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1 than IgA(+/+) mice (13 vs 75% survival after virus challenge).
2 n provide protection against any influenza A virus challenge.
3 e given a lethal western equine encephalitis virus challenge.
4 rred protection against homologous wild-type virus challenge.
5  to homosubtypic, as well as heterosubtypic, virus challenge.
6 rotected ferrets from an unmatched 2007 H1N1 virus challenge.
7 tment protects mice against lethal influenza virus challenge.
8 logous and heterologous H1N1 as well as H5N1 virus challenge.
9 lizing antibody and protective immunity upon virus challenge.
10 uenza virus was protective against influenza virus challenge.
11  and 50% protection against lethal H5N1 HPAI virus challenge.
12  MVA-NP+M1 vaccination followed by influenza virus challenge.
13 NA-antibody-based protection against in vivo virus challenge.
14 r homologous or, in some cases, heterologous virus challenge.
15 course of ST-246 and survive lethal vaccinia virus challenge.
16 d its durability against heterosubtypic H5N1 virus challenge.
17 and the absence of viremia in pigs following virus challenge.
18 from the nasal cavity in all pigs after live virus challenge.
19 re measured at enrollment and again prior to virus challenge.
20 ould these mice inhibit RSV replication upon virus challenge.
21 dy was able to protect mice in a lethal H2N2 virus challenge.
22 olled virus load but did not protect against virus challenge.
23 rotection to mice against a lethal influenza virus challenge.
24 ation retain the ability to respond to local virus challenge.
25  against a highly pathogenic avian influenza virus challenge.
26 ponse, and incomplete protection from p-H1N1 virus challenge.
27 ociated with complete protection from p-H1N1 virus challenge.
28 re autoinflammatory disease in response to a virus challenge.
29 ainst a heterologous simian immunodeficiency virus challenge.
30 cted mice from a lethal recombinant vaccinia virus challenge.
31 s fully protected ferrets from parental HPAI virus challenge.
32 rosubtypes protected against lethal CA/E3/09 virus challenge.
33 d L1R were protected against lethal vaccinia virus challenge.
34 ted neutralizing antibody response following virus challenge.
35 ng the potential for rapid mobilization upon virus challenge.
36 ion against the heterologous avian influenza virus challenge.
37 e and ferrets from homologous wild-type (wt) virus challenge.
38  are required based on the route of vaccinia virus challenge.
39  complete protection against lethal vaccinia virus challenge.
40 ry CD8(+) T cells to the lung airways during virus challenge.
41 cted mice against a lethal systemic vaccinia virus challenge.
42 boosted as a recall response after monkeypox virus challenge.
43 on and the rapid kinetics of expansion after virus challenge.
44 nses and providing protection against lethal virus challenge.
45 ver survived and were readily recalled after virus challenge.
46 ntranasal route of a lethal dose of vaccinia virus challenge.
47 sponses, which were reactivated rapidly upon virus challenge.
48  100% protection from disease after virulent virus challenge.
49 dy response or to provide protection against virus challenge.
50 2 genome copies in dorsal root ganglia after virus challenge.
51 st resistant transgenic plant lines prior to virus challenge.
52 h the levels of Gag-specific immunity before virus challenge.
53 at the site of infection following influenza virus challenge.
54 ection from detectable infection by virulent virus challenge.
55 d CD8+ memory T cells can confer immunity to virus challenge.
56  production of infectious virus after a live-virus challenge.
57 is and interstitial pneumonitis after a live-virus challenge.
58 protected adult AG129 mice against lethal D1 virus challenge.
59 protects guinea pigs from lethal Ebola Zaire virus challenge.
60 mice and ferrets from lethal H5N1 homologous virus challenge.
61 rferon were produced by CD4(+) T cells after virus challenge.
62 e recombinant virus but only against mucosal virus challenge.
63 ogression following a highly pathogenic AIDS virus challenge.
64 sue virus titers observed on day 5 post-H5N1 virus challenge.
65 rotected unvaccinated mice from lethal Ebola virus challenge.
66 mitted systemically in response to localized virus challenge.
67 veral criteria, including protection against virus challenge.
68 re than 50% of the control fish succumbed to virus challenge.
69 n-human primates against viraemia after Zika virus challenge.
70 ) and develop tumors following radiation and virus challenge.
71  CTLp in mice against cross-strain influenza virus challenge.
72 n and mortality following a lethal influenza virus challenge.
73 tes more rapid recovery after heterosubtypic virus challenge.
74 nd protected chickens against wild-type H5N1 virus challenge.
75 ection or hepatitis during 2 years following virus challenge.
76  elaboration measured either 6 or 24 h after virus challenge.
77 cilitate virus clearance upon heterosubtypic virus challenge.
78 iding for at least a month after the initial virus challenge.
79 ces can elicit protection against parenteral virus challenge.
80 ed some evidence of infection at the site of virus challenge.
81 erring protection in a stringent influenza A virus challenge.
82 ntibodies and protect mice against influenza virus challenge.
83 ing antibody titers and survival rates after virus challenge.
84  subsequent virulent simian immunodeficiency virus challenge.
85 y heightened vascular permeability following virus challenge.
86 es shows better protection against influenza virus challenge.
87 mplete protection when administered prior to virus challenge.
88 d was able to protect mice against influenza virus challenge.
89 e-VLP were protected against homologous H1N1 virus challenge.
90 nea pigs from lethal disease when given post-virus challenge.
91 de protective host immunity against a lethal virus challenge.
92 mice and their efficacy against lethal Ebola virus challenge.
93  administration in ferrets after NiV and HeV virus challenge.
94 iated protective responses against influenza virus challenge.
95 nt to mediate protection against respiratory virus challenge.
96 fornia/07/2009, protects mice against lethal virus challenge.
97  vaccine candidate to protect against lethal virus challenge.
98 re to ATCV-1 in vitro for up to 72 h after a virus challenge.
99 highly susceptible to secondary heterologous virus challenge.
100 systemic disease and encephalitis after H5N1 virus challenge.
101 stem were protected against lethal influenza virus challenge.
102 ed in cornea pathology in response to ocular virus challenge.
103 cell immunity against heterologous influenza virus challenge.
104  48, or 72 hours after A/Anhui/1/2013 (H7N9) virus challenge.
105 ow and conferred protective immunity against virus challenge.
106 uited regulatory cells and neutrophils after virus challenge.
107 e amplification observed following influenza virus challenge.
108 mmalian and avian species exposed to similar virus challenges.
109 en reported against neutralization-sensitive virus challenges.
110 ect all TDF treated animals against multiple virus challenges.
111 tely prevented infection, even after mucosal virus challenges.
112 d heterosubtypic [A/Philippines/2/82 (H3N2)] virus challenges.
113 magnitude to protect against pathogenic AIDS virus challenges.
114 gainst homologous and heterologous influenza virus challenges.
115 ce from 8 of 9 lethal heterologous influenza virus challenges.
116 ut was ineffective against repeated low-dose virus challenges.
117 eterosubtypic H1N1, H3N2, and H5N1 influenza virus challenges.
118 otection in pigs but only against homologous virus challenges.
119 tion against homo- and heterosubtypic lethal virus challenges.
120 gainst homologous and heterologous influenza virus challenges.
121  heterologous protection against influenza A virus challenges.
122  protected aged mice from 2009 pandemic H1N1 virus challenge 16 months after vaccination.
123 cutaneous vaccination followed by a virulent virus challenge 6 months later.
124 esponses was examined with two separate live-virus challenges administered at 4 and 24 weeks after th
125 yed no protection against the heterosubtypic virus challenge after immunization with PC nanogel-adjuv
126 es complete protection from lethal influenza virus challenge after intranasal administration.
127                Interestingly, at day 7 after virus challenge, all of the fish vaccinated with the IHN
128                              Following Lassa virus challenge, all unvaccinated animals died (0% survi
129  confer protection against a normally lethal virus challenge, although the CTL appear fully functiona
130 ogical outcomes following virulent influenza virus challenge, although the effect is not clearly corr
131 n host) for the immune responses to a rabies virus challenge, an immunotypic disease model that descr
132 te protection against lethal homologous H5N1 virus challenge and a reduction in virus shedding and di
133 an initial H1N1pdm09 infection survived H5N1 virus challenge and cleared virus from the respiratory t
134 -primed mice protected from lethal influenza virus challenge and enhanced survival with less weight l
135  for lethality prediction following vaccinia virus challenge and for gaining insight into protective
136 severity after heterologous clade 2.2.1 H5N1 virus challenge and increased virus-specific serum and n
137       Infant macaques can respond rapidly to virus challenge and mount strong innate immune responses
138 body 14G7 is protective against lethal Ebola virus challenge and recognizes a distinct linear epitope
139 enuated SIVmac239Delta3 against heterologous virus challenge and suggest that even live, attenuated v
140 lular immune response to secondary influenza virus challenges and offer an additional parameter to co
141  Gag-Pol, in the control of immunodeficiency virus challenges and the protection of CD4(+) cells.
142 t in the blood and most tissues 3 days after virus challenge, and severe inflammatory lesions were fo
143           Immunized mice were protected from virus challenge, and survival times increased following
144 rovide prolonged protection against multiple virus challenges, and different administration times wit
145 :123) with the establishment of infection in virus-challenged animals.
146   Lymphocyte recruitment to the vagina after virus challenge appeared to involve memory lymphocytes,
147                                           In virus challenge assays, treatment with Intrepid-2F prior
148                                        After virus challenge both CD4(+) T cells and NK cells in feta
149 cytolytic (granzyme B) response to influenza virus challenge, both of which have been shown to correl
150 V) protected ferrets against homologous H3N2 virus challenge but provided minimal to no protection ag
151 odels of CCHFV infection reliably succumb to virus challenge but vary in their ability to reflect sig
152 ute and chronic lymphocytic choriomeningitis virus challenges, but did not affect the ability to clea
153  correlated to complete protection from live virus challenge by a single vaccination at a dose ten ti
154 iratory disease (ERD) in mice following H3N2 virus challenge by demonstrating increased lung patholog
155 D4 T-cell-mediated protection from influenza virus challenge by HA-specific memory T cells and hetero
156 an initial line of defense against secondary virus challenge by limiting early viral replication at t
157 rovide protection from secondary respiratory virus challenge by limiting early viral replication.
158 ombinant gp160 vaccines against the uncloned virus challenge by the intrarectal route compared with t
159 t bNAb-mediated protection against a mucosal virus challenge can involve clearance of infectious viru
160                        Thus, within hours of virus challenge, CD8(+) memory T cells display the stand
161 anisms involved in mediating protection from virus challenge compared to those that control an establ
162 ved protection against Listeria and vaccinia virus challenges compared with the Armstrong boost.
163 ction in lung tissue following H5N1 and 1918-virus challenge, compared with wild-type control mice.
164 ors in protective immunity against influenza virus challenge conferred by NP DNA.
165                                    Following virus challenge, control animals experienced a rapid and
166                           Protection from wt virus challenge correlated well with the level of serum
167 body b12 serum concentrations at the time of virus challenge corresponded to approximately 400 (25 mg
168 ) or IFNGR1(-/-) mice followed by intranasal virus challenge demonstrated both that IFN-gamma produce
169 against lethal heterosubtypic H5N1 influenza virus challenge despite the absence of detectable H5N1 n
170  the older monkeys required a 150-fold-lower virus challenge dose than the neonates (P=3.3 x 10(-5)).
171 escribed that uses an empirically determined virus challenge dose, a single dilution of antiserum, an
172 ed in the lungs of IFN-gamma(-/-) mice after virus challenge, either Th1- or Th2-biased responses cou
173 ined TLR/CD40 immunization, because vaccinia virus challenge elicited primarily OX40L-dependent CD4 r
174 , but FcgammaRIIB blockade during homologous virus challenge enhanced the secondary CD8 T cell respon
175 cells may be present at the time and site of virus challenge, establishing a high level of CD8(+) T c
176 ompletely protected against lethal influenza virus challenge even 120 days after immunization.
177                                   After live virus challenge, expansion of Th1 cells seems to facilit
178 nd discuss the outcome and interpretation of virus challenge experiments in animals.
179  nasal washes of homologous and heterologous virus challenged ferrets.
180 s, a group of eight infectious salmon anemia virus-challenged fish were included to observe T cell re
181                       However, upon a second virus challenge following BCD pretreatment, the majority
182 educed protective efficacy against wild-type virus challenge following vaccination.
183 model based on repeated low-dose influenza A virus challenges given within a short period.
184 ow-dose H1N1 virus infection against an H3N2 virus challenge, given 4 weeks later.
185  and protected animals from lethal influenza virus challenge, highlighting the potential clinical use
186 of DBA/2 mice against lethal wild-type pH1N1 virus challenge; however, at a lower dose (1 mg/kg), HF5
187  were not protected against lethal monkeypox virus challenge if their CD4(+) cell count was <300 cell
188 trolled a highly pathogenic immunodeficiency virus challenge in a rhesus macaque model.
189  T-cell responses and protected mice against virus challenge in an infectious disease model and provi
190                    BnAbs can protect against virus challenge in animal models, and many such antibodi
191 tfusion F can also induce protection against virus challenge in animals.
192 mmune responses against homologous secondary virus challenge in both asthmatic and nonasthmatic mice,
193 ng is functional using a heterologous lethal virus challenge in ferrets.
194  elicited sterilizing immunity against Lassa virus challenge in guinea pigs and marmosets and virus-s
195 erred complete protection against homologous virus challenge in mice, and the serum antibodies direct
196 rotection against a lethal dose of influenza virus challenge in mice, demonstrating the potential of
197 s-strain protection against a lethal dose of virus challenge in mice.
198 luated following highly pathogenic influenza virus challenge in mice.
199 -MS immunization provided protection against virus challenge in mice.
200  CTL and cross-strain protection from lethal virus challenge in mice.
201 ted flies, confer passive protection against virus challenge in naive animals.
202 nd provided partial protection (55%) against virus challenge in outbred New Zealand White rabbits.
203 8+ T cells, which protected against a lethal virus challenge in the absence of other mechanisms, incl
204  an H5N1 LAIV against highly pathogenic H5N1 virus challenge in the absence of significant pulmonary
205 unogenicity and protection against wild-type virus challenge in the ferret model.
206 y in reducing viral loads after an influenza virus challenge in the ferret model.
207 -NA antibodies protect from lethal influenza virus challenge in the mouse model and correlate inverse
208 tested by passive antibody transfer and oral virus challenge in the rhesus macaque model for EBV infe
209 erred complete protection from homologous wt virus challenge in the upper respiratory tract.
210 es in vitro and protected mice against Ebola virus challenge in vivo.
211  displayed effector functions in response to virus challenge in vivo.
212 nst a lethal heterologous A/Puerto Rico/8/34 virus challenge in vivo.
213 to raise protection against immunodeficiency virus challenges in rhesus macaques.
214 gent, heterologous, neutralization-resistant virus challenges in rhesus monkeys.
215  protection against neutralization-resistant virus challenges in rhesus monkeys.
216 inst acquisition of neutralization-resistant virus challenges in rhesus monkeys.
217 ighly protective against homologous virulent virus challenges in type I interferon receptor (IFNAR)-k
218 ot result in enhanced disease following live-virus challenge, in contrast to the histopathology seen
219 tal YFV-17D were not protected against DEN-2 virus challenge, indicating that protection was mediated
220  upregulated in the vaginal epithelium after virus challenge, indicating that virus-specific memory T
221                    When allowed free choice, virus-challenged individuals chose a higher protein diet
222 a high level of protection against wild-type virus challenge infection compared to the strain with th
223 icant protection against a heterologous H1N1 virus challenge infection in the upper respiratory tract
224 rotective activities against a lethal rabies virus challenge infection, with SPBN-Cyto c(+) revealing
225 red lung T(CD8) during heterotypic influenza virus challenge infection.
226 challenged and simian-human immunodeficiency virus-challenged macaques.
227 nst homologous and heterologous wild-type H7 virus challenge, making it suitable for use in protectin
228 cific CD8(+) T-lymphocyte response following virus challenge may exert suppressive effects on primed
229 aditional models based on a single high-dose virus challenge may have limitations.
230                          Thus, during lethal virus challenge, memory CD8(+) T cells are required for
231 ed into the central nervous systems of DEN-2 virus challenged mice.
232 ically, conferring enhanced survival of H5N1 virus-challenged mice when treatment was begun 72 h afte
233 nferred Fc-dependent protection to influenza virus-challenged mice.
234                               Upon influenza virus challenge, mice vaccinated with the hyperglycosyla
235 able animal model for dengue, a human dengue virus challenge model (ie, a controlled live dengue viru
236 ll recipients using a tumor and an influenza virus challenge model.
237 vaccines was confirmed in a lethal influenza virus challenge model.
238 ) antigens A33R and B5R in a murine vaccinia virus challenge model.
239 vided protection for >2 years in a monkeypox virus challenge model.
240 n than intramuscular vaccination in a lethal virus challenge model.
241 points during human A/California/2009 (H1N1) virus challenge monitored using mass cytometry along wit
242 s in the plasma calculated to protect 99% of virus-challenged monkeys was 1:38.
243 bolished the transmission capacity of dengue virus-challenged mosquitoes.
244 d ST-246 in prairie dogs against a monkeypox virus challenge of 65 times the 50% lethal dose (LD(50))
245                                         Live virus challenge of animals given SARS or MERS vaccines r
246 research and development, a single high-dose virus challenge of animals is used to evaluate vaccine e
247 her to provide reinforced protection against virus challenge of rhesus macaques.
248 g a pathogenic simian-human immunodeficiency virus challenge of rhesus monkeys vaccinated with plasmi
249 acy against homologous and heterologous live virus challenge of the resulting VLPs were tested after
250                          Using two disparate virus challenges of mice, we show that splenic CD8(+) me
251 0-1074) in blocking repeated weekly low-dose virus challenges of the clade B SHIVAD8.
252 ection were protected against herpes simplex virus challenge only if the gC antibodies blocked C3b bi
253                                        After virus challenge, only the Fluzone/CLDC-vaccinated animal
254 prophylaxis (beginning seven days before the virus challenge) or treatment (beginning at the time of
255 onstrated enhanced protection from wild-type virus challenge over that for mice vaccinated with an rP
256 D and SIV(mac251) in subsequent intravaginal virus challenges (P = 0.63), despite the potent antivira
257 y the absence of TNF-alpha induction in H5N1 virus-challenged pigs, coincided with greater cell death
258 20-fold reduction of chemokine expression in virus-challenged PLNs, CXCR5 remained essential for B-ce
259 ce tolerized to alphaMYHC are protected from virus challenge proving pathogenesis depends upon autoim
260 ponse to HA and confer immunity to influenza virus challenge relative to the commercial vaccines Fluz
261  delay in transferring NAbs until 24 h after virus challenge resulted in infection in two of two monk
262                             Corneal vaccinia virus challenge resulted in the infiltration of B cells,
263                             Recent monkeypox virus challenge studies have established the black-taile
264  Results of both natural history studies and virus challenge studies with macaques indicate that resp
265                            For both of these virus challenge studies, significant protection from vir
266 n a large scale serially sampled respiratory virus challenge study we quantify the diagnostic advanta
267 prophylactic treatment in a mouse intranasal virus challenge study, and systemic administration of th
268 ct mice against a lethal intranasal vaccinia virus challenge, suggesting that both IMV- and EEV-speci
269                                         Upon virus challenge, TAM-deficient DCs display type I IFN re
270 provided better protection against H5N1 HPAI virus challenge than did PIV5-NP-HN/L.
271 rbohydrate (C) were more likely to survive a virus challenge than those restricted to diets with a lo
272  T cells exhibited protection from influenza virus challenge that occurred in the presence of CD8-dep
273 t is T cells already resident at the site of virus challenge that offer superior immune protection.
274                         After heterosubtypic virus challenge, the accumulation of CD8 T cells in the
275 longer the delay between MVC application and virus challenge, the less protection (half life of appro
276 irus (SIV) and simian-human immunodeficiency virus challenges, the specific immune responses that con
277 nt work on hepatitis A virus and hepatitis E virus challenges this long-held tenet.
278 s directed protective responses to influenza virus challenge through intrinsic effector mechanisms, r
279 memory responses after a secondary influenza virus challenge, thus indicting the nonredundant functio
280                             Within 3 days of virus challenge, vaccinated mice showed high levels of a
281  of signs of disease and of detectable Ebola virus challenge virus.
282 allenged with homologous and heterologous H5 viruses, challenge virus replication was reduced in the
283 v) gene was analyzed in relation to route of virus challenge, virus load, and neutralizing antibody (
284 al protection against heterologous influenza virus challenge was achieved following either IM/IM or I
285 a-specific memory CD4 T cells in response to virus challenge was completely abrogated by CTLA4Ig with
286 unized mice against recombinant HCV-vaccinia virus challenge was higher than that observed in HCV DNA
287       Similarly, the mortality from vaccinia virus challenge was significantly greater in RGKO mice t
288 sponses and protective immunity to influenza virus challenges was evaluated using a DNA vaccine encod
289 r understand the overall response to Marburg virus challenge, we undertook a transcriptomic analysis
290 ibody, on the control of an immunodeficiency virus challenge, we vaccinated Mamu-A*01(+) macaques wit
291 after infection with a high-dose, oral-nasal virus challenge were protected from disease, whereas all
292 ated monkeys (DNA or HDCV) survived a rabies virus challenge, whereas monkeys vaccinated with only th
293                   HA seroconverters survived virus challenge, whereas unvaccinated controls and vacci
294 nce the immune response to primary influenza virus challenge while preventing potentially damaging ch
295  immunized with either gD or gHt-gL survived virus challenge, while many control animals died.
296 hamsters remained active following wild-type virus challenge, while mock-immunized hamsters displayed
297 ted with reduced shedding of a pandemic H1N1 virus challenge, while vaccination with MVA encoding nuc
298                              Intranasal live virus challenge with a recombinant vaccinia virus expres
299  and conferred complete lung protection from virus challenge, with no ERD signs in the form of alveol
300  a lethal A/Duck/Laos/25/06 (H5N1) influenza virus challenge, with no evidence of morbidity, mortalit

 
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