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1 enovirus or EC material during all phases of virus production).
2 ytoplasmic virion envelopment and infectious virus production.
3 hese processes are coordinated for efficient virus production.
4 ormation of the VAC for efficient infectious virus production.
5 efficient virion envelopment and infectious virus production.
6 unable to suppress viral DNA replication or virus production.
7 portantly, is required for infectious dengue virus production.
8 ich E7 replaces UL97 are still defective for virus production.
9 oit AAK1 and GAK during entry and infectious virus production.
10 ct on JFH1 genome replication but attenuated virus production.
11 d in E1 transport to the plasma membrane and virus production.
12 n levels and ultimately promoting infectious-virus production.
13 kedly depends on the host cell line used for virus production.
14 ion but are defective for infectious progeny virus production.
15 s yet another role for NS2 in later steps in virus production.
16 e the role of the F protein CT in infectious virus production.
17 these two proteins also moderately inhibited virus production.
18 s to alter the cellular environment to favor virus production.
19 ks had various levels of impaired infectious virus production.
20 ity of ORF57 to support KSHV replication and virus production.
21 induces little viral gene expression and no virus production.
22 mbryonated chicken eggs, a common source for virus production.
23 adenovirus (Ad) infection to achieve optimal virus production.
24 of IRES-mediated translation and infectious virus production.
25 c domains play important roles in infectious virus production.
26 e active conformation required for efficient virus production.
27 ion of many KSHV genes, and is essential for virus production.
28 ression, viral DNA packaging, and infectious virus production.
29 residue to be essential for infectious H77S virus production.
30 m more favorable for replication and progeny virus production.
31 were most effective when added early during virus production.
32 plays an important, as-yet-undefined role in virus production.
33 ed culture with immune suppressants enhanced virus production.
34 NAs; however, the majority are defective for virus production.
35 ase of the cell cycle was more efficient for virus production.
36 beneficial role in viral gene expression and virus production.
37 s cytopathic but had no effect on infectious virus production.
38 on nonviral RNA, preserving the protein for virus production.
39 re' strategies targeting multiple sources of virus production.
40 , RNA and protein expression, and infectious virus production.
41 els and an approximately 10-fold decrease in virus production.
42 aired both in RNA replication and infectious virus production.
43 acellular compartments and severely inhibits virus production.
44 reduction in MVC DNA replication and progeny virus production.
45 pression, viral DNA synthesis, or infectious virus production.
46 2 protease activity but decreased infectious virus production.
47 tein processing, replication, and infectious virus production.
48 ial but poorly understood role in infectious virus production.
49 th HCV subgenomic replication and infectious virus production.
50 cytoplasmic densities near sites of prolific virus production.
51 viral transcription influences the level of virus production.
52 of CDK13 leads to a significant increase in virus production.
53 notype, susceptibility to ASFV infection and virus production.
54 the in vitro protein binding efficiency and virus production.
55 V entry, viral gene expression or infectious virus production.
56 eins Gag and Env and subsequently suppresses virus production.
57 d by viral protein production and infectious virus production.
58 g mutations in E2, p7, and NS2 all increased virus production.
59 rmation, and envelopment to complete de novo virus production.
60 her than macrophages, are the main source of virus production.
61 anscription, DNA replication, and infectious virus production.
62 th a heme analog, led to marked increases in virus production.
63 almitoylation are functionally important for virus production.
64 me appears both necessary and sufficient for virus production.
65 s an important, not fully understood role in virus production.
66 s HCV genotype 2a replication and infectious virus production.
67 lways reflect an association with infectious virus production.
68 information in the absence of any infectious virus production.
69 p7 in vitro, drastically impaired infectious virus production.
70 osome sorting machinery to enable infectious virus production.
71 icted transmembrane domain are important for virus production.
72 eus and also led to inhibition of infectious-virus production.
73 3 is essential for WNV-NY to achieve maximum virus production.
74 ering RNA resulted in reduction of influenza virus production.
75 K8alpha, and K8.1 expression and infectious virus production.
76 AAV5 proteins necessary to achieve efficient virus production.
77 ulation at early times without affecting net virus production.
78 M protein, which is essential for infectious virus production.
79 ytoplasmic virion envelopment and infectious virus production.
80 the nonpermissive cell to ensure infectious virus production.
81 V-infected cells were accompanied by reduced virus production.
82 ian cells leads to viral RNA replication and virus production.
83 r the UEV Ub binding function contributes to virus production.
84 t myeloid cells are not an in vivo source of virus production.
85 to inhibit virion envelopment and infectious virus production.
86 ons, which was associated with a decrease in virus production.
87 -1 pathway and enhances EBV reactivation and virus production.
88 alization in transfected cells and abolished virus production.
89 ction in the absence of infectious cell-free virus production.
90 siRNA) or Mdivi-1 caused marked reduction in virus production.
91 essential for EBV replication and infectious virus production.
92 IV genome demonstrated further inhibition of virus production.
93 d leading to a much reduced viral spread and virus production.
94 ep in the process of assembly and infectious virus production.
95 l virus, Nipah virus) to suppress infectious virus production.
96 interfere with virus particle formation and virus production.
97 protein as the determinant for heterologous virus production.
98 igomers triggers viral filament assembly and virus production.
99 packaging of DIP genomes can interfere with virus production.
100 molecule inhibitors also reduces infectious virus production.
101 lasma HIV-1 RNA from ex vivo measurements of virus production.
102 ytoplasmic virion envelopment and infectious virus production.
103 nfectivity without any significant impact on virus production.
104 05) in M that is critical for RSV infectious virus production.
105 n synthesis, virion assembly, and infectious virus production.
106 some-lysosome fusion, resulting in increased virus production.
107 orylation-dependent regulation of infectious virus production.
108 xogenous glucose is not required for maximal virus production.
109 duced stress-induced apoptosis and increased virus production.
110 in NS5A hyperphosphorylation and infectious virus production.
111 whose propagation adversely affects its host virus' production.
112 d also caused a 10- to 100-fold reduction in virus production, along with decreased viral DNA replica
113 ein likely functions primarily in infectious virus production, although little is known about the det
114 ved a maximum 50-fold decrease in infectious virus production and a 10- to 40-fold reduction in Ad DN
115 an enhanced growth phenotype with respect to virus production and accumulation of virus-encoded mRNAs
116 yl phorbol acetate/n-butyrate resulted in no virus production and an aberrant gene expression pattern
118 mutants exhibited more pronounced defects in virus production and DNA synthesis in quiescent cells as
120 tion activates signaling pathways to enhance virus production and facilitate virus reactivation from
121 due 76 (Y76A), were essential for infectious virus production and filament formation while having lim
122 protein that drastically reduces infectious virus production and filament formation with minimal eff
123 d gKDelta31-68 mutant viruses for infectious-virus production and for gKDelta31-68/gBDelta28syn-media
125 ap the determinants necessary for infectious virus production and gain further insight into the multi
126 /6 mice, supported high levels of infectious virus production and high viral protein expression level
128 ated that a Q221N mutation minimally rescued virus production and led to a second-site I399V mutation
129 imilarly, I399V alone allowed only low-level virus production and led to selection of an I286V mutati
130 treatment with XX-650-23 reduced infectious-virus production and limited lesion formation compared t
131 ike M gene, showed an early surge in progeny virus production and more severe pathology and extrapulm
132 H2 but showed wild-type levels of infectious virus production and no increase in ICP0 expression in l
133 the NEC in infected cells and also decreased virus production and nuclear egress in the absence of ma
134 as L-domain activity essential for efficient virus production and pathogenicity but is not essential
135 mphoid tissues (LTs), the principal sites of virus production and persistence before initiating ART.
136 bition of HIV replication was due to reduced virus production and reduced infectivity of produced vir
138 irus showed further cooperative increases in virus production and severity of infection in vitro and
139 ecause apoptosis of infected cells can limit virus production and spread, some viruses have co-opted
140 s, and FAS are all required for maximal KSHV virus production and that these pathways appear to parti
141 ositive correlation (r=0.64, P=.001) between virus production and the number of CD25+/HLA-DR+ T cells
145 virus were disrupted at sequential stages of virus production and were visualized by atomic force mic
152 o caspase-mediated capsid cleavage increased virus production approximately 3- to 5-fold in CrFK cell
155 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 v10 by 80% resulted in a 2-fold reduction in virus production but no discernible impact on the infect
163 fect on the efficiency of protein binding or virus production, but mutation of a nucleotide in the mi
164 ild-type helical pitch resulted in increased virus production, but some exhibited decreased virus rel
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
171 ignificant cytopathic effects and infectious virus production by day 14; genome copy numbers were equ
172 ed rate of genome replication and infectious virus production by EG PV without impacting the final yi
174 Rather, SLFN11 acts at the late stage of virus production by selectively inhibiting the expressio
178 with different amounts of XMRV and monitored virus production by using quantitative real-time PCR.
180 approximately 1-log reduction in infectious virus production compared to that of the wild-type virus
181 omain 1 of the helicase which fully restored virus production, confirming the involvement of both maj
182 he host protein milieu at the time of robust virus production, depicting changes in cellular processe
183 d, demonstrating that the DDR contributes to virus production, despite its recognized antivirus role.
184 partner, ORF38, are required for infectious virus production due to their important role in the tegu
185 portant and perhaps essential for infectious virus production during reactivation in vivo, this prote
187 ed with a significant decrease in infectious virus production equivalent to the impaired T-cell tropi
188 oplasmic envelopment, egress, and infectious virus production, followed by the double deletion of UL1
190 nomes results in a 5- to 7-fold decrement in virus production following lytic induction, indicating t
191 ase active-site mutant HIV-1 yielded de novo virus production following subsequent T cell activation.
192 Notably, adaptive mutations known to enhance virus production from GT 1a-2a chimeric genomes further
193 ntributions of ongoing virus replication and virus production from HIV-1 reservoirs to persistent low
194 ed with HIV-1 infectious clones, or as HIV-1 virus production from resting CD4+ T cells isolated from
197 ion might lead to HIV persistence by causing virus production, generating new target cells, enabling
198 _G209 substitution mutants had any effect on virus production; however, the deletion mutant (DeltaG20
199 to HIV-1 pathogenesis through modulation of virus production, impairment of the adaptive immune resp
200 , in vivo delivery of anti-D5 siRNAs reduced virus production in a mouse model of VACV infection.
201 : 408, 410, 411, and 413) reduced infectious virus production in a position-dependent fashion but wer
205 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
210 roviruses, along with evidence of continuing virus production in LT despite ART, indicated two import
211 ic cells (FDCs) increase HIV replication and virus production in lymphocytes by increasing the activa
213 expression substantially enhanced infectious virus production in quiescent cells, but did not complem
214 we observed a significant reduction of HIV-1 virus production in Src homology 2 domain-containing leu
215 ing that UL97-dependent defects in cell-free virus production in strains with full-length ULb' region
216 Mutant spectrum analyses and kinetics of virus production in the absence and presence of drugs in
217 ne the effect of disruption of the domain on virus production in the context of the virus genome by u
218 g time points, providing evidence of ongoing virus production in the gut and equilibrium of HIV-1 bet
219 M1 suppressor mutations restored infectious virus production in the presence of M2Y76A and mediated
221 from wild-type virus in terms of infectious virus production in the trigeminal ganglia during acute
225 lly recapitulates HCV entry, replication and virus production in vitro to re-examine the issue of HCV
228 absent v-chemokine supplementation inhibited virus production, indicative of autocrine effects of end
231 ly down modulated during HIV-1 infection and virus production inversely co-related with HspBP1 expres
232 LLINI treatment, and compound potency during virus production is independent of the level of LEDGF/p7
234 h LAT sRNA2 was less effective at inhibiting virus production, it inhibited expression of infected ce
235 r intracellular and extracellular infectious virus production late in the infection, suggesting that
236 ntracellular ERK, however, failed to inhibit virus production, likely due to maintenance of residual
237 wn, have significant inhibitory effects upon virus production, making PRF essential for HIV-1 replica
239 ivity in vitro prior to in vivo inoculation, virus production methods may differentially affect stock
241 dy-state levels of the HIV-1 Gag protein and virus production; Mov10 was efficiently incorporated int
242 om all major HCV genotypes, we observed that virus production occurred in a genotype- and isolate-dep
243 , no enhancement of viral DNA replication or virus production occurred in cGAS or STING shRNA-targete
244 products, indicating that a block to progeny virus production occurs after the initiation of virus ge
246 ificantly inhibited viral spread and progeny virus production of mut-Ad3GFP but not of wt-Ad3GFP.
248 demonstrated no discernible impact on either virus production or infectivity of the resultant particl
252 size, intracellular genomic RNA levels, and virus production progressively decreased with decreasing
253 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
265 t3 activation, as a Stat3 inhibitor restored virus production to levels observed without IL-10 stimul
266 could at least partially restore infectious virus production to M2-deficient influenza A viruses.
267 of these mutations into the chimera rescued virus production to various levels, suggesting a genetic
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
275 tency in the spleen was also seen when lytic virus production was inhibited by treating mice infected
282 infectious virus in transfected cells, while virus production was rescued to near-wild-type levels in
286 xamine the consequences of MVB targeting for virus production, we investigated 29/31KE particle produ
288 role of this cytoplasmic tail in infectious virus production, we used reverse genetics to generate a
289 of reduced viral gene expression and progeny virus production were also observed in normal fibroblast
293 tors robustly induce HIV-1 transcription and virus production when directly compared with maximum rea
294 led to a substantial decrease in infectious virus production, whereas starving infected cells of exo
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
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