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1 nity are still ambiguous during experimental visceral leishmaniasis.
2 mania donovani, causative agent of the fatal visceral leishmaniasis.
3 protozoa, Leishmania donovani chagasi causes visceral leishmaniasis.
4 r systematic subunit vaccine testing against visceral leishmaniasis.
5 that are used to treat the parasitic disease visceral leishmaniasis.
6 herapeutic design and vaccine strategies for visceral leishmaniasis.
7 it with IL-4, plays a protective role during visceral leishmaniasis.
8 Leishmania donovani, the causative agent of visceral leishmaniasis.
9 on into skin but disseminates to cause fatal visceral leishmaniasis.
10 a live attenuated vaccine candidate against visceral leishmaniasis.
11 evelopment of new therapeutic agents against visceral leishmaniasis.
12 ve agent of the tropical infectious disease, visceral leishmaniasis.
13 mployed a well-defined experimental model of visceral leishmaniasis.
14 pool of sera from Brazilians with documented visceral leishmaniasis.
15 shmania chagasi, the cause of South American visceral leishmaniasis.
16 ing host immunity and liver pathology during visceral leishmaniasis.
17 d vaccinia virus-based vaccine against human visceral leishmaniasis.
18 it causes cutaneous, diffuse cutaneous, and visceral leishmaniasis.
19 ive CD8(+) T cells after vaccination against visceral leishmaniasis.
20 e pathogenesis as well as vaccine studies of visceral leishmaniasis.
21 se reported for subclinical canine and human visceral leishmaniasis.
22 orrelated with the probability of developing visceral leishmaniasis.
23 e immunity to Leishmania chagasi, a cause of visceral leishmaniasis.
24 tion is a risk factor for the development of visceral leishmaniasis.
25 the results of a vaccine trial against human visceral leishmaniasis.
26 of new drug targets and their inhibitors for visceral leishmaniasis.
27 inst parasite challenge in a murine model of visceral leishmaniasis.
28 with the life-threatening disease now called visceral leishmaniasis.
29 We tested this strategy in a murine model of visceral leishmaniasis.
30 ally) represent a major advance for treating visceral leishmaniasis.
31 ognostic utility of rK39 in detecting active visceral leishmaniasis.
32 pproved oral drug for treating cutaneous and visceral leishmaniasis.
33 activated late in the course of experimental visceral leishmaniasis.
34 of this strategy to reduce the incidence of visceral leishmaniasis.
35 l drugs have long been the mainstay to treat visceral leishmaniasis.
36 sized and tested against the murine model of visceral leishmaniasis.
37 perties to enter preclinical development for visceral leishmaniasis.
38 ortisol levels have also been found in human visceral leishmaniasis.
39 stage of infection, causing life-threatening visceral leishmaniasis.
40 manifesting as cutaneous, mucocutaneous, and visceral leishmaniasis.
41 iltefosine for Eastern African children with visceral leishmaniasis.
42 frequently after apparent clinical cure from visceral leishmaniasis.
43 al leishmaniasis (PKDL), clinical sequela of visceral leishmaniasis.
44 ted in cultures recovered from patients with visceral leishmaniasis.
45 No vaccine exists against visceral leishmaniasis.
46 d immunity and subsequent protection against visceral leishmaniasis.
47 parasites, in a Brazilian city endemic with visceral leishmaniasis.
48 ense regulation in the liver in experimental visceral leishmaniasis.
49 ni and L. infantum - cause the fatal disease visceral leishmaniasis.
50 L. donovani, the etiological agent of deadly visceral leishmaniasis.
51 ed 287 individuals, including 77 with active visceral leishmaniasis, 26 with post-kala-azar dermal le
53 these events, their role remains elusive in visceral leishmaniasis, a disease associated with macrop
54 plicated in the clinical expression of human visceral leishmaniasis, a disease-exacerbating T helper
56 establish models for studying recurrence of visceral leishmaniasis, a growing problem in T cell-defi
57 for controlling and preventing the spread of visceral leishmaniasis, a major public health concern in
58 histosomiasis, onchocerciasis, trachoma, and visceral leishmaniasis, a mean delay of 2-3 years for a
60 Africa is the world region most affected by visceral leishmaniasis, accounting for 45% of cases glob
63 nducted a Phase II trial in 30 children with visceral leishmaniasis, aged 4-12 years, to test whether
65 d, may be the first effective oral agent for visceral leishmaniasis, an intracellular protozoal infec
66 ishmania donovani parasites are the cause of visceral leishmaniasis and are transmitted by bites from
67 IL-17A is present in sera from patients with visceral leishmaniasis and decreases after successful tr
68 ctivation observed in patients with American visceral leishmaniasis and human immunodeficiency virus
69 Leishmania donovani is the dermal sequel of Visceral Leishmaniasis and importantly, is the proposed
70 d key roles in promoting inflammation during visceral leishmaniasis and malaria-two important parasit
71 e findings confirm that patients with active visceral leishmaniasis and patients with post-kala-azar
74 phatic filariasis, trachoma, onchocerciasis, visceral leishmaniasis, and gambiense sleeping sickness)
75 phatic filariasis, onchocerciasis, trachoma, visceral leishmaniasis, and human African trypanosomiasi
76 ing effects regulate outcome in experimental visceral leishmaniasis, and IL-10R blockade represents a
77 Leishmania donovani, the causative agent of visceral Leishmaniasis, and Leishmania tropica, the caus
78 me and response to treatment of experimental visceral leishmaniasis, and MAb targeting of T-cell cost
79 ania donovani, the main etiological agent of visceral leishmaniasis, and the autophagic machinery of
80 esponses are critical for the progression of visceral leishmaniasis, and the pleiotropic cytokine int
81 may overcome compromised T cell responses in visceral leishmaniasis, and this has an important implic
83 rotection found in vaccine studies of murine visceral leishmaniasis are significantly lower than for
85 ng diseases (gambiense sleeping sickness and visceral leishmaniasis) are likely to have fewer cases b
86 of Leishmania donovani, the causal agent of visceral leishmaniasis, are conditionally lethal mutatio
87 eglected tropical diseases aims to eliminate visceral leishmaniasis as a public health problem and to
91 ite burden in a 45-day BALB/c mouse model of visceral leishmaniasis at a dosage of 10 mg/kg/day as de
92 bundant in bone marrows of humans with acute visceral leishmaniasis but not in those of uninfected co
95 ote intracellular infection, including human visceral leishmaniasis, by disabling Th1 cell-type respo
96 -beta inhibits Th1-associated cure of murine visceral leishmaniasis caused by L. chagasi, independent
97 ature of many infectious diseases, including visceral leishmaniasis caused by Leishmania donovani.
98 of IL-10 in susceptibility to cutaneous and visceral leishmaniasis caused by Leishmania major and Le
102 Progressive disease in the hamster model of visceral leishmaniasis, caused by Leishmania donovani, i
104 eglected tropical diseases by WHO, including visceral leishmaniasis, Chagas disease, strongyloidiasis
106 hough human immunodeficiency virus (HIV) and visceral leishmaniasis coinfection is recognized as a ma
108 eishmania donovani, the etiological agent of visceral leishmaniasis, confer polyamine auxotrophy to t
111 ible factor 1 alpha in BALB/c mouse model of visceral leishmaniasis decreased liver and spleen parasi
112 rial splenic aspirates from 27 patients with visceral leishmaniasis during monotherapy with interfero
113 y, transmission competence and the impact of visceral leishmaniasis elimination campaigns.Parasitemia
114 -line treatment in different formulations in visceral leishmaniasis endemic areas of Bihar, India.
115 protozoan parasites, the causative agent of visceral leishmaniasis, establish an infection partly by
116 h receptors potential therapeutic targets in visceral leishmaniasis for engagement (TLR4) or blockade
119 ted Leishmania donovani (LdCen(-/-)) against visceral leishmaniasis has been reported extensively.
122 However, in contrast to its role in human visceral leishmaniasis, IL-10 may not play a key immunos
124 of such polarized CD4(+) T cells facilitates visceral leishmaniasis in BALB/c mice in a clear contras
125 077 patients aged >/=14 years with confirmed visceral leishmaniasis in Bihar, eastern India, found th
126 etween IL-2R mutations and susceptibility to visceral leishmaniasis in children infected with Leishma
130 nvenient, safe, and effective treatments for visceral leishmaniasis in Eastern African children are l
133 is from dogs with clinical manifestations of visceral leishmaniasis in Governador Valadares, an endem
134 This study is nested within the Predicting Visceral Leishmaniasis in HIV-InfectedPatients (PreLeisH
135 ys using crude antigens for the diagnosis of visceral leishmaniasis in human immunodeficiency virus t
136 hmania donovani, the main causative agent of visceral leishmaniasis in humans, and successfully appli
142 ling framework for analyzing the dynamics of visceral leishmaniasis in the Indian sub-continent (VL),
145 ling but scarring cutaneous lesions to fatal visceral leishmaniasis in which parasites disseminate to
148 with cutaneous, visceral, and post-kala azar visceral leishmaniasis indicated that a majority of indi
156 sness of patients for the sand fly vector of visceral leishmaniasis is linked to parasites found in t
160 unity and pathogen clearance in experimental visceral leishmaniasis (Leishmania donovani) but more se
161 In stark contrast, the causative agent of visceral leishmaniasis, Leishmania donovani, does not pr
163 from self-healing cutaneous lesions to fatal visceral leishmaniasis, mucosal leishmaniasis and diffus
164 shmania chagasi, the cause of South American visceral leishmaniasis, must survive antimicrobial respo
165 ed on an index patient with thymoma, chronic visceral leishmaniasis, myasthenia gravis, and a marked
168 ed patients with clinically confirmed active visceral leishmaniasis or post-kala-azar dermal leishman
169 sness to the sandfly vector of patients with visceral leishmaniasis or post-kala-azar dermal leishman
170 oint was the proportion of participants with visceral leishmaniasis or post-kala-azar dermal leishman
172 ases, such as invasive fungal infections and visceral leishmaniasis, particularly for patients who ar
173 he relevance of asymptomatic and symptomatic visceral leishmaniasis patients as infection reservoirs.
175 hat selection for parasite resistance within visceral leishmaniasis patients who have been exposed to
179 also displayed efficacy in a murine model of visceral leishmaniasis, reducing liver parasitemia by 37
181 encing of TCTP in an infected mouse model of visceral leishmaniasis showed decreased parasite burden
182 ansmitted helminthiases (STH), trachoma, and visceral leishmaniasis, shows that the impact of this di
183 taneous leishmaniasis and a hamster model of visceral leishmaniasis, soluble antigen induces a leishm
185 -HLA-DQA1 HLA class II region contributes to visceral leishmaniasis susceptibility in India and Brazi
187 5 mm) had a significantly lower frequency of visceral leishmaniasis than non-responders (27/375 [7.2%
189 , suggesting shared genetic risk factors for visceral leishmaniasis that cross the epidemiological di
191 ce of kala-azar, a clinical manifestation of visceral leishmaniasis, to below 1 in 10,000 by 2020.
193 lent, faces the highest burden world-wide of visceral leishmaniasis (VL) and human immunodeficiency v
194 Little is known about CD8 T cells in human visceral leishmaniasis (VL) and it is unclear if these c
195 ds to analyze longitudinal incidence data on visceral leishmaniasis (VL) and its sequela, post-kala-a
196 another promising preclinical candidate for visceral leishmaniasis (VL) and, in combination with ben
197 +) T cell effector responses during clinical visceral leishmaniasis (VL) are associated with elevated
199 emic spread of Leishmania parasites in human visceral leishmaniasis (VL) are not well understood.
200 -27/TCCR pathway in the host defense against visceral leishmaniasis (VL) by monitoring the course of
203 miR-21 in regulating immune responses during visceral leishmaniasis (VL) caused by Leishmania donovan
205 l ibrutinib as a host-targeted treatment for visceral leishmaniasis (VL) caused by Leishmania donovan
206 eport a detrimental role of Ly6C(hi) iMOs in visceral leishmaniasis (VL) caused by Leishmania donovan
207 is also a vaccine antigen candidate against visceral leishmaniasis (VL) caused by Leishmania infantu
210 immunodeficiency virus (PWH) with recurrent visceral leishmaniasis (VL) could potentially drive Leis
212 , sodium stibogluconate) in the treatment of visceral leishmaniasis (VL) has fallen from more than 85
213 r residual spraying (IRS) is used to control visceral leishmaniasis (VL) in India, but it is poorly q
214 ne had demonstrated very good cure rates for visceral leishmaniasis (VL) in India, Nepal, and Banglad
216 s study was to identify the risk factors for visceral leishmaniasis (VL) in renal transplant recipien
218 with human immunodeficiency virus (HIV) and visceral leishmaniasis (VL) in the VL-endemic areas of B
220 sed approach to identify infected cells in a visceral leishmaniasis (VL) infection, which revealed pa
238 high miltefosine treatment failure rates for visceral leishmaniasis (VL) on the Indian subcontinent.
239 a dermal form of the disease, occurs in some visceral leishmaniasis (VL) patients following treatment
243 shmania parasites is critical for evaluating visceral leishmaniasis (VL) treatment response at an ear
244 ns of people across the world, in particular visceral leishmaniasis (VL) which is fatal unless treate
246 ficant number of individuals may progress to visceral leishmaniasis (VL), a deadly disease that threa
248 ere is an urgent need for new treatments for visceral leishmaniasis (VL), a parasitic infection which
249 percentage of people who have been cured of visceral leishmaniasis (VL), and it contributes to trans
250 KDL) are usually extrapolated from those for visceral leishmaniasis (VL), but drug pharmacokinetics (
253 leishmaniasis (PKDL), a cutaneous sequela of visceral leishmaniasis (VL), develops in some patients a
255 shmania donovani (LD), responsible for fatal visceral leishmaniasis (VL), faces increasing challenges
256 is (PKDL), a heterogeneous dermal sequela of visceral leishmaniasis (VL), is challenging in terms of
257 diseases tegumentary leishmaniasis (TL) and visceral leishmaniasis (VL), is comparatively less well
258 Miltefosine (MIL), the only oral drug for visceral leishmaniasis (VL), is currently the first-line
259 te Leishmania donovani, a causative agent of visceral leishmaniasis (VL), require a potent host proin
260 In Tbilisi, Georgia, an endemic area for visceral leishmaniasis (VL), sand flies are abundant for
264 velopment of new oral treatment regimens for visceral leishmaniasis (VL), there is a need for early m
265 to infection with L. donovani, the cause of visceral leishmaniasis (VL), was determined by Northern
267 oral drug available for treatment of Indian visceral leishmaniasis (VL), which was shown to have an
268 ent years to be highly efficient in treating visceral leishmaniasis (VL)-the life-threatening form of
281 no effective vaccine is available for human visceral leishmaniasis(VL) caused by Leishmania donovani
282 nsor construction, canine serum positive for visceral leishmaniasis was added to its surface and show
286 treatment of the neglected tropical disease visceral leishmaniasis, were identified in a phenotypic
287 245/DDD01305143, a preclinical candidate for visceral leishmaniasis which acted through inhibition of
288 nly orally bioavailable drug for the disease visceral leishmaniasis, which is caused by the protozoan
289 n African trypanosomiasis, Buruli ulcer, and visceral leishmaniasis, which relies on intensified dise
290 gnificant risk factor for the development of visceral leishmaniasis, which results from skin inoculat
291 ic test is the primary diagnostic method for visceral leishmaniasis, while cutaneous leishmaniasis is