 MK1) with short hairpin RNA (shRNA) inhibits HIV infection, no specific small-molecule inhibitor of L
227 ation.IMPORTANCE More than 150,000 pediatric HIV infections occur yearly, despite the availability of
233 ent study, we hypothesized that METH impacts HIV infection of neural progenitor cells (NPCs) by a mec
234 myeloid-only mice (MoM), we demonstrate that HIV infection of tissue macrophages is rapidly suppresse
236 or anal intercourse with at least 1 man with HIV infection or unknown serostatus within 90 days.
237 l transduction and autophagy in single-round HIV infection or with nonreplicative HIV-1-derived lenti
244 se progression to AIDS in infants.IMPORTANCE HIV infection progresses much more rapidly in pediatric
245 d may reduce viral reservoirs during chronic HIV infection, providing validation for IFN-I blockade a
246 The main model outcomes were the number of HIV infections, quality-adjusted life-years (QALYs), and
247 -five patients with stage I to III SCCAC and HIV infection received CRT: 45 to 54 Gy radiation therap
252 HIV DNA-containing cells.IMPORTANCE Cure of HIV infection requires an intervention that reduces the
253 Blocking or reducing GJ communication during HIV infection resulted in aberrant TNT cell-to-cell cont
254 dividuals with human immunodeficiency virus (HIV) infection, resulting in death in approximately 40%
255 esistant to nucleoside analogs used to treat HIV infections reveal that the ground state binding is w
256 e members with human immunodeficiency virus (HIV) infection revealed 19 (18.6%) cases of M. genitaliu
257 tive tract (FRT) is hypothesized to increase HIV infection risk by interfering with barrier protectio
258 , even among US black women at high risk for HIV infection, sample size requirements for an RCT with
259 usceptibility of people with disabilities to HIV infection seems to be shaped by social and environme
261 duodenum were studied at different stages of HIV infection, starting from the seronegative phase.
262 There was no significant association between HIV infection status and rectovaginal GBS carriage.
265 y and motor function with advanced stages of HIV infection suggests that these two domains are most s
266 To be considered for HCT, patients must have HIV infection that is responsive to combination antiretr
267 5, among 573 ART-naive PWUD (18% with recent HIV infection), the overall TDR prevalence was 9.8% (95%
269 with advanced human immunodeficiency virus (HIV) infection, the rate of death from infection (includ
271 r already in the seronegative phase of acute HIV infection, thereby inducing microbial translocation
272 HCV infected subjects who developed incident HIV infection to determine if IL-18 increases with coinf
273 ne resistance testing early in the course of HIV infection to guide ART selection among PWUD in our s
274 isease (including hemodialysis patients), or HIV infection; travelers to HBV-endemic regions; and adu
275 integration of fungal diseases into existing HIV infection, tuberculosis infection, diabetes, chronic
276 inistered by injection that prevented simian-HIV infection upon repeat intrarectal challenge in male
278 ll detection rate of people unaware of their HIV infection was 0.5 persons per day, and the detection
280 R3(+)CCR6(+)CCR4(-) (Th1*) phenotype, aTB or HIV infection was associated with a contraction of this
288 nodeficiency virus (HIV) on the incidence of HIV infection, we analyzed the association between the i
289 CD4(+) T cell memory inflation occurs during HIV infection, we used HLA-DR7 (DRB1*07:01) tetramers lo
290 eir HIV status, 90% of people with diagnosed HIV infection will receive antiretroviral treatment (ART
292 ared with uninfected individuals, those with HIV infection with a recent biomarker of more severe imm
293 compare anal cancer incidence in people with HIV infection with the general population, used Poisson
294 losis deaths worldwide were in children with HIV infections, with 31 000 (36%, 19 000-59 000) in the
295 as this subtype accounts for the majority of HIV infections worldwide, but well-ordered clade C Env t
298 etermine whether ART initiation during acute HIV infection would attenuate changes in these biomarker
299 eceptors CD4 and CCR5, that are required for HIV infection yet are dispensable for cellular prolifera
300 sion, and T cell exhaustion are hallmarks of HIV infection, yet the mechanisms driving these processe
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