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1 fection, or inhibitors significantly reduces cryptococcal ability to traverse the HBMEC monolayer, in
2 d IL-13) and IL-10 in lung leukocytes and in cryptococcal Ag-pulsed splenocytes, 3) diminished IgE pr
3 central nervous system (CNS) involvement are cryptococcal and coccidioidal, so CSF BG screening can b
4                                              Cryptococcal and nontuberculous mycobacterial infections
5 ced lateral flow immunoassay (LFA) to detect cryptococcal antigen (CRAG) is reportedly more rapid and
6                                          The cryptococcal antigen (CRAG) lateral flow assay (LFA) had
7                                          The cryptococcal antigen (CRAG) lateral flow assay (LFA) has
8              Retrospective data suggest that cryptococcal antigen (CrAg) screening in patients with l
9 ians with CD4 <150 cells/mL underwent plasma cryptococcal antigen (CRAG) screening.
10                         Geometric mean serum cryptococcal antigen (CRAG) titers in CNS disease were 5
11 th CD4 T-cell counts </=100 cells/microL for cryptococcal antigen (CrAg) using the CrAg lateral flow
12 x regression; longitudinal patterns in serum cryptococcal antigen (SCrAg) titers and the probability
13                   Prognostic implications of cryptococcal antigen and outcomes associated with centra
14 cultured for fungal organisms and tested for cryptococcal antigen by ELISA.
15 ity support consisted of screening for serum cryptococcal antigen combined with antifungal therapy fo
16 (95% CI 195 500-340 600) people positive for cryptococcal antigen globally and 223 100 (95% CI 150 60
17 l count <100 cells/microL and negative serum cryptococcal antigen initiating antiretroviral therapy i
18                                          The cryptococcal antigen lateral flow assay (CrAg LFA) was e
19 ens, which were originally negative with the Cryptococcal Antigen Latex Agglutination System (CALAS),
20 andard care group received a home visit or a cryptococcal antigen screen rather than only standard ca
21 nt clinic-based services combined with serum cryptococcal antigen screening.
22 or subsequent culture, should not be used if cryptococcal antigen testing is needed.
23  have late-onset disease, fungemia, or serum cryptococcal antigen titer more than 1:64 even in the pr
24 ttransplantation (late-onset disease), serum cryptococcal antigen titer more than 1:64, and fungemia
25 S<15 and these patients had lower median CSF cryptococcal antigen titers (P = .042) and CCL2 (P = .00
26 to develop IRS, irrespective of serum or CSF cryptococcal antigen titers and fungemia.
27 (DCs) can phagocytose C. neoformans, present cryptococcal antigen, and kill C. neoformans.
28 aining, acid-fast staining, and lactic acid, cryptococcal antigen, histoplasma antigen, herpes simple
29 ented by screening patients for sub-clinical cryptococcal antigenaemia (CRAG) at antiretroviral-thera
30                                              Cryptococcal antigenaemia prevalence by country was deri
31                                     Based on cryptococcal antigenaemia prevalence in each country and
32               We estimated an average global cryptococcal antigenaemia prevalence of 6.0% (95% CI 5.8
33                                              Cryptococcal antigenemia (CrAg+) in the absence of CM ca
34 cal meningitis and asymptomatic, subclinical cryptococcal antigenemia (CRAG+) is unknown.
35        Eleven participants (5%) had isolated cryptococcal antigenemia with a negative CSF CRAG and cu
36 talized with acute respiratory infection for cryptococcal antigenemia, even in the absence of meningi
37       Analysis with inhibitors revealed that cryptococcal association, invasion, and transmigration r
38 that defines the fungal-BBB interface during cryptococcal attachment to, and internalization by, the
39                       An unsolved problem in cryptococcal biology is whether the PSs composing the ca
40 ver, the molecular mechanism involved in the cryptococcal blood-brain barrier traversal is poorly und
41 EC monolayer, which is the critical step for cryptococcal brain infection and development of meningit
42 nd p38 MAPK, but not ERK activation, and the cryptococcal capsule blocked this extracellular recognit
43 ributes to the structure and function of the cryptococcal capsule is not known.
44 stand how chronological age could impact the cryptococcal capsule properties, we compared the elastic
45                                              Cryptococcal capsule size ex vivo is an important contri
46                           The ability of the cryptococcal capsule to activate the complement cascade
47  our understanding of a major polymer of the cryptococcal capsule.
48                   Our results establish that cryptococcal capsules are highly dynamic structures that
49            Additionally, Cin1 interacts with cryptococcal Cdc42 and Wsp1 (a WASP homologue) proteins
50 ess known as nonlytic exocytosis whereby the cryptococcal cell is released from the macrophage into t
51    This article reviews current knowledge of cryptococcal cell wall and capsule biosynthesis and outs
52 pase B1 (Plb1) enzyme, which is required for cryptococcal cell wall integrity and virulence, was redu
53 tigations of the role of alpha glucan in the cryptococcal cell wall.
54 opy revealed structural changes and ruptured cryptococcal cell walls following treatment.
55                                              Cryptococcal cells disrupted in their alpha glucan synth
56                                 Phagocytosed cryptococcal cells exhibited less viability than nonphag
57                                  A subset of cryptococcal cells in the lungs differentiate into enlar
58                                              Cryptococcal cells isolated from Anxa2-deficient (Anxa2(
59                             The inability of cryptococcal cells that lacked the Cch1-Mid1 channel to
60  pathogenesis-a balanced interaction between cryptococcal cells, macrophages, endothelial cells, and
61 the mammalian immune response to respiratory cryptococcal challenge remain poorly defined.
62 and macrophages), and, ultimately, effective cryptococcal clearance from the infected lungs.
63 thase and correlated with the known onset of cryptococcal clearance in this strain of mice.
64 ts in the stimulation of local Th1-type anti-cryptococcal CMI responses and the development of protec
65 cant differences in the rate of clearance of cryptococcal colony-forming units (CFU) in CSF samples a
66  neoformans, but ultimately has no effect on cryptococcal control by adaptive immunity.
67 y alveolar macrophages, critical elements in cryptococcal control.
68        In the present study, deletion of the cryptococcal copper-dependent transcription factor 1 (Cu
69 Participants receiving sertraline had faster cryptococcal CSF clearance and a lower incidence of immu
70 f available copper was constructed using the cryptococcal CUF1-dependent copper transporter, CTR4.
71  .0089) were lower in those who achieved CSF cryptococcal culture negativity compared to those with p
72 mined by results of serial, quantitative CSF cryptococcal cultures.
73 rated that osmotic lysis was responsible for cryptococcal death.
74 ting antiretroviral therapy (ART) may reduce cryptococcal disease and deaths.
75 g of the importance of antigen detection for cryptococcal disease and invasive aspergillosis, the use
76 e setting of opportunistic illnesses such as cryptococcal disease and tuberculosis.
77 -eight of those patients lacked a history of cryptococcal disease and were the focus of this study.
78 gs suggest that transplantation after recent cryptococcal disease may not be a categorical exclusion
79 ated immunity for resistance to the disease (cryptococcal disease) caused by Cryptococcus neoformans
80  IL-17 have been implicated in resistance to cryptococcal disease, but it is not clear whether IL-23-
81                                  Donors with cryptococcal disease, including those with unrecognized
82  analysis is often deferred in patients with cryptococcal disease, particularly in the absence of neu
83 substantial ongoing burden of HIV-associated cryptococcal disease, primarily in sub-Saharan Africa.
84 timate of global incidence of HIV-associated cryptococcal disease.
85 immunity places individuals at high risk for cryptococcal disease.
86 does not appear to be wholly attributable to cryptococcal disease.
87 ntigen (CrAg) is invaluable for establishing cryptococcal disease.
88 pathology, elevated serum IgE, fungemia, and cryptococcal dissemination in the central nervous system
89 , only surviving IL-17RA(-/-) mice exhibited cryptococcal dissemination to the blood.
90             In the absence of CD40, systemic cryptococcal dissemination was increased, and mice died
91 ed 79 whose silencing significantly affected cryptococcal engulfment.
92 ctivated effector phenotype characterized by cryptococcal-enhanced production of inducible nitric oxi
93                Our data identified the first cryptococcal gene associated with elevated intracranial
94 nase enzymes; however, blast searches of the cryptococcal genome were unable to identify any homologu
95  there is no cyclooxygenase homologue in the cryptococcal genome.
96 d was associated with higher serum titers of cryptococcal glucuronoxylomannan.
97         Survival of infected mice; pulmonary cryptococcal growth and pathology; immunological paramet
98                  Human pDCs can also inhibit cryptococcal growth by a mechanism similar to that of mu
99 more, deletion of CXT1 led to attenuation of cryptococcal growth in a mouse model of infection, sugge
100 emonstrate that CD40 helps limit progressive cryptococcal growth in the lung and protects against let
101 e fungistatic against C. neoformans, whereas cryptococcal growth was uncontrolled within macrophages
102 enzymes, specifically cathepsin B, inhibited cryptococcal growth.
103                     Characterizations of the cryptococcal hexokinases and trehalose mutants support t
104                  The incidence of recognized cryptococcal immune reconstitution inflammatory syndrome
105 emental cost-effectiveness ratio (ICER) of 3 cryptococcal induction regimens: (1) amphotericin B deox
106 cantly lower rates of tuberculosis (P=0.02), cryptococcal infection (P=0.01), oral or esophageal cand
107                            The prevalence of cryptococcal infection among advanced AIDS patients in t
108 gnificant differences in the pathogenesis of cryptococcal infection among inbred mice and associate t
109 rtant element of antifungal defenses against cryptococcal infection and CNS dissemination.
110 val infection model to assess the process of cryptococcal infection and disease development sequentia
111      We aimed to determine the prevalence of cryptococcal infection and outcomes of those infected am
112 nction of macrophages in normal clearance of cryptococcal infection and the defects present in uncont
113      Screening and pre-emptive treatment for cryptococcal infection combined with a short initial per
114 elation prior to establishing a diagnosis of cryptococcal infection for patients with first-time posi
115        BALB/c mice progressively cleared the cryptococcal infection in the lungs and showed a Th1-ske
116 immunophenotype that develops in response to cryptococcal infection in the lungs.
117                Thus, high-content imaging of cryptococcal infection in vivo demonstrates how very ear
118 tudy, we performed a comparative analysis of cryptococcal infection in wild-type versus CD40-deficien
119  that IL-23 dampens the allergic response to cryptococcal infection through IL-17-independent suppres
120 s suggest a role for ANXA2 in the control of cryptococcal infection, macrophage function, and fungal
121              We calculated those at risk for cryptococcal infection, specifically those with CD4 less
122  associations with clearance outcomes during cryptococcal infection, we compared C57BL/6, BALB/c, and
123 velopment of the adaptive immune response to cryptococcal infection, wild-type (TLR9+/+) and TLR9 kno
124  fungal control during the afferent phase of cryptococcal infection.
125 nts without meningitis are rarely tested for cryptococcal infection.
126 e cells to the initial host response against cryptococcal infection.
127 ungal expansion during the afferent phase of cryptococcal infection.
128  the deleterious effects of Th2 cells during cryptococcal infection.
129 nts with a CD4 count </=100 cells/microL for cryptococcal infection.
130  the global escalation of the AIDS pandemic, cryptococcal infections are increasing and are of signif
131                                              Cryptococcal infections are primarily caused by two rela
132  to play a major role in the pathogenesis of cryptococcal infections, including the enzyme phospholip
133 ctive host immunity against future pulmonary cryptococcal infections.
134 , a receptor not previously evaluated during cryptococcal infections.
135 o such damage, could be valuable in treating cryptococcal infections.
136 we identified a multi-modular protein, Cin1 (cryptococcal intersectin 1), whose domain structure is s
137                                              Cryptococcal Kcs1 converts IP6 to PP-IP5/IP7, but the ki
138                                              Cryptococcal killing by bone marrow-derived ExMs was CCR
139 se in proliferation and a 2-fold increase in cryptococcal killing within the phagosome.
140 ith its enzymatic inhibitors led to enhanced cryptococcal killing.
141 ted the role of Rac in NK cell mediated anti-cryptococcal killing.
142 depletion or genetic deletion of the primary cryptococcal laccase (lac1 Delta) resulted in a loss of
143                         Next we investigated cryptococcal laccase, an enzyme known to bind polyphenol
144 associated with central nervous system (CNS) cryptococcal lesions in solid organ transplant recipient
145           The comparison of brain and spleen cryptococcal loads at weeks 2, 3, and 4 postinfection re
146               At days 7 to 14, the number of cryptococcal lung CFU continued to increase in both untr
147 tudy, we used an established murine model of cryptococcal lung infection and flow cytometric analysis
148 ates that PD-1 signaling promotes persistent cryptococcal lung infection and identifies this pathway
149 stent infections, as evidenced by studies of cryptococcal lung infection in IL-10-deficient mice.
150                We conclude that clearance of cryptococcal lung infection requires the CCR2-mediated m
151 lization of lung DC and Mvarphi in mice with cryptococcal lung infection.
152 ssive fungal disease using a murine model of cryptococcal lung infection.
153                                 Mitogen- and cryptococcal mannoprotein (CMP)-activated (CD25+CD134+)
154    Responses were assessed following ex vivo cryptococcal mannoprotein stimulation, using 13-color fl
155 e played by mannosylation, an immunoreactive cryptococcal mannoprotein was expressed recombinantly in
156                                              Cryptococcal mannoproteins (MP) are highly mannosylated
157 lasma CRAG titers >1:640, 96% (27 of 28) had cryptococcal meningitis (cerebrospinal fluid CRAG-positi
158 (25[OH]D) were measured in 150 patients with cryptococcal meningitis (CM) and 150 HIV-infected contro
159 uman immunodeficiency virus (HIV)-associated cryptococcal meningitis (CM) and is lower in patients on
160                      Ocular complications in cryptococcal meningitis (CM) are commonly attributed to
161 ated to raise intracranial pressure (ICP) in cryptococcal meningitis (CM) by mechanical obstruction o
162 y virus (HIV)-infected patients with treated cryptococcal meningitis (CM) commencing combination anti
163 human immunodeficiency virus/AIDS-associated cryptococcal meningitis (CM) frequently experience clini
164                                              Cryptococcal meningitis (CM) is a leading cause of death
165                                              Cryptococcal meningitis (CM) is a leading cause of HIV-a
166                                              Cryptococcal meningitis (CM) is a major cause of death a
167 uman immunodeficiency virus (HIV)-associated cryptococcal meningitis (CM) is characterized by high fu
168                                              Cryptococcal meningitis (CM) is one of the most common c
169 study to determine the national incidence of cryptococcal meningitis (CM), and describe characteristi
170                                              Cryptococcal meningitis (CM)-related immune reconstituti
171                                              Cryptococcal meningitis (CM)-related mortality may be pr
172  patient, who defaulted from care, died from cryptococcal meningitis (CM).
173                                              Cryptococcal meningitis accounts for 20 to 25% of acquir
174 nal fluid (CSF) samples for the diagnosis of cryptococcal meningitis against that of existing diagnos
175 val of HIV-infected persons with symptomatic cryptococcal meningitis and asymptomatic, subclinical cr
176 e in the treatment of fungal infections like cryptococcal meningitis and C. albicans infections.
177  mouse IgG1 currently in clinical trials for cryptococcal meningitis and for the design of antibody t
178 ed adults in Uganda and South Africa who had cryptococcal meningitis and had not previously received
179 body screening in four current patients with cryptococcal meningitis and identified and tested 103 ar
180 nvasive aspergillosis, invasive candidiasis, cryptococcal meningitis and mucosal and urinary Candida
181 mortality among patients with HIV-associated cryptococcal meningitis and was associated with more adv
182 uman immunodeficiency virus (HIV)-associated cryptococcal meningitis are poorly defined.
183                                              Cryptococcal meningitis associated with human immunodefi
184  measured in 44 patients with HIV-associated cryptococcal meningitis at baseline and during follow-up
185 lucytosine) is the recommended treatment for cryptococcal meningitis but has not been shown to reduce
186 an Africa accounted for 73% of the estimated cryptococcal meningitis cases in 2014 (162 500 cases [95
187                        In the United States, cryptococcal meningitis causes approximately 3400 hospit
188 iagnosis prompted screening of patients with cryptococcal meningitis for anticytokine autoantibodies.
189 0 (95% CI 150 600-282 400) incident cases of cryptococcal meningitis globally in 2014.
190                             One patient with cryptococcal meningitis had autoantibodies only against
191                              No persons with cryptococcal meningitis had negative fingersticks.
192                                              Cryptococcal meningitis has been described in immunocomp
193 r a trial on the treatment of HIV-associated cryptococcal meningitis in Mbarara, Uganda.
194 antibodies are associated with some cases of cryptococcal meningitis in otherwise immunocompetent pat
195 p, open-label trial of induction therapy for cryptococcal meningitis in patients with human immunodef
196                                Patients with cryptococcal meningitis in sub-Saharan Africa frequently
197 recruited adult patients with HIV-associated cryptococcal meningitis in Vietnam, Thailand, Indonesia,
198                      Early ART initiation in cryptococcal meningitis increased CSF cellular infiltrat
199                                              Cryptococcal meningitis is a metric of HIV treatment pro
200                               HIV-associated cryptococcal meningitis is associated with an estimated
201                                              Cryptococcal meningitis is the leading cause of adult me
202                                              Cryptococcal meningitis is the most common cause of adul
203                                              Cryptococcal meningitis is the most frequent cause of me
204                     Antifungal treatment for cryptococcal meningitis relies on three old, off-patent
205                                              Cryptococcal meningitis remains a significant cause of d
206 n ART should be initiated after diagnosis of cryptococcal meningitis remains unanswered.
207 r antiretroviral therapy (ART) initiation in cryptococcal meningitis resulted in higher mortality com
208                     Altered mental status in cryptococcal meningitis results in poorer survival, but
209 ccus gattii isolated from serial episodes of cryptococcal meningitis that were separated by at least
210  and 189 ART-naive Ugandans with symptomatic cryptococcal meningitis treated with amphotericin (CM co
211 rring ART for 5 weeks after the diagnosis of cryptococcal meningitis was associated with significantl
212                                    Globally, cryptococcal meningitis was responsible for 15% of AIDS-
213                             One patient with cryptococcal meningitis was successfully treated.
214             Patients with a first episode of cryptococcal meningitis were enrolled, and their immune
215 duals assessed, 172 HIV-infected adults with cryptococcal meningitis were enrolled.
216                    Annual global deaths from cryptococcal meningitis were estimated at 181 100 (95% C
217 ntiretroviral naive patients presenting with cryptococcal meningitis were randomized to 4 treatment a
218 tibodies in an otherwise healthy female with cryptococcal meningitis who later developed pulmonary al
219 , we recruited HIV-infected individuals with cryptococcal meningitis who presented to Mulago Hospital
220 mmunodeficiency virus-infected patients with cryptococcal meningitis who received antifungal therapy
221 iciency virus-infected patients with treated cryptococcal meningitis who start combination antiretrov
222  identified seven HIV-negative patients with cryptococcal meningitis who tested positive for high-tit
223 tive participants, 138 (93%) had evidence of cryptococcal meningitis with a positive CSF CRAG.
224 We review the antifungal drugs used to treat cryptococcal meningitis with respect to clinical effecti
225          Nine CSF samples from patients with cryptococcal meningitis yielded positive results using b
226 meningitis and sepsis), fungal (for example, cryptococcal meningitis) and parasitic (for example, mal
227 ormans var. grubii is the causative agent of cryptococcal meningitis, a significant source of mortali
228  is an important determinant of mortality in cryptococcal meningitis, but its use in aiding clinical
229 uman immunodeficiency virus (HIV)-associated cryptococcal meningitis, screened for the Cryptococcal O
230 s the most attractive treatment strategy for cryptococcal meningitis, though the rising price may be
231 mulating factor (GM-CSF) autoantibodies with cryptococcal meningitis.
232  important contributor to virulence in human cryptococcal meningitis.
233 be considered for point-of-care diagnosis of cryptococcal meningitis.
234 sease severity and outcome in HIV-associated cryptococcal meningitis.
235 rebrospinal fluid samples from patients with cryptococcal meningitis.
236 tosine as first-line induction treatment for cryptococcal meningitis.
237 to safe and effective antifungal therapy for cryptococcal meningitis.
238 d with improved survival among patients with cryptococcal meningitis.
239 lus 5-FC for the treatment of HIV-associated cryptococcal meningitis.
240 , but their use is untested in patients with cryptococcal meningitis.
241  of people who are developing and dying from cryptococcal meningitis.
242 colony-stimulating factor autoantibodies and cryptococcal meningitis; anti-interleukin (IL)-6 autoant
243                                          CNS cryptococcal meningoencephalitis in both HIV positive (H
244                                              Cryptococcal meningoencephalitis is a fungal infection t
245                                              Cryptococcal meningoencephalitis is a lethal infection w
246                                              Cryptococcal meningoencephalitis is an AIDS-defining ill
247                                              Cryptococcal meningoencephalitis is the most common fung
248 l disease, including those with unrecognized cryptococcal meningoencephalitis may transmit the infect
249                            A murine model of cryptococcal meningoencephalitis was used.
250 lay an important role in the pathogenesis of cryptococcal meningoencephalitis.
251 ly detection and intervention strategies for cryptococcal meningoencephalitis.
252 cterize the phenotypic features of different cryptococcal molecular types.
253 s, suggesting that Znf2 might interfere with cryptococcal neurotropism upon extrapulmonary disseminat
254 sted no influence of a-alpha interactions on cryptococcal neurotropism, irrespective of the route of
255           The 25-hydroxyvitamin D levels and cryptococcal notifications were analyzed for evidence of
256 ery early in infection and that increases in cryptococcal number are driven by intracellular prolifer
257 ed cryptococcal meningitis, screened for the Cryptococcal Optimal ART Timing (COAT) trial in Uganda a
258 rebrospinal fluid (CSF) and serum during the Cryptococcal Optimal ART Timing (COAT) trial.
259                Despite extensive research on cryptococcal pathogenesis, host genes involved in the in
260 at has been implicated in multiple stages of cryptococcal pathogenesis, including initiation and pers
261 e of these strains in mice suggests that the cryptococcal PDK1, PKC, and likely the TOR pathways play
262 hese findings underscore the contribution of cryptococcal-phagocyte interactions and laccase-dependen
263                                        Thus, cryptococcal PIK1, RUB1, and ENA1 differentially contrib
264                                 Deletions of cryptococcal PIK1, RUB1, and ENA1 genes independently re
265 s and additional effector cells in mice with cryptococcal pneumonia.
266 onse to Cryptococcus neoformans in mice with cryptococcal pneumonia.
267 scopy with (15)N-labeled peptide mimetics of cryptococcal polysaccharide antigen (Ag).
268                                          The cryptococcal polysaccharide capsule is a leading candida
269                  In this study, we show that cryptococcal production of both PGE(2) and PGF(2 alpha)
270 g with an inability to control intracellular cryptococcal proliferation, even in the presence of reac
271 a demonstrate a critical role for laccase in cryptococcal prostaglandin production, and provides insi
272 l laccase (lac1 Delta) resulted in a loss of cryptococcal prostaglandin production.
273                                              Cryptococcal-related mortality is associated with monocy
274 wever, the magnitude of the impact of LPs on cryptococcal-related mortality is unknown.
275                  To dissect the mechanism of cryptococcal resistance to MBL, we compared MBL binding
276  DC lysosome fungicidal activity against all cryptococcal serotypes.
277  the virulence composites of both pathogenic cryptococcal species.
278                                              Cryptococcal-specific CD4(+) T-cell responses were chara
279                    The relationships between cryptococcal-specific CD4(+) T-cell responses, clinical
280                                              Cryptococcal-specific peripheral CD4(+) T-cell responses
281            Moreover, high CTR4 expression by cryptococcal strains from 24 solid organ transplant pati
282                                              Cryptococcal strains producing larger ex vivo capsules i
283          We examined DC lysosomal killing of cryptococcal strains, anti-fungal activity of purified l
284 were also seen to play a role as a niche for cryptococcal survival.
285                                          The cryptococcal transcript for the extracellular mannoprote
286 dc42, and their activations are required for cryptococcal transmigration across the HBMEC monolayer.
287 monolayer, indicating their positive role in cryptococcal transmigration.
288 formans-derived microvesicles can facilitate cryptococcal traversal across the BBB and accumulate at
289  host regulators that specifically influence cryptococcal uptake.
290 group significantly and specifically altered cryptococcal uptake; one of them encoded CaMK4, a calciu
291              Collectively, these data define cryptococcal urease as a pulmonary virulence factor that
292 Thus, our studies define a novel role of the cryptococcal Vad1 protein as a central regulator of cryp
293 occal Vad1 protein as a central regulator of cryptococcal virulence and illustrate that Vad1 promotes
294 and the exopolysaccharide capsule, a primary cryptococcal virulence determinant.
295 ity and retention of mannoproteins and known cryptococcal virulence factors in the cell wall of C. ne
296 rge set of clinical isolates for established cryptococcal virulence traits to evaluate the contributi
297  RUB1, and ENA1 differentially contribute to cryptococcal virulence, in correlation with their differ
298 e is known about the contribution of Plb1 to cryptococcal virulence.
299 nd CNA2580) were not previously described in cryptococcal virulence.
300                    The gene, termed CXT1 for cryptococcal xylosyltransferase 1, encodes a 79-kDa type

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