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1 tinued with mT2* <5 ms and 1 died (suspected central nervous system infection).
2 tion was unchanged, with no signs of ongoing central nervous system infection.
3 issemination was increased, and mice died of central nervous system infection.
4 terized cellobiose PTS system is involved in central nervous system infection.
5 c switching could influence the outcome of a central nervous system infection.
6 neurons from virus-induced injury following central nervous system infection.
7 CCR3 appears critical in central nervous system infection.
8 ecessary in certain difficult- to- eradicate central nervous system infections.
9 existence of theiloviruses that cause human central nervous system infections.
10 d in respiratory viral, gastrointestinal, or central nervous system infections.
11 oup A Streptococcus (GAS) is a rare cause of central nervous system infections.
12 100 viruses have been associated with acute central nervous system infections.
13 icroglia are important host defense cells in central nervous system infections.
14 ment and receipt of disability pension after central nervous system infections.
15 dly growing mycobacteria are rarely found in central nervous system infections.
16 robable WNF infection, of whom 352 had acute central-nervous-system infections.
18 Borna disease virus (BDV) causes persistent central nervous system infection and behavioral disturba
19 alomyelitis virus (TMEV) induce a persistent central nervous system infection and demyelinating disea
20 V replication in disseminated infections and central nervous system infections, and is superior to ac
21 in barrier, a key step in the development of central nervous system infections, and the lack of avail
22 pathogenesis and the immune response during central nervous system infection as well as further clin
23 alomyelitis virus (TMEV) induce a persistent central nervous system infection associated with an infl
24 al fluid is the recommended test to document central nervous system infection, but this test may not
25 s of this disease, and new manifestations of central nervous system infection by polyomavirus JC have
26 es is their interference with the control of central nervous system infections by the immune system.
27 ia fowleri causes an acute and rapidly fatal central nervous system infection called primary amebic m
28 ytic clearance or chronic viral persistence; central nervous system infection can result in T-cell-de
29 bic meningoencephalitis (PAM) is a fulminant central nervous system infection caused by the thermophi
30 yelitis virus (TMEV) results in a persistent central nervous system infection (CNS) and immune-mediat
32 rate a critical role for IRF-3 in control of central nervous system infection following HSV-1 challen
33 es of cerebrospinal fluid from patients with central nervous system infections have shown that the ol
36 w-neurovirulence TMEV result in a persistent central nervous system infection in mice, leading to an
37 viruses cause serious and potentially fatal central nervous system infections in humans and are high
38 viruses, cause serious and potentially fatal central nervous system infections in humans for which no
39 gnized as a cause of renal, respiratory, and central nervous system infections in immunosuppressed pa
40 RTANCE Astroviruses are an emerging cause of central nervous system infections in mammals, and astrov
41 a contributing aetiology to tsunami lung and central nervous system infections in near-drowning victi
43 y contribute to the establishment of chronic central nervous system infection including brain abscess
44 of nonspecific symptoms to supposed ongoing central nervous system infection is a major factor perpe
45 JCV targets a highly specialized cell in the central nervous system, infection is widespread, with mo
46 ophageal (n=9), lung (n=8), blood (n=6), and central nervous system infections (n=3), and sinusitis w
47 and Infections of the Cardiovascular System, Central Nervous System Infections, Ocular Infections, So
48 cific reactivation and different patterns of central nervous system infection of HSV-1 and HSV-2.
50 hemorrhage, subdural hematoma, brain tumor, central nervous system infection, or ischemic stroke wer
52 f HHV-6 encephalitis or other type of active central nervous system infection should not be made with
54 l as the anticipated pattern of a persistent central nervous system infection, the application of Koc
56 f TBM, a rabbit model of acute mycobacterial central nervous system infection was set up (8-day study
60 e the interaction of this important agent of central nervous system infection with endothelial cells
61 (TLRs) in the innate immune response during central nervous system infection with HSV-1 have not bee
62 found in individuals who have recovered from central nervous system infections with human herpesvirus
64 sent in 105 (69.1%) patients; 47 (30.9%) had central nervous system infection, with or without lung i
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