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1  suggesting an immunopathogenic component to neurovirulence.
2 tures associated with HIV-1 neurotropism and neurovirulence.
3 ents leads to reversions that increase virus neurovirulence.
4 tructural coding regions contributed to AR86 neurovirulence.
5  the central nervous system and in increased neurovirulence.
6  the spike are also important in determining neurovirulence.
7 ), which were essential for AR86 adult mouse neurovirulence.
8 ting OPVs, with a lower risk of reversion to neurovirulence.
9 t Sindbis virus background confers increased neurovirulence.
10 aky-late (VP16) promoter exhibited wild-type neurovirulence.
11 Oral poliovirus vaccine can mutate to regain neurovirulence.
12 ace of neural cells, contributing to greater neurovirulence.
13 res nPTB binding, translation initiation and neurovirulence.
14 ge in these residues might be linked to EEEV neurovirulence.
15 s that has been selected in vivo for extreme neurovirulence.
16 f the Fr98 envelope gene are associated with neurovirulence.
17 s nonstructural protein genes in adult mouse neurovirulence.
18 TMEV) is divided into two subgroups based on neurovirulence.
19 tutions were engineered and tested for mouse neurovirulence.
20 ell-specific translational control and viral neurovirulence.
21 o directly address the role of the S gene in neurovirulence.
22 t these differences appear to correlate with neurovirulence.
23  plays an important role in conferring mouse neurovirulence.
24 sFrKP41 (KP41), which differ dramatically in neurovirulence.
25 macrophages in other tissues underlies HIV-1 neurovirulence.
26 reatest effect on early viremia kinetics and neurovirulence.
27  identification of molecular determinants of neurovirulence.
28 ys, in DEN2 E as being responsible for mouse neurovirulence.
29 e noncoding control region are necessary for neurovirulence.
30 ucidating the molecular basis of mumps virus neurovirulence.
31 ibit OL differentiation, irrespective of MLV neurovirulence.
32 ection of neural cells, thereby facilitating neurovirulence.
33  replicative pathway contribute to increased neurovirulence.
34 ediated arrest of both viral replication and neurovirulence.
35 mbrane portion of envelope and/or nef confer neurovirulence.
36 l and sufficient for complete attenuation of neurovirulence.
37 ficantly reduced virus neuroinvasion but not neurovirulence.
38 he attenuation of vesicular stomatitis virus neurovirulence.
39 al functional interactions influencing HSV-2 neurovirulence.
40 E Env glycosylation features could influence neurovirulence.
41  the neurological signs observed during H5N1 neurovirulence.
42 ed host, which is required for full reovirus neurovirulence.
43 n processes involved in neuroattenuation and neurovirulence.
44 c stability, and less potential to reacquire neurovirulence.
45 as the gE/gI interaction is critical for VZV neurovirulence.
46  innate immune responses and thereby enhance neurovirulence.
47 V can be classified into two groups based on neurovirulence: a highly virulent group, e.g., GDVII vir
48 in the RABV glycoprotein had greatly reduced neurovirulence after intracerebral inoculation in suckli
49 been used successfully in the past to reduce neurovirulence and abolish neuroinvasiveness of TBEV, na
50             SARS-CoV protein 6 increases MHV neurovirulence and accelerates MHV infection kinetics in
51 tor of IFN genes (STING) exhibit exacerbated neurovirulence and atypical lymphotropic dissemination o
52 tion, oral polio vaccine (OPV) can revert to neurovirulence and cause paralytic poliomyelitis.
53 p V of the 5'-non-coding region (NCR) reduce neurovirulence and cell-specific cap-independent transla
54      To study the role of these mutations in neurovirulence and demyelination, we prepared a recombin
55 f the rVSV genome, vectors that have reduced neurovirulence and enhanced immunogenicity can be made.
56                Thus, the RBD determined both neurovirulence and folding instability.
57                                The levels of neurovirulence and immunogenicity of the chimeric viruse
58 lymphoblasts at a sequence essential for JCV neurovirulence and in cerebrospinal fluid of immunosuppr
59                   In parallel with increased neurovirulence and increased viral replication, Sindbis
60 types were confirmed, another determinant of neurovirulence and its molecular basis was characterized
61 sal infection of two HPAI strains of varying neurovirulence and lethality.
62 y attenuated in the skin and yet retains its neurovirulence and may reactivate and damage sensory neu
63  39ns1, demonstrated significantly increased neurovirulence and morbidity, including weight loss and
64 tant of BHV-5 displayed a wild-type level of neurovirulence and neural spread in the olfactory pathwa
65 ecular basis for the observed differences in neurovirulence and neuroattenuation, the complete genome
66 R altered virus neuroinvasiveness, decreased neurovirulence and neuroinflammatory responses, and prev
67 9 deletion recombinant was generated and its neurovirulence and neuroinvasive properties were compare
68 ture and pathogenic properties, particularly neurovirulence and neuroinvasiveness for SCID mice, gene
69 e derivative, strain E5, exhibit significant neurovirulence and neuroinvasiveness in normal mice, alb
70 -5 Us9-deleted virus but conferred increased neurovirulence and neuroinvasiveness in our rabbit seizu
71 ells, with the E138K mutation abrogating the neurovirulence and neuroinvasiveness of Japanese encepha
72 pairs of Sindbis virus variants differing in neurovirulence and neuroinvasiveness were derived by lim
73 erent risk of the Sabin strains to revert to neurovirulence and reacquire greater transmissibility th
74  (HSV-1) ICP34.5 protein strongly influences neurovirulence and regulates several cellular antiviral
75 tion of the HIV envelope and viral clades to neurovirulence and residual virus replication in the CNS
76  strongly suggest that (i) the phenotypes of neurovirulence and spontaneous reactivation are separabl
77         These studies unveil determinants of neurovirulence and stability in Japanese encephalitis vi
78  attenuated recombinant viruses show reduced neurovirulence and that peripheral immunization blocks t
79  for the spike gene, differ in the extent of neurovirulence and the ability to induce demyelination.
80 1)Sabin were assessed, a correlation between neurovirulence and the ability to replicate in primary h
81      Further tests in mice demonstrated high neurovirulence and the age-dependent neuroinvasiveness o
82 in-specific differences in neuroinvasion and neurovirulence and their contribution to differences in
83 Such derivative viruses often have increased neurovirulence and transmissibility, and in some cases t
84       gK 8mer treatment also increased viral neurovirulence and viral induced CS in ocularly infected
85 tural proteins are important contributors to neurovirulence and viral tissue tropism.
86           Here, we describe the attenuation, neurovirulence, and immunogenicity of rVSV vectors expre
87 of these amino acid changes in neurotropism, neurovirulence, and neuroattenuation is discussed.
88 hown that the herpes simplex virus 1 (HSV-1) neurovirulence- and autophagy-modulating protein ICP34.5
89 tragenic suppressor mutation does not affect neurovirulence; and (iii) the attenuated gamma34.5 mutan
90 pe 1 (HSV-1) mutants that are attenuated for neurovirulence are being used for the treatment of cance
91 isms by which these amino acid changes alter neurovirulence are not known.
92 , the domain that binds beclin1 and controls neurovirulence, are necessary for interactions with PGAM
93 9 reversion caused a significant increase in neurovirulence as determined by the 50% lethal dose and
94                       When tested in our rat neurovirulence assay against the respective parental str
95                                 Reversion to neurovirulence, assessed as paralysis of transgenic mice
96  vitro demonstrate a partial recovery of the neurovirulence associated with HSV-1; and (ii) vvD54-M00
97 e gene, MyD116, and the herpes simplex virus neurovirulence-associated gene, ICP34.5.
98 ghlighting a potential strategy to develop a neurovirulence-attenuated vaccine against chickenpox and
99                     Recently, high levels of neurovirulence attenuation were achieved with geneticall
100 l nonstructural genes (except 3B) of the low-neurovirulence BeAn virus strain for cell death.
101 a mutation at residue 103(Lys) had decreased neurovirulence but did induce demyelination.
102  major role in determining organ tropism and neurovirulence but that other genes also play important
103 ropism and suggest that a strategy to reduce neurovirulence by deleting gI could prolong active infec
104 he genetic basis of MuV neuroattenuation and neurovirulence by generating a series of recombinant vir
105 s the first viral protein shown to influence neurovirulence by inhibiting CD8+ T cell protection.
106 CP34.5 (ICP, infected cell protein) enhances neurovirulence by negating antiviral functions of the IF
107                                              Neurovirulence can be attenuated by point mutations or b
108                   In a standardized test for neurovirulence, ChimeriVax-JE and YF-Vax were compared i
109 lone, ps51, was significantly attenuated for neurovirulence compared to that derived from ps55.
110                                      The low-neurovirulence DA strain uses sialic acid as a corecepto
111 solution of the crystal structure of the low-neurovirulence DA virus in complex with the sialic acid
112 llustrate that (i) the protein synthesis and neurovirulence defects observed in gamma34.5 mutant viru
113                                          One neurovirulence determinant mapped to the N-terminal port
114 ama virus, four of which are predicted to be neurovirulence determinants based on various sequence co
115 em for investigating the molecular basis for neurovirulence determinants encoded within the JE E prot
116 estigate ZIKV-host interactions and identify neurovirulence determinants of ZIKV.
117 iral genome that correlate with the level of neurovirulence determined by the monkey neurovirulence t
118 es a potential mechanism for modulating TMEV neurovirulence during persistence in the mouse central n
119 nce of markers of virus neuroattenuation and neurovirulence, ensuring mumps vaccine safety has proven
120 of the MV genome which are required for full neurovirulence equivalent to CAM/RB.
121     Our data show that HSV-1 0DeltaNLS lacks neurovirulence even in highly immunocompromised mice lac
122 ta indicate that the MuV SH protein is not a neurovirulence factor and highlight the importance of di
123 mplex virus 1 (HSV-1) defective in the viral neurovirulence factor infected cell protein 34.5 (ICP34.
124 lence the expression of ICP34.5, a key viral neurovirulence factor, and that miR-III is able to silen
125 ression of lytic cycle genes (especially the neurovirulence factor, ICP34.5) and suggest a mechanism
126 utions lie outside the coding region for the neurovirulence factor, ICP34.5.
127  is blocked completely when viruses lack the neurovirulence factor, infected cell protein 34.5, or wh
128 90% of the ORF encoding ORF-34.5, a putative neurovirulence factor, which is transcribed from the opp
129 f the HSV gamma(1)34.5 gene, which encodes a neurovirulence factor.
130  neurotropism through ICP34.5, a major viral neurovirulence factor.
131 I reduces expression of ICP34.5, a key viral neurovirulence factor.
132 e that VP1 is the main determinant of EV-D68 neurovirulence following IM injection of neonatal SW mic
133 hat has a nearly 1 million-fold reduction in neurovirulence following intracerebral (i.c.) inoculatio
134                                              Neurovirulence following intracerebral inoculation of mi
135                Even though LGT has low-level neurovirulence for humans, it, and its more attenuated e
136 sage of dengue and YF viruses have increased neurovirulence for mice but reduced viscerotropism for h
137 and 172 in the E2 glycoprotein determine the neurovirulence for mice of different ages and the effici
138 ve isolates of each lineage showed increased neurovirulence for PVR-Tg21 transgenic mice.
139 uroblastoma cells and reduced its peripheral neurovirulence for SCID mice.
140 ted herpes simplex virus lacking its ICP34.5 neurovirulence gene (HSVDelta34.5).
141      The herpes simplex virus type 1 (HSV-1) neurovirulence gene encoding ICP34.5 controls the autoph
142 ut this response is antagonized by the HSV-1 neurovirulence gene product, ICP34.5.
143 EV) consist of two groups, the high- and low-neurovirulence groups, based on lethality in intracerebr
144 afety test with which to measure mumps virus neurovirulence has also hindered analysis of the neuropa
145 del that mimics systemic DEN disease without neurovirulence has been an obstacle, but DENV-2 models t
146  of cluster-specific reversions could confer neurovirulence; however, residue 138 of the E protein (E
147 roteins of Sindbis virus have been linked to neurovirulence; however, the molecular mechanisms by whi
148 dies have mapped an important determinant of neurovirulence in adult mice to a single amino acid chan
149 protein 1 (nsP1) 538 that is associated with neurovirulence in adult mice.
150  oral poliovirus vaccine (OPV) is tested for neurovirulence in animals and also for the presence of n
151 els can serve as a host determinant of viral neurovirulence in C57BL/6 mice, reflecting the direct in
152 102/103 in an sPV1(M) background restored wt neurovirulence in CD155 transgenic (tg) mice and suppres
153 le genetically and phenotypically, including neurovirulence in CD155 transgenic mice, the large major
154  for poliovirus recombinants with attenuated neurovirulence in experimental animals that corroborate
155 ble molecular mechanisms of enhanced B virus neurovirulence in humans, which results in an 80% mortal
156 e virus, the ICP47- mutant expressed reduced neurovirulence in immunologically normal mice, and T cel
157 g1 vectors demonstrated dramatically reduced neurovirulence in mice following direct intracranial ino
158 rtedly implicated in the different levels of neurovirulence in mice infected with WNV NY99 or Eg101.
159  However, the ICP47- mutant exhibited normal neurovirulence in mice that were acutely depleted of CD8
160 valuated for growth in cultured cells or for neurovirulence in mice.
161 s virus (SV) is a critical determinant of SV neurovirulence in mice.
162 ess, TBEV/DEN4Delta30 virus exhibited higher neurovirulence in monkeys than either LGTV or YF 17D, su
163 e primary target of MeV infection, abrogates neurovirulence in neonatal H-2(d) congenic C57BL/6 mice.
164 ited replication in C6/36 cells, and lack of neurovirulence in newborn ICR mice.
165 use of this vaccine candidate in humans, its neurovirulence in nonhuman primates needed to be evaluat
166 ed for clinical evaluation when assessed for neurovirulence in nonhuman primates.
167 rhinovirus type 2 resulted in attenuation of neurovirulence in primates.
168 is a determinant of Sindbis virus growth and neurovirulence in suckling mice as well as persistent in
169 ese results suggest that the determinants of neurovirulence in the envelope gene may influence the ef
170 ls that may not allow accurate prediction of neurovirulence in the human host.
171 phalitis virus/dengue virus) abolished virus neurovirulence in the mature mouse CNS.
172 dues as virus-specific determinants of mouse neurovirulence in this chimeric system.
173  beta in the brain represents a correlate of neurovirulence in this disease, whereas the TNF response
174 rate convergence between nAb evasion and CNS neurovirulence in vivo by a frequent JCPyV-PML VP1 mutat
175  plays an important role in cell tropism and neurovirulence in vivo.
176 x virus type 1 (HSV-1) is required for viral neurovirulence in vivo.
177 an neuronal cells, exhibited increased mouse neurovirulence in vivo.
178 y for replication (neurotropism) and damage (neurovirulence) in the brain and an 88-1961 wild-type vi
179 -specific propagation deficit and eliminates neurovirulence inherent in poliovirus without affecting
180 any aspects of viral pathogenesis; promoting neurovirulence, inhibiting interferon-induced shutoff of
181 ike gene, we have previously shown that high neurovirulence is associated with the JHM spike protein,
182                                              Neurovirulence is determined by the sequence of the vira
183                                              Neurovirulence is determined by the sequence of the vira
184  heterokaryon analyses revealed that loss of neurovirulence is due to trans-dominant repression of PV
185                                         EEEV neurovirulence is influenced by the interaction of the v
186                           This difference in neurovirulence is not the complete explanation for the f
187  molecular and cellular basis of coronavirus neurovirulence is poorly understood.
188 tigate a possible role for HE in MHV-induced neurovirulence, isogenic recombinant MHV-A59 viruses wer
189  in primary neuronal cultures, the increased neurovirulence it conferred may be due in part to the in
190       L/ST-4BS was completely attenuated for neurovirulence (LD50 > 10(6) PFU) relative to wild-type
191  relationship between macrophage tropism and neurovirulence, macaques were inoculated with two recomb
192 nants of simian immunodeficiency virus (SIV) neurovirulence map to the env and nef genes.
193 alysis of the Cas-Br-E genome indicates that neurovirulence maps to the env gene, which encodes the s
194                                        Since neurovirulence may be determined at the early stages of
195      These findings suggest that coronavirus neurovirulence may depend on a novel discriminatory abil
196 nse silent transmission, whereas the reduced neurovirulence may have contributed to the absence of pa
197 oliovirus vaccine strain, known to attenuate neurovirulence, may further restrict tropism by eliminat
198                                The increased neurovirulence mediated by the virus encoding glycine at
199 tified sites in the LGT genome that promoted neurovirulence/neuroinvasiveness.
200      However, when tested in a stringent NHP neurovirulence (NV) model, this vector was not adequatel
201 EV SA14-14-2 E protein, as shown by the high neurovirulence of an analogous YFV/JEV Nakayama chimera
202 n vivo relationship between hsp72 levels and neurovirulence of an hsp72-responsive virus using the mo
203 r-normal trigeminal ganglion replication and neurovirulence of an ICP34.5 mutant in IFN-alpha/betaR-/
204 , CD8+ T cell depletion did not increase the neurovirulence of an unrelated, attenuated HSV-1 glycopr
205  of the gE epitope significantly reduced the neurovirulence of BHV-5 in rabbits.
206 (HS) as an attachment receptor increases the neurovirulence of cell culture-adapted strains of Sindbi
207   We investigated the genetic basis of mouse neurovirulence of dengue virus because it might be direc
208  this interaction contributes to the extreme neurovirulence of EEEV.
209 eduction in viral replication and associated neurovirulence of HSV.
210           Here, we demonstrate that the high neurovirulence of JHM is associated with accelerated spr
211 oprotein GP2 has been shown to attenuate the neurovirulence of JUNV in suckling mice.
212                             In contrast, the neurovirulence of LGTV exhibited the reverse profile, pr
213  is likely an important factor in the severe neurovirulence of MHV-JHM in wild-type mice.
214 n animal model that can reliably predict the neurovirulence of mumps virus vaccine candidates in huma
215 immune recognition because a decrease in the neurovirulence of mutant viruses was observed in neonata
216              We now show that attenuation of neurovirulence of PV/HRV2 chimeras is not confined to CD
217                                              Neurovirulence of several mumps virus strains was assess
218 sence and extent of faecal shedding, and the neurovirulence of shed virus.
219 s than for the parental GDVII virus, and the neurovirulence of the adapted virus in intracerebrally i
220 ne envelope residues were found to influence neurovirulence of the Friend murine polytropic retroviru
221                                  The reduced neurovirulence of the ICP47- mutant was due to a protect
222                                              Neurovirulence of the mutant virus was determined in a t
223 iated three amino acid changes with enhanced neurovirulence of the neuroadapted vaccine strain: one e
224 se and three amino acid changes with reduced neurovirulence of the neuroattenuated wild-type strain:
225  a significant (P = 0.031) difference in the neurovirulence of the two recombinants.
226 rvous system (CNS) enables alteration of the neurovirulence of the virus and control of the neuropath
227                   We found that the level of neurovirulence of the virus correlates with its differen
228 anslation initiation, and attenuation of the neurovirulence of the virus without a marked effect on v
229 ese modifications also affected the residual neurovirulence of the virus, but it remained immunogenic
230 he capsid-specific mutations strongly affect neurovirulence of the virus.
231                                          The neurovirulence of these "spongiogenic retroviruses" is d
232                           The relative human neurovirulence of these strains was proportional to the
233 ue sections indicated that the variations in neurovirulence of these viruses could not be explained b
234                                          The neurovirulence of these viruses has long been known to b
235 Deletion of gamma134.5 greatly decreases the neurovirulence of this mutant virus but also reduces its
236 ain, and may be a key reason for the greater neurovirulence of TSE prions relative to many other auto
237                                The increased neurovirulence of vaccine derivatives has been known sin
238     These results suggest that the decreased neurovirulence of VarK may be due to its failure to effi
239                                          The neurovirulence of VSV in animal models requires the atte
240 nts of HRV2 and FMDV severely attenuated the neurovirulence of VSV without perturbing its oncolytic p
241 nize/evade immune responses, and the extreme neurovirulence of wild-type NA-EEEV may be a consequence
242 patients (JCPyV-PML) but whether they confer neurovirulence or escape from virus-neutralizing antibod
243 o determine those structures responsible for neurovirulence (or attenuation) of these chimeric viruse
244 infections may contribute to the adult mouse neurovirulence phenotype of S.A.AR86.
245 s responsible for the observed change of the neurovirulence phenotype.
246 dicate that the assay correctly assesses the neurovirulence potential of mumps viruses in humans and
247 rat model may prove useful in evaluating the neurovirulence potential of new live, attenuated vaccine
248                         We describe here the neurovirulence properties of a herpes simplex virus type
249                                              Neurovirulence properties of these recombinant viruses w
250       We aimed to characterize antigenic and neurovirulence properties of WPV1-SOAS silently circulat
251 r of potentially causal genes, including the neurovirulence protein ICP34.5 (RL1).
252  alphaherpesvirus that lacks the herpesviral neurovirulence protein ICP34.5.
253  virus 1 (HSV-1) encodes the multifunctional neurovirulence protein ICP34.5.
254 y is antagonized by the herpes simplex virus neurovirulence protein, ICP34.5.
255 ave indicated that sequences responsible for neurovirulence reside within the env gene.
256 sociated with persistent virus and increased neurovirulence, RJHM(N514S) was not more virulent than t
257 ines have neurovirulent properties, a monkey neurovirulence safety test (MNVT) is performed.
258 tates, to test a novel rat-based mumps virus neurovirulence safety test.
259                            A trend of higher neurovirulence scores was observed in monkeys inoculated
260                            Low- but not high-neurovirulence strains use sialic acid as an attachment
261 gy data from an exploratory nonhuman primate neurovirulence study indicated that some of these attenu
262 irus strains was assessed in a prototype rat neurovirulence test and compared to results obtained in
263 SH protein (rMuVDeltaSH) are attenuated in a neurovirulence test using newborn rat brains and may be
264 re apathogenic in a sensitive suckling mouse neurovirulence test, and were similar in immunogenicity
265 nt DEN virus tetravalent vaccine in a formal neurovirulence test, as well as its protective efficacy
266 ompared to that of YF-VAX in a formal monkey neurovirulence test.
267 d compared to results obtained in the monkey neurovirulence test.
268 l of neurovirulence determined by the monkey neurovirulence test.
269 st national regulatory organizations require neurovirulence testing of virus seeds used in the produc
270 , NB15a did not differ from YF5.2iv in mouse neurovirulence testing, based on mortality rates and ave
271 s and CD155 receptor-specific antibodies and neurovirulence tests in CD155 transgenic mice confirmed
272 ally stable (ie, lower risks of reverting to neurovirulence) than the Sabin monovalent OPV2 (mOPV2),
273 etic elements that contribute to adult mouse neurovirulence, the neurovirulent Sindbis virus strain A
274                                     The high-neurovirulence Theiler's murine encephalomyelitis virus
275   Infection of susceptible mice with the low-neurovirulence Theiler's murine encephalomyelitis virus
276                                      The low-neurovirulence Theiler's murine encephalomyelitis viruse
277 the sequence of the envelope gene determines neurovirulence, this effect appears to operate through a
278 esidues 68 to 87 significantly contribute to neurovirulence through an unknown mechanism.
279  that M1-D macrophages infected with the low-neurovirulence TMEV BeAn virus became apoptotic through
280  In this study, we demonstrate that the high-neurovirulence TMEV GDVII virus uses the glycosaminoglyc
281                                          Low-neurovirulence TMEV result in a persistent central nervo
282 5 mutation in the suppressor mutant restores neurovirulence to wild-type levels.
283 stinct clusters were required to restore the neurovirulence typical of the YFV/JEV Nakayama virus.
284                                              Neurovirulence was assayed in a mouse model for MV encep
285  surveillance isolates were sequenced, their neurovirulence was determined using transgenic mouse exp
286 fectious particles yielded virus whose mouse neurovirulence was highly attenuated.
287 the contribution of nsP1 Thr 538 to S.A.AR86 neurovirulence was provided by experiments in which a th
288 enetic basis of mumps virus neurotropism and neurovirulence was until recently not understood, largel
289 e only feature that correlated with relative neurovirulence was viral burden as measured by both vira
290 s system (CNS) infection that correlate with neurovirulence, we compared two neurovirulent MuLV, Fr98
291    To identify the molecular determinants of neurovirulence, we constructed an infectious simian immu
292 this hyperactive membrane fusion activity in neurovirulence, we discovered that the growth of JHM in
293         To investigate how histidine confers neurovirulence, we examined the various stages of the vi
294  better understand the determinants of HIV-1 neurovirulence, we isolated viruses from brain tissue sa
295 andidate host genes that modulate alphavirus neurovirulence, we utilized GeneChip Expression analysis
296                            No differences in neurovirulence were seen between the wild-type and the S
297 ruses passaged in vivo demonstrate decreased neurovirulence, whereas those passaged in vitro demonstr
298 aviruses attenuates S.A.AR86 for adult mouse neurovirulence, while introduction of Thr at position 53
299 viruses (mouse hepatitis virus) of different neurovirulences with primary cell cultures of brain immu
300 is important for efficient neural spread and neurovirulence within the CNS and could not be replaced

 
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