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1 s its derivative, clone 13 (Cl-13), causes a persistent infection.
2 hat vIL-10 may play a functional role during persistent infection.
3 bud from the plasma membrane and establish a persistent infection.
4 ic treatment for the prolonged duration of a persistent infection.
5 that are maintained in their rodent hosts by persistent infection.
6 n for replication in macaques to establish a persistent infection.
7 gens to evade immune clearance and establish persistent infection.
8 nge of clinical presentations and a lifelong persistent infection.
9 e virus in the establishment of a long-term, persistent infection.
10 rus-induced cardiac disease during acute and persistent infection.
11 in response to hypoxia in vivo, resulting in persistent infection.
12 t support a potential role in primary and/or persistent infection.
13 r phagosomes of the host cells and establish persistent infection.
14 ly important hepatitis B and C viruses cause persistent infection.
15  specimens obtained from subjects developing persistent infection.
16        Ten recipients developed prolonged or persistent infection.
17 elope proteins from HBV in order to maintain persistent infection.
18 vade the host immune response to establish a persistent infection.
19  low in KE37 and BJAB cells, which support a persistent infection.
20 se host microenvironments, thus facilitating persistent infection.
21 ar evolution of that virus during 5 years of persistent infection.
22 urface, rendering them highly susceptible to persistent infection.
23 ll responses and reduce the risk of a second persistent infection.
24 mosquito cell line, wStr maintains a robust, persistent infection.
25 reached germinal center B cells to establish persistent infection.
26 alcitrant nasal polyps, suggesting a link to persistent infection.
27 ful conditions in the host and to maintain a persistent infection.
28 nterobactin and salmochelin are required for persistent infection.
29 ive of a partial protective immunity against persistent infection.
30 stress and antibiotics, and to be sources of persistent infection.
31 in mouse models of acute colitis and chronic persistent infection.
32 nfection of basal cells is a requirement for persistent infection.
33 may be caused by reactivation of a low-level persistent infection.
34 on, ultimately facilitating clearance of the persistent infection.
35     GBV-C is a lymphotropic virus capable of persistent infection.
36 CV infection may facilitate and maintain HCV persistent infection.
37 HTLV-2 or APH-2 mutant viruses established a persistent infection.
38 ral T cell immunity and likely contribute to persistent infection.
39 ant viruses may be the forms responsible for persistent infection.
40 glycoproteins of NDV in the establishment of persistent infection.
41 arance or in mitigating the fitness costs of persistent infection.
42 hers control the pathogen as an asymptomatic persistent infection.
43 o escape host immune clearance and establish persistent infection.
44 cating the presence of a tissue reservoir of persistent infection.
45  mediate a stable standoff during controlled persistent infections.
46 comes a more complex issue in the context of persistent infections.
47 h similar but nonsignificant HRs for 6-month persistent infections.
48 biofilms are responsible for a wide range of persistent infections.
49 med to identify risk factors associated with persistent infections.
50 tunistic pathogen that can cause devastating persistent infections.
51 y 10 to 20% of infections are established as persistent infections.
52  induce a protective immune response against persistent infections.
53 as been documented, leading to nonpathogenic persistent infections.
54 itopes in E2 remained intact throughout both persistent infections.
55 ction detection, but cannot reliably predict persistent infections.
56 issue injury or promote the establishment of persistent infections.
57 ifferentiation is not clear, particularly in persistent infections.
58 or efforts to develop control strategies for persistent infections.
59 tous human pathogens that establish lifelong persistent infections.
60 immune activation and disease progression in persistent infections.
61 omplications occur frequently, especially in persistent infections.
62 nnate inflammatory responses elicited during persistent infections.
63 therapeutic intervention to prevent or treat persistent infections.
64 s and in mice that develop acute followed by persistent infections.
65 o overcome immune dysfunction and thus fight persistent infections.
66 l RNA and is activated by viruses that cause persistent infections.
67 pounds are a promising solution for treating persistent infections.
68 tation and innate immunity in the control of persistent infections.
69 eath, thereby promoting the establishment of persistent infections.
70 ation in the host and serve as catalysts for persistent infections.
71 ral approaches to probe the small numbers in persistent infections.
72 ppeared to be contagious and associated with persistent infections.
73 asive fungi can impair clearance and promote persistent infections.
74 osure with implications for cancer and other persistent infections.
75  difference between responses to primary and persistent infection, 13 long-term carriers were screene
76 E) at 48 months was assessed against 6-month persistent infection (6MPI) with low-risk HPV types in t
77                               To establish a persistent infection,A. baumannii must overcome the detr
78 ey B cells in vitro and reproduces acute and persistent infection after oral inoculation of macaques.
79 itro, and successfully established acute and persistent infection after oral inoculation of rhesus ma
80 tently infected patients (P = .043) and with persistent infection among CT patients (P = .033).
81 d human pathogen that establishes a lifelong persistent infection and can cause severe disease in imm
82 . pylori-induced immunomodulation, promoting persistent infection and conferring protection against a
83 i-MPyV CD8 T cells are primed de novo during persistent infection and contribute to maintenance of th
84 squitoes have evolved mechanisms to tolerate persistent infection and developed efficient antiviral s
85 nique hysteretic memory switch may result in persistent infection and enhanced host-to-host spreading
86 egy and is required for the establishment of persistent infection and for viral spread to additional
87 IL-1beta was able to establish a significant persistent infection and immune activation in BALB/c mic
88 nced ability to replicate in mice and caused persistent infection and immune activation in the BALB/c
89         Hepatitis C virus (HCV) often causes persistent infection and is an increasingly important fa
90 associated herpesvirus (KSHV) cause lifelong persistent infection and play causative roles in several
91  LRV1-positive patients (27%) presented with persistent infection and symptomatic relapse that requir
92 dicate that chronic Lyme disease is due to a persistent infection and that extended antibiotic therap
93 at suboptimal Ag presentation contributes to persistent infection and that limiting Ag presentation i
94 t this is a bacterial adaptation to maximize persistent infection and transmission to a new host unde
95 ed by Brucella to establish an intracellular persistent infection and will aid in the development of
96       As the possible exception, VEs against persistent infection and/or CIN 2/3 due to HPV-31 A/B an
97 18, -31, -33, -35, -45, and -51 resulting in persistent infection and/or CIN 2/3 were matched (ratio,
98  reprogram host cells to establish long-term persistent infection and/or to produce viral progeny.
99 iruses, such as hepatitis C virus, establish persistent infections and cause chronic disease are of f
100 ationships of viruses that are able to cause persistent infections and exist with high incidences of
101 ay have an intrinsic ability to cause highly persistent infections and later adverse outcomes.
102 Antiviral resistance is a relevant factor in persistent infections and needs to be investigated in va
103 tory responses in infected ECs, resulting in persistent infections and potential carcinogenesis.
104 s a potential good diagnostic marker for MAP persistent infections and predictor of disease specific
105 otential new target for the immunotherapy of persistent infections and should be accounted for and su
106 90% reduction of incident infection, 6-month persistent infection, and ASCUS+, respectively.
107  This may contribute to the mechanism of HCV persistent infection, and suggest that blockade of HCVc
108                                  During many persistent infections, antiviral T cells are maintained
109  of Msp2 variants expressed during long-term persistent infection are mosaics, derived by recombinati
110                                              Persistent infections are common, and there is currently
111                          Because repeated or persistent infections are correlated with serious compli
112  mechanisms associated with establishment of persistent infections are poorly elucidated.
113 lococcus aureus biofilms, a leading cause of persistent infections, are highly resistant to immune de
114                                           In persistent infection, arginase-expressing gMDSCs (and ci
115 ctive immune responses and, thereby, promote persistent infections, as evidenced by studies of crypto
116 n persist in large numbers during controlled persistent infections, as exemplified by rare HIV-infect
117  virus infections, which can cause acute and persistent infections associated with chronic inflammati
118 mal disease at cutaneous sites but developed persistent infection at the mucosal sites including thos
119 y associated with lower risk of incident and persistent infection, atypical squamous cells of undeter
120 s, such as Epstein-Barr virus, can establish persistent infection, but the underlying virus-host inte
121 infections might be due to reactivation of a persistent infection, but this hypothesis has been diffi
122  approximately 2000 years ago as a result of persistent infection by a fungal endophyte, Ustilago esc
123 oprotein of hepatitis C virus contributes to persistent infection by evolving escape mutations that a
124                          HVR1 contributes to persistent infection by evolving mutations that escape f
125 r understand the dynamic interaction between persistent infection by HTLV-I and virus-specific host i
126  regions of HCV genomes appear to facilitate persistent infection by masking the genome from RNase L
127 proteasomal degradation and is necessary for persistent infection by Mtb.
128                                              Persistent infection by specific oncogenic human papillo
129                                         This persistent infection can cause severe disease in immunoc
130 de of these pathways either before or during persistent infection can promote viral clearance.
131 ght to be important in the dissemination and persistent infection caused by ranavirus.
132                                              Persistent infections caused by pathogens such as hepati
133 ble-stranded DNA viruses that cause lifelong persistent infections characterized by periods of quiesc
134                                              Persistent infection (chronic Q fever) develops in 1%-5%
135  virus-specific CD8 T cells recruited during persistent infection contribute to preservation of funct
136  work in the murine norovirus (MNV) model of persistent infection demonstrates that innate immunity c
137 ms that the parasite utilizes to establish a persistent infection despite activation of a potent immu
138               Many bacterial pathogens cause persistent infections despite repeated antibiotic exposu
139 cobacterium tuberculosis (Mtb) establishes a persistent infection, despite inducing antigen-specific
140 letion of genes from the wca operon caused a persistent-infection E. coli strain to become sensitive
141                                     In fact, persistent infections following antibiotic treatment are
142 n, human herpesvirus 6 (HHV-6) establishes a persistent infection for life.
143 ibular salivary gland (SMG), a major site of persistent infection for many viruses, contains a large
144 ient-derived hepatitis B virus can establish persistent infection for over 30 days in a self-assembli
145 Here, we show that NPHV, like HCV, can cause persistent infection for over a decade, with high titers
146 eficiency virus type 1 (HIV-1) establishes a persistent infection for which there remains no feasible
147                         Incident and 6-month persistent infections for HPV 6 and 11 did not differ by
148                                     Lifelong persistent infection has also been linked with the devel
149 populations during the course of a lifelong, persistent infection has generated interest in the virus
150 fic CD4 T cells primed during an established persistent infection have diminished ability to develop
151             Prior studies in mouse models of persistent infection have suggested that ineffective ada
152 tramacrophage environment may be a niche for persistent infection; however, mechanisms by which the b
153    Whereas immune-compromised mice developed persistent infection, immune-competent mice cleared the
154 V infection is that it establishes long-term persistent infection in 10 to 70% of infected stallions
155      It provides the only example to date of persistent infection in a chimpanzee challenged with cel
156                  We explore the emergence of persistent infection in a closed region where the diseas
157   However, E. coli has been shown to cause a persistent infection in a minority of cases.
158 LB/c, and C3H/HeN mice and induced lethal or persistent infection in a route- and dose-dependent mann
159 ewcastle disease virus (NDV) could establish persistent infection in a tumor cell line, resulting in
160 ingly, pp65 was not required for primary and persistent infection in animals.
161                     Alphaviruses establish a persistent infection in arthropod vectors which is essen
162 ies to hijack infected host cells, establish persistent infection in B cells, and evade antiviral imm
163 hagic fever in macaques but an asymptomatic, persistent infection in baboons.
164 in neonatal-infected mice diversified during persistent infection in both the brain and spleen, while
165         Biofilms facilitate colonization and persistent infection in gallbladders of humans and mouse
166  CD4(+) T cells are the largest reservoir of persistent infection in HIV-1-positive subjects.
167 e that this anatomical site is the source of persistent infection in humans.
168 ubiquitous virus that establishes a lifetime persistent infection in humans.
169 M. tuberculosis that allows establishment of persistent infection in lymph nodes.
170                 The inability to establish a persistent infection in mice, even in immunocompromised
171 utritional immunity in macrophages and cause persistent infection in mice.
172          Hepatitis C virus (HCV) establishes persistent infection in most infected patients, and even
173                            HIV-1 establishes persistent infection in part due to its ability to evade
174 /ESI-MS may be a very sensitive indicator of persistent infection in patients on antibiotic therapy f
175 wn as hepatitis delta virus) can establish a persistent infection in people with chronic hepatitis B,
176       We also detected a higher frequency of persistent infection in PML(-)/(-) peritoneal cells.
177                         Hantaviruses cause a persistent infection in reservoir hosts that is attribut
178 re large-genome DNA viruses that establish a persistent infection in sensory neurons and commonly man
179 was required for MRSA to achieve high-level, persistent infection in the bladder.
180 ment of macrophages and establish long term, persistent infection in the host against the control of
181 form of the virus and thought to establish a persistent infection in the host urinary tract.
182 mavirus (JCPyV) establishes an asymptomatic, persistent infection in the kidneys of the majority of t
183  may also contribute to the establishment of persistent infection in the liver.
184               Hepatitis C virus (HCV) causes persistent infection in the majority of infected individ
185 emiological and clinical features, including persistent infection in the male reproductive tract and
186  DeltacheY2-infected ticks did not develop a persistent infection in the murine host.
187 full MCMV infectivity in macrophages and for persistent infection in the salivary gland.
188 mia suggest the ability of ZIKV to establish persistent infection in the seminiferous tubules, an imm
189 rus has the distinctive ability to establish persistent infection in the stallion's reproductive trac
190  including severe congenital manifestations, persistent infection in the testes, and neurologic seque
191 that plays an essential role in establishing persistent infection in their respective host species.
192 g human pathogens maintained by noncytolytic persistent infection in their rodent reservoir hosts.
193 hagocytic or endothelial cells and establish persistent infection in their vertebrate reservoir hosts
194 that is consistent with the establishment of persistent infection in tissue macrophages.
195                       Thus, establishment of persistent infection in vitro involves viral genetic cha
196 coma-associated herpesvirus (KSHV) establish persistent infections in B cells.
197 omaviruses are characterized by establishing persistent infections in healthy hosts and generally cau
198 as aeruginosa biofilm formation is linked to persistent infections in humans.
199 ve genus of retroviruses that cause chronic, persistent infections in mammals, including humans.
200 t the surprising finding that during ongoing persistent infections in mice, a major fraction of the p
201 y feature of viruses that establish lifelong persistent infections in the face of strong immune respo
202 re zoonotic viruses that cause asymptomatic, persistent infections in their rodent hosts but can lead
203  difficile Spo0A protein plays a key role in persistent infection, including recurrence and host-to-h
204                   The accelerated control of persistent infection induced by blocking IFN-I signaling
205 tection, 214 were untreated (n = 137) or had persistent infection (infection duration >/=26 weeks) at
206                                              Persistent infection is a key feature of hepatitis C vir
207 ommon cause of infectious mononucleosis, and persistent infection is associated with multiple cancers
208 or therapy in immunocompromised persons with persistent infection is limited because of cost, determi
209 heck-point function of the spleen to promote persistent infection is not clear.
210  of naive CD4 T cells primed in the midst of persistent infection is unclear.
211           How such enteric viruses establish persistent infections is not well understood.
212 esistant Staphylococcus aureus (MRSA) during persistent infection leads to antimicrobial resistance b
213                                         Such persistent infections may provide the opportunity for th
214  murine cytomegalovirus (MCMV) was used as a persistent infection model to study heterologous immunit
215 o spontaneously cleared HCV (n = 285) or had persistent infection (n = 509).
216                    Other potential causes of persistent infection need to be evaluated.
217 ogic loads of M. genitalium, suggesting that persistent infection occurs with minimal direct damage t
218 f DC vaccine in preventing and combating the persistent infection of HCV or other chronic viruses.
219                                              Persistent infection of hepatitis C virus (HCV) is one o
220 may have evolved to allow HBoV1 to establish persistent infection of human airway epithelia.
221 nded to persist over time, suggesting either persistent infection of individuals or cycles of reinfec
222 ising in the viral capsid protein VP1 during persistent infection of mice.
223                                        Thus, persistent infection of phagocytes produced a CD4(+) T c
224                                  We detected persistent infections of Mycoplasma ovipneumoniae, the p
225       Despite this, SCVs are associated with persistent infections of the bloodstream, bones, and pro
226 iasis (CMC) is characterized by recurrent or persistent infections of the skin, nail, oral, and genit
227 ndpoint was vaccine efficacy against 6-month persistent infection or cervical intraepithelial neoplas
228 ndpoint was vaccine efficacy against 6-month persistent infection or cervical intraepithelial neoplas
229 r efficacy, vaccine efficacy against 6-month persistent infection or CIN1+ associated with HPV 16/18
230 e efficacy against HPV 16/18-related 6-month persistent infection or CIN1+ was significant in all age
231 aintenance, function, and response to latent persistent infection, particularly against CMV, which ex
232 comparing temporally dispersed isolates from persistent infections (persistent isolates) originating
233 cells were infected with Sendai virus (SeV), persistent infection (PI) was established.
234            Of these 15 patients, 3 died from persistent infection postoperatively, whereas 8 underwen
235 ic CD4 T cells primed during the established persistent infection provide help to B cells, but only l
236    ART usage was associated with a higher TV persistent infection rate among those receiving the sing
237 erfering with chronic IFN-I signaling during persistent infection redirects the immune environment to
238 hough the evolving immune environment during persistent infection reshapes established CD4 T-cell res
239 nd Ab-mediated immunity to control acute and persistent infection, respectively.
240 he host defense system to facilitate its own persistent infection, resulting in a compromise of the m
241  following an RC treatment (RCT) can lead to persistent infections, resulting in treatment failure an
242  2 mutations arising in clinical MRSA during persistent infection: RpoB H(4)(8)(1)Y, which is linked
243   Unlike human malaria parasites that induce persistent infection, some rodent malaria parasites, lik
244   Deletion of genes in the wca operon from a persistent-infection strain resulted in a reduction of m
245 er is a tolerogenic environment exploited by persistent infections, such as hepatitis B (HBV) and C (
246 SHV proteins v-FLIP and v-cyclin during KSHV persistent infection that reshapes autophagy.
247 gulation of metabolic processes during early persistent infection that was linked to changes in expre
248 us or human herpesvirus 8 (HHV-8), establish persistent infections that cause chronic illnesses, incl
249                                       During persistent infection, the E2 proteins from many papillom
250                                To maintain a persistent infection, the expression of ap2-g is limited
251 indeed EBV-2 utilizes T cells to establish a persistent infection, this could provide one mechanism f
252 ance of a limited CD8 T cell response during persistent infections, this response is not sufficiently
253 ctively, this study shows that CTLs adapt to persistent infection through a positive feedback pathway
254 s a common human pathogen that establishes a persistent infection through latency in B cells, where i
255 ology during RCT has the potential to reduce persistent infections through vital cell detection and a
256 g acute infection, the role of vIL-10 during persistent infection was analyzed in rhesus macaques inf
257                                              Persistent infection was associated with increased and s
258                                 In contrast, persistent infection was asymptomatic and led to establi
259  that clear infection and those that develop persistent infection was demonstrated to occur earlier t
260 CAR3) with a recombinant low-pathogenic NDV, persistent infection was established in a subset of tumo
261             The risk of incident and 6-month persistent infection was not associated with baseline se
262                                              Persistent infection was observed in all cases.
263 ptomatic (because they were healthy troops), persistent infection we called the primary multiple scle
264                Using the J-Lat 10.6 model of persistent infection, we demonstrate that proliferation
265                                              Persistent infections were acquired at an earlier age, a
266 demonstrated that E. coli strains that cause persistent infections were more motile than those that c
267 limited by reduced antigen expression during persistent infection, whereas ESAT-6-specific T cells be
268  viral genome into the host cell, leading to persistent infection wherein HIV-1 can remain transcript
269 n worldwide, predominantly originates from a persistent infection with a high-risk human papillomavir
270 lidity of results of attempts to demonstrate persistent infection with B. burgdorferi has not been es
271                Due to the high prevalence of persistent infection with BKV in the general population,
272                                   This first persistent infection with cell culture-produced HCV prov
273                              Here, we report persistent infection with chronic hepatitis in a chimpan
274                Liver disease associated with persistent infection with hepatitis B virus (HBV) contin
275                                              Persistent infection with hepatitis C virus (HCV) causes
276 shed that chronic antigen stimulation during persistent infection with hepatitis C virus is associate
277 host and body louse vector niches, producing persistent infection with high titer bacterial loads in
278                                              Persistent infection with high-risk human papillomavirus
279 ion is harmless and clears spontaneously but persistent infection with high-risk human papillomavirus
280 nt cross-protective efficacy against 6-month persistent infection with HPV 31 (65.8%, 96.2% CI 24.9-8
281 -protective vaccine efficacy against 6-month persistent infection with HPV 31 (79.1%, 97.7% CI 27.6-9
282          Cervical cancer is a consequence of persistent infection with human papillomaviruses (HPV).
283                            Immune control of persistent infection with Mycobacterium tuberculosis (Mt
284                                              Persistent infection with oncogenic Human Papillomavirus
285                                              Persistent infection with oncogenic human papillomavirus
286 uman lymphocytes survive while maintaining a persistent infection with species C adenovirus, we compa
287 ne appears to have moderate efficacy against persistent infections with a number of low-risk HPV type
288 nd immune pathology associated with acute or persistent infections with an unrelated virus.
289                                              Persistent infections with cytomegalovirus (CMV) differe
290 ociated with sex, birth characteristics, and persistent infections with cytomegalovirus (CMV) or EBV.
291                                              Persistent infections with hepatitis B virus (HBV) or he
292  fundamentally in their ability to establish persistent infections with markedly different patterns o
293 i infection display features common to other persistent infections with signs of T cell exhaustion.
294 of that ST in that herd (index case) and all persistent infections with that PTE ST, represented 40%
295 cy virus positive (HIV+), both prevalent and persistent infections with Trichomonas vaginalis (TV) ar
296 h hepatitis C virus (HCV) typically leads to persistent infection, with >170 million people estimated
297 nd potent responses are uncommon even during persistent infection, with only a subset of adults devel
298 e samples as a result of niche adaptation to persistent infection within a host.
299  evasion strategies used by HCV to establish persistent infection within the liver, as well as how ho
300 f Staphylococcus aureus disease in humans is persistent infections without development of protective

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