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1 e; however, this was less pronounced than in viral encephalitis.
2 yme 1 (DBR1) is a rare etiology of brainstem viral encephalitis.
3 were selected due to their susceptibility to viral encephalitis.
4  experimental models of acute and persistent viral encephalitis.
5 yme disease, babesiosis, anaplasmosis, and a viral encephalitis.
6 and autoimmune neurological diseases or with viral encephalitis.
7 hagy) and increases susceptibility to lethal viral encephalitis.
8 is one of the leading etiologies of sporadic viral encephalitis.
9 provides a well-characterized model to study viral encephalitis.
10 ms or types of presentations often suggest a viral encephalitis.
11 es a role for pathogenic Th17 cells in fatal viral encephalitis.
12 nhances survival in a murine model of lethal viral encephalitis.
13 ne orchestration of leukocyte recruitment in viral encephalitis.
14 as plausible therapeutic targets in treating viral encephalitis.
15 only recently been appreciated as a cause of viral encephalitis.
16 s virus (JEV) is the leading global cause of viral encephalitis.
17 toimmune and inflammatory diseases including viral encephalitis.
18 y be useful adjunct therapy in some types of viral encephalitis.
19 es in the induction of acute seizures during viral encephalitis.
20 ting pathologic immune responses in nonlytic viral encephalitis.
21  targeting ICAM-1 signaling may help control viral encephalitis.
22 tem neuronal dysfunction seen in fatal Nipah viral encephalitis.
23 cephalitis virus (JEV) is a leading cause of viral encephalitis.
24 a promising and novel treatment strategy for viral encephalitis.
25 mergence of novel mechanisms of transmitting viral encephalitis.
26 hat has become a significant global cause of viral encephalitis.
27 itate the development of immunotherapies for viral encephalitis.
28 lity by preventing the development of lethal viral encephalitis.
29 ic early radiographic manifestations of this viral encephalitis.
30  test was positive in 12 of 24 patients with viral encephalitis.
31 ive approach, we have used a murine model of viral encephalitis and an in vivo imaging system that ca
32 system (CNS) provides a model for studies of viral encephalitis and demyelinating disease.
33 mans and is the leading etiological agent of viral encephalitis and eye infections.
34 s emerged as a significant cause of epidemic viral encephalitis and flaccid limb paralysis, yet the m
35 ented to identify patients hospitalized with viral encephalitis and meningitis.
36 ing viral infections, such as other forms of viral encephalitis and other HSV-1 diseases in particula
37 in the T-cell-mediated IL-10 response during viral encephalitis and persistence.
38 s viral neuropathogenesis and contributes to viral encephalitis are not well understood.
39 , factors that confer neuroprotection during viral encephalitis are poorly understood.
40 focuses on some of the most common agents of viral encephalitis, as well as important emerging viral
41 titers in the brain after day 6, and died of viral encephalitis between days 7 and 12.
42 e CNS but enhances morbidity associated with viral encephalitis by increasing the ratio of IFN-gamma
43  role for NKG2D in host defense during acute viral encephalitis by selectively enhancing CTL activity
44                                              Viral encephalitis caused by neuroadapted yellow fever 1
45         Thus, the rapid monocyte response to viral encephalitis constitutes an indirect antiviral pat
46 etal dynamics, the worldwide epidemiology of viral encephalitis continues to evolve in surprising way
47                                   IMPORTANCE Viral encephalitis contributes to illness and death in c
48 3 sera from New York patients with suspected viral encephalitis demonstrated concordance with results
49  cohort of 11 adult Italian patients in whom viral encephalitis developed.
50                               The fourth had viral encephalitis during infancy.
51 oreover, recent investigations indicate that viral encephalitis (e.g., herpes simplex) can trigger sy
52  such as acute flaccid myelitis (EV-D68) and viral encephalitis (EV-A71).
53   The largest effect association was between viral encephalitis exposure and Alzheimer's disease.
54 e found that brain tissue from patients with viral encephalitis expresses increased levels of phospho
55                                Patients with viral encephalitis have a 16-fold increased risk of deve
56  genes, and its dysfunction is implicated in viral encephalitis, HIV, ALS, and cancer.
57 ovirus, was attributed to large outbreaks of viral encephalitis; however, compelling evidence suggest
58 se encephalitis (JE) is the leading cause of viral encephalitis in Asia, resulting in 70,000 cases ea
59 quito-borne flavivirus, is the main cause of viral encephalitis in Asia.
60 st Nile virus (WNV) is an important cause of viral encephalitis in birds and animals, including human
61  of severe hand, foot, and mouth disease and viral encephalitis in children across the Asia-Pacific r
62 e Flaviviridae family, is a leading cause of viral encephalitis in Europe and Asia.
63 roportion of patients once suspected to have viral encephalitis in fact have an autoimmune etiology f
64                WEEV is an important cause of viral encephalitis in humans and horses in the Americas,
65                                  While rare, viral encephalitis in humans is often fatal and survivor
66 s emerged globally as a significant cause of viral encephalitis in humans, especially in immunocompro
67  virus (WNV) is responsible for outbreaks of viral encephalitis in humans, horses, and birds, with pa
68 cephalitis (HSE) is the most common sporadic viral encephalitis in humans.
69 s emerged globally as a significant cause of viral encephalitis in humans.
70             Indeed, the overall mortality of viral encephalitis in immunocompetent individuals is low
71 litis (HSE) is the most common form of acute viral encephalitis in industrialized countries.
72                               MAV-1 produces viral encephalitis in its natural host, providing a good
73 been used to study the pathogenesis of acute viral encephalitis in mice for many years.
74 RNA afforded robust protection against fatal viral encephalitis in mice.
75 WNV has become the leading cause of epidemic viral encephalitis in North America.
76 aviridae) are the leading cause of pediatric viral encephalitis in North America.
77 le virus has become the most common cause of viral encephalitis in several states.
78 virus (LACV) is a primary cause of pediatric viral encephalitis in the United States but rarely cause
79 le virus (WNV) has been the leading cause of viral encephalitis in the United States since 1999.
80  the Flavivirus genus, is a leading cause of viral encephalitis in the United States(1).
81 WNV is now the most common cause of epidemic viral encephalitis in the United States, and it will lik
82 rus (LACV) is the primary cause of pediatric viral encephalitis in the United States.
83 ic Bunyavirus, is a major cause of pediatric viral encephalitis in the United States.
84 virus (LACV) is the major cause of pediatric viral encephalitis in the United States; however, the me
85 pes simplex virus (HSV) is the main cause of viral encephalitis in the Western world, and the type I
86               The primary treatment for most viral encephalitis, including LACV, is palliative care,
87     Neurologic complications associated with viral encephalitis, including seizures and cognitive imp
88 sfusion-associated and transplant-associated viral encephalitis, including West Nile virus, rabies vi
89 halitis virus is the most important emerging viral encephalitis; interferon alpha was not effective a
90                                              Viral encephalitis is a major cause of morbidity and mor
91                                              Viral encephalitis is a serious condition that causes ac
92 ated astrocytes undergo apoptosis.IMPORTANCE Viral encephalitis is a significant cause of worldwide m
93                                        Acute viral encephalitis is believed to result from direct vir
94 pid monocyte recruitment into the CNS during viral encephalitis is dispensable for T cell migration a
95 migration of lymphocytes into the CNS during viral encephalitis is hindered by the blood-brain barrie
96                                              Viral encephalitis is most commonly caused by herpesviru
97                     One of the key events in viral encephalitis is the ability of virus to enter the
98  of neuroinflammation in the pathogenesis of viral encephalitis is unclear.
99 branching enzyme 1 (DBR1) underlie brainstem viral encephalitis is unknown.
100 acy of the inhibitor in protecting mice from viral encephalitis, JNK inhibition represents a promisin
101 ctive role of Ifit2 is established for acute viral encephalitis, less is known about its influence du
102 sfusion-associated and transplant-associated viral encephalitis may be an underrecognized risk of the
103 anding of neuroinflammatory responses during viral encephalitis may facilitate the development of new
104 ndard for diagnosing the etiologic agent for viral encephalitis, may not clearly differentiate betwee
105                                         In a viral encephalitis model in mice, disease depended on CT
106 and serum specimens taken from patients with viral encephalitis or a presumed viral infection involvi
107           Investigation found no evidence of viral encephalitis or other recognized causes of rapid-o
108  of nonmalarial cause (bacterial meningitis, viral encephalitis, or unknown cause).
109 cy is a broad mechanism of death in cases of viral encephalitis, plethysmography was evaluated in mic
110 patients with several types of autoimmune or viral encephalitis, PNH, or mutations of the Caspr2-enco
111 IL-1 signaling within the hippocampus during viral encephalitis prevents synapse recovery and promote
112            Using newly established models of viral encephalitis recovery in adult animals, we show th
113                                        Acute viral encephalitis requires rapid pathogen elimination w
114 easures will address the gap in treatment of viral encephalitis such as those caused by the neurotrop
115 encephalomyelitis virus (TMEV) is a model of viral encephalitis that causes behavioral seizures along
116 neurological cells in patients with types of viral encephalitis that have not been treatable in the p
117 ort of patients with a diagnosis of definite viral encephalitis (VE) and AE from February 2005 to Dec
118 he central nervous system (CNS) during acute viral encephalitis was studied in vivo using fluorescent
119                                        Acute viral encephalitis was thus induced in CCL2-deficient (C
120 ain after HIV-1 infection, a murine model of viral encephalitis was used to study relationships, over
121 ribute to age-dependent resistance to lethal viral encephalitis, we compared central nervous system (
122 ioral assessment under healthy conditions or viral encephalitis, we studied seizures and postictal sy
123 E.P. became profoundly amnesic in 1992 after viral encephalitis, which damaged his medial temporal lo
124 RNA virus clearance and neurotoxicity during viral encephalitis with a focus on the cytokines essenti
125       HSV-1 is the leading cause of sporadic viral encephalitis, with mortality rates approaching 30%
126 and remains the most common type of sporadic viral encephalitis worldwide.

 
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