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1 ternalized with CD63, which is necessary for virus production.
2 l DNA replication, late gene expression, and virus production.
3 protein as the determinant for heterologous virus production.
4 igomers triggers viral filament assembly and virus production.
5 packaging of DIP genomes can interfere with virus production.
6 molecule inhibitors also reduces infectious virus production.
7 lasma HIV-1 RNA from ex vivo measurements of virus production.
8 ytoplasmic virion envelopment and infectious virus production.
9 05) in M that is critical for RSV infectious virus production.
10 n synthesis, virion assembly, and infectious virus production.
11 some-lysosome fusion, resulting in increased virus production.
12 ides a promising target for interfering with virus production.
13 orylation-dependent regulation of infectious virus production.
14 xogenous glucose is not required for maximal virus production.
15 duced stress-induced apoptosis and increased virus production.
16 in NS5A hyperphosphorylation and infectious virus production.
17 ytoplasmic virion envelopment and infectious virus production.
18 hese processes are coordinated for efficient virus production.
19 ormation of the VAC for efficient infectious virus production.
20 efficient virion envelopment and infectious virus production.
21 unable to suppress viral DNA replication or virus production.
22 portantly, is required for infectious dengue virus production.
23 ich E7 replaces UL97 are still defective for virus production.
24 ct on JFH1 genome replication but attenuated virus production.
25 d in E1 transport to the plasma membrane and virus production.
26 n levels and ultimately promoting infectious-virus production.
27 kedly depends on the host cell line used for virus production.
28 ion but are defective for infectious progeny virus production.
29 s yet another role for NS2 in later steps in virus production.
30 e the role of the F protein CT in infectious virus production.
31 , and POU2F1 knockdown diminished infectious virus production.
32 these two proteins also moderately inhibited virus production.
33 s to alter the cellular environment to favor virus production.
34 ks had various levels of impaired infectious virus production.
35 ity of ORF57 to support KSHV replication and virus production.
36 induces little viral gene expression and no virus production.
37 mbryonated chicken eggs, a common source for virus production.
38 adenovirus (Ad) infection to achieve optimal virus production.
39 of IRES-mediated translation and infectious virus production.
40 c domains play important roles in infectious virus production.
41 xpression, protein abundance, and infectious-virus production.
42 e active conformation required for efficient virus production.
43 ion of many KSHV genes, and is essential for virus production.
44 ression, viral DNA packaging, and infectious virus production.
45 residue to be essential for infectious H77S virus production.
46 required for efficient KSHV reactivation and virus production.
47 m more favorable for replication and progeny virus production.
48 were most effective when added early during virus production.
49 plays an important, as-yet-undefined role in virus production.
50 ed culture with immune suppressants enhanced virus production.
51 NAs; however, the majority are defective for virus production.
52 ase of the cell cycle was more efficient for virus production.
53 beneficial role in viral gene expression and virus production.
54 s cytopathic but had no effect on infectious virus production.
55 on nonviral RNA, preserving the protein for virus production.
56 , RNA and protein expression, and infectious virus production.
57 els and an approximately 10-fold decrease in virus production.
58 aired both in RNA replication and infectious virus production.
59 es that promote viral genome replication and virus production.
60 acellular compartments and severely inhibits virus production.
61 reduction in MVC DNA replication and progeny virus production.
62 pression, viral DNA synthesis, or infectious virus production.
63 ype I interferon transcripts to thus inhibit virus production.
64 2 protease activity but decreased infectious virus production.
65 tein processing, replication, and infectious virus production.
66 ial but poorly understood role in infectious virus production.
67 th HCV subgenomic replication and infectious virus production.
68 viral transcription influences the level of virus production.
69 of CDK13 leads to a significant increase in virus production.
70 the in vitro protein binding efficiency and virus production.
71 V entry, viral gene expression or infectious virus production.
72 eins Gag and Env and subsequently suppresses virus production.
73 d by viral protein production and infectious virus production.
74 ranslation of viral structural proteins, and virus production.
75 g mutations in E2, p7, and NS2 all increased virus production.
76 her than macrophages, are the main source of virus production.
77 anscription, DNA replication, and infectious virus production.
78 nd sustaining its expression to culminate in virus production.
79 omplex to overcome host defences and promote virus production.
80 by a reverse genetics method of recombinant virus production.
81 re' strategies targeting multiple sources of virus production.
82 r the UEV Ub binding function contributes to virus production.
83 siRNA) or Mdivi-1 caused marked reduction in virus production.
84 interfere with virus particle formation and virus production.
85 hibits a pronounced kinetic delay in progeny virus production.
86 nfectivity without any significant impact on virus production.
87 oit AAK1 and GAK during entry and infectious virus production.
88 cytoplasmic densities near sites of prolific virus production.
89 notype, susceptibility to ASFV infection and virus production.
90 rmation, and envelopment to complete de novo virus production.
91 th a heme analog, led to marked increases in virus production.
92 information in the absence of any infectious virus production.
93 ulation at early times without affecting net virus production.
94 M protein, which is essential for infectious virus production.
95 ytoplasmic virion envelopment and infectious virus production.
96 the nonpermissive cell to ensure infectious virus production.
97 V-infected cells were accompanied by reduced virus production.
98 ian cells leads to viral RNA replication and virus production.
99 t myeloid cells are not an in vivo source of virus production.
100 to inhibit virion envelopment and infectious virus production.
101 ons, which was associated with a decrease in virus production.
102 -1 pathway and enhances EBV reactivation and virus production.
103 alization in transfected cells and abolished virus production.
104 ction in the absence of infectious cell-free virus production.
105 sion after the onset of DNA replication, and virus production.
106 essential for EBV replication and infectious virus production.
107 IV genome demonstrated further inhibition of virus production.
108 d leading to a much reduced viral spread and virus production.
109 ep in the process of assembly and infectious virus production.
110 l virus, Nipah virus) to suppress infectious virus production.
111 whose propagation adversely affects its host virus' production.
112 s reestablish a resting state without active virus production after extended culture and maintain a s
113 d also caused a 10- to 100-fold reduction in virus production, along with decreased viral DNA replica
114 otides on HIV-1 RNA abundance and infectious virus production and also enhanced the production of mur
117 mutants exhibited more pronounced defects in virus production and DNA synthesis in quiescent cells as
119 tion activates signaling pathways to enhance virus production and facilitate virus reactivation from
120 due 76 (Y76A), were essential for infectious virus production and filament formation while having lim
121 protein that drastically reduces infectious virus production and filament formation with minimal eff
122 d gKDelta31-68 mutant viruses for infectious-virus production and for gKDelta31-68/gBDelta28syn-media
124 ap the determinants necessary for infectious virus production and gain further insight into the multi
125 /6 mice, supported high levels of infectious virus production and high viral protein expression level
127 ated that a Q221N mutation minimally rescued virus production and led to a second-site I399V mutation
128 imilarly, I399V alone allowed only low-level virus production and led to selection of an I286V mutati
129 treatment with XX-650-23 reduced infectious-virus production and limited lesion formation compared t
130 ike M gene, showed an early surge in progeny virus production and more severe pathology and extrapulm
131 H2 but showed wild-type levels of infectious virus production and no increase in ICP0 expression in l
132 the NEC in infected cells and also decreased virus production and nuclear egress in the absence of ma
133 as L-domain activity essential for efficient virus production and pathogenicity but is not essential
134 mphoid tissues (LTs), the principal sites of virus production and persistence before initiating ART.
135 bition of HIV replication was due to reduced virus production and reduced infectivity of produced vir
137 irus showed further cooperative increases in virus production and severity of infection in vitro and
138 ecause apoptosis of infected cells can limit virus production and spread, some viruses have co-opted
140 ow that decreasing IFI44L expression impairs virus production and that IFI44L expression negatively m
141 ow that decreasing IFI44L expression impairs virus production and that IFI44L expression negatively m
142 s, and FAS are all required for maximal KSHV virus production and that these pathways appear to parti
144 virus were disrupted at sequential stages of virus production and were visualized by atomic force mic
145 critical role for these cells in suppressing virus production and/or reactivation in vivo under ART.I
151 BRA, amplifies the lytic cascade, increasing virus production, and, importantly, prevents the abortiv
152 o caspase-mediated capsid cleavage increased virus production approximately 3- to 5-fold in CrFK cell
153 he period between infection and the start of virus production), as well as the rate at which infectio
156 ter, short-term transcription, and long-term virus production assays revealed that both pUL138-L and
157 on has been unclear, although it facilitates virus production at a late assembly or release step.
158 that these pathways appear to participate in virus production at different stages of the viral life c
159 t disrupt these salt bridges were lethal for virus production, because the mutant proteins assembled
160 ing early infection, allowing for sufficient virus production before RNase L activation is detectable
161 v10 by 80% resulted in a 2-fold reduction in virus production but no discernible impact on the infect
164 fect on the efficiency of protein binding or virus production, but mutation of a nucleotide in the mi
165 2 86 alone provides some complementation for virus production, but the correct temporal expression of
166 inhibited HCV replication and/or infectious virus production by >100-fold, with one (quinidine) inhi
167 , with one (quinidine) inhibiting infectious virus production by 450-fold relative to HCV replication
168 for several weeks and could be activated to virus production by a combination of a histone deacetyla
169 IIalpha siRNAs decreased HCV replication and virus production by almost 100%, they had no effect on i
170 ignificant cytopathic effects and infectious virus production by day 14; genome copy numbers were equ
171 ed rate of genome replication and infectious virus production by EG PV without impacting the final yi
172 ode US11, an immune antagonist that promotes virus production by preventing shutdown of protein trans
174 Rather, SLFN11 acts at the late stage of virus production by selectively inhibiting the expressio
178 mide 1 (DPH1) gene, which enable both robust virus production by transfection and evaluation of DTA-e
179 with different amounts of XMRV and monitored virus production by using quantitative real-time PCR.
181 approximately 1-log reduction in infectious virus production compared to that of the wild-type virus
182 omain 1 of the helicase which fully restored virus production, confirming the involvement of both maj
183 d, demonstrating that the DDR contributes to virus production, despite its recognized antivirus role.
184 of RNase L during infection typically limits virus production dramatically, we used CRISPR-Cas9 gene
185 partner, ORF38, are required for infectious virus production due to their important role in the tegu
186 ture, including differences in the amount of virus production, extracellular virus release, and cell-
187 oplasmic envelopment, egress, and infectious virus production, followed by the double deletion of UL1
189 nomes results in a 5- to 7-fold decrement in virus production following lytic induction, indicating t
190 ase active-site mutant HIV-1 yielded de novo virus production following subsequent T cell activation.
191 Notably, adaptive mutations known to enhance virus production from GT 1a-2a chimeric genomes further
192 ntributions of ongoing virus replication and virus production from HIV-1 reservoirs to persistent low
198 ion might lead to HIV persistence by causing virus production, generating new target cells, enabling
199 _G209 substitution mutants had any effect on virus production; however, the deletion mutant (DeltaG20
200 to HIV-1 pathogenesis through modulation of virus production, impairment of the adaptive immune resp
201 , in vivo delivery of anti-D5 siRNAs reduced virus production in a mouse model of VACV infection.
206 ession of BGLF2 induced BZLF1 expression and virus production in EBV-infected gastric carcinoma cells
207 otein (NP) level and inhibition of influenza virus production in infected cell lines (MDCK and A549).
208 tion mechanisms have focused on the stage of virus production in infected cells, when large numbers o
209 roviruses, along with evidence of continuing virus production in LT despite ART, indicated two import
210 ic cells (FDCs) increase HIV replication and virus production in lymphocytes by increasing the activa
212 expression substantially enhanced infectious virus production in quiescent cells, but did not complem
213 we observed a significant reduction of HIV-1 virus production in Src homology 2 domain-containing leu
214 ing that UL97-dependent defects in cell-free virus production in strains with full-length ULb' region
215 Mutant spectrum analyses and kinetics of virus production in the absence and presence of drugs in
216 g time points, providing evidence of ongoing virus production in the gut and equilibrium of HIV-1 bet
217 M1 suppressor mutations restored infectious virus production in the presence of M2Y76A and mediated
219 from wild-type virus in terms of infectious virus production in the trigeminal ganglia during acute
223 lly recapitulates HCV entry, replication and virus production in vitro to re-examine the issue of HCV
226 drial ROS production strongly suppresses RSV virus production, including in a mouse model with concom
227 absent v-chemokine supplementation inhibited virus production, indicative of autocrine effects of end
229 ly down modulated during HIV-1 infection and virus production inversely co-related with HspBP1 expres
230 LLINI treatment, and compound potency during virus production is independent of the level of LEDGF/p7
231 h LAT sRNA2 was less effective at inhibiting virus production, it inhibited expression of infected ce
232 Although N-803 alone did not reactivate virus production, its administration after the depletion
233 r intracellular and extracellular infectious virus production late in the infection, suggesting that
234 ntracellular ERK, however, failed to inhibit virus production, likely due to maintenance of residual
235 wn, have significant inhibitory effects upon virus production, making PRF essential for HIV-1 replica
237 ivity in vitro prior to in vivo inoculation, virus production methods may differentially affect stock
239 dy-state levels of the HIV-1 Gag protein and virus production; Mov10 was efficiently incorporated int
240 om all major HCV genotypes, we observed that virus production occurred in a genotype- and isolate-dep
241 , no enhancement of viral DNA replication or virus production occurred in cGAS or STING shRNA-targete
243 ificantly inhibited viral spread and progeny virus production of mut-Ad3GFP but not of wt-Ad3GFP.
246 demonstrated no discernible impact on either virus production or infectivity of the resultant particl
251 lls showed a significant reduction in budded virus production, providing further evidence for the inv
255 cells overexpressing Bim restored levels of virus production similar to those seen with virus-infect
257 ilencing NRAV suppressed IAV replication and virus production, suggesting that reduction of NRAV is p
259 led to 1,000- to 250,000-fold-higher progeny virus production than in the absence of tetracycline, wh
260 nction significantly extends the timespan of virus production, thereby increasing the chances for vir
261 lso VZV DNA accumulation, transcription, and virus production, thereby prolonging the life of VZV-inf
262 However, a subset of mutations still led to virus production, thus revealing the key IRES-ribosome i
264 t3 activation, as a Stat3 inhibitor restored virus production to levels observed without IL-10 stimul
265 could at least partially restore infectious virus production to M2-deficient influenza A viruses.
266 ains unknown the contribution of spontaneous virus production to the expansion of KSHV-infected tumor
267 of these mutations into the chimera rescued virus production to various levels, suggesting a genetic
268 oduction of cells and viruses, with enhanced virus production under carbon-limiting growth conditions
269 of-function phenotype, increasing infectious virus production up to 1 log more than in the wild-type
270 ed that nucleolin was required for efficient virus production, viral DNA synthesis, and the expressio
271 ques that did not develop SIVE, more ex vivo virus production was detected from monocyte-derived macr
273 e contribution of Rad18 levels to infectious virus production was examined with small interfering RNA
282 infectious virus in transfected cells, while virus production was rescued to near-wild-type levels in
285 xamine the consequences of MVB targeting for virus production, we investigated 29/31KE particle produ
287 role of this cytoplasmic tail in infectious virus production, we used reverse genetics to generate a
288 of reduced viral gene expression and progeny virus production were also observed in normal fibroblast
292 tors robustly induce HIV-1 transcription and virus production when directly compared with maximum rea
293 led to a substantial decrease in infectious virus production, whereas starving infected cells of exo
294 B (HIV-1B) infection of macrophages enhanced virus production, while CCL2 immuno-depletion reversed t
295 ormation and drastic reduction in infectious virus production, while mutation of C82 and C243 caused
297 d indirect effects of nutrient limitation on virus production within hosts, we manipulated soil nitro
299 of pp150, significantly reducing infectious virus production without affecting the formation of the