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1 om entering G(2)/M also did not reduce HIV-1 cytopathicity.
2 somal secretion affect viral replication and cytopathicity.
3 g-pol and vpu, tat, and rev did not mitigate cytopathicity.
4 e resilience of macrophages to HIV-1-induced cytopathicity.
5 rough active virus replication and resulting cytopathicity.
6 blasts, which are resistant to virus-induced cytopathicity.
7 ated in primary lymphocytes without inducing cytopathicity.
8 ght into the viral component responsible for cytopathicity.
9 sceptible as wild-type Jurkat cells to HIV-1 cytopathicity.
10 s that render macrophages sensitive to viral cytopathicity.
11 tics of viral replication in baboon PBMC and cytopathicity.
12  which has been previously implicated in HIV cytopathicity.
13 diated clearance and/or elimination by viral cytopathicity.
14  sufficient for the development of increased cytopathicity.
15 on of lysosomal proteases can modulate viral cytopathicity.
16 rticular coreceptor is associated with viral cytopathicity.
17 with the P2X7R in the absence of significant cytopathicity.
18 e viral replication kinetics and single-cell cytopathicity.
19 m induction but was not a key determinant of cytopathicity.
20 expression of bcl-2 did not prevent eventual cytopathicity.
21 at Tat also influences virus infectivity and cytopathicity.
22 g its protective effect against ZIKV-induced cytopathicity.
23 s replication while preventing virus-induced cytopathicity.
24 ted against virus replication and associated cytopathicity.
25 sistant to both apoptosis and other types of cytopathicity after infection with La Crosse virus, reaf
26 m suggests that CD4(+) T cell-directed viral cytopathicity alone cannot explain the course of disease
27 ved to balance virus infectivity, stability, cytopathicity and antibody vulnerability.
28 ignated mycolactone was isolated that causes cytopathicity and cell cycle arrest in cultured L929 mur
29 from T cells in terms of decreased to absent cytopathicity and for active accumulation of new progeny
30 ies, implicating M as a primary regulator of cytopathicity and host transcriptional suppression.IMPOR
31 al RNA (sfRNA), a noncoding RNA that induces cytopathicity and pathogenesis.
32 hila, despite lacking both contact-dependent cytopathicity and regulated sodium sensitivity.
33 but not Fas or TRAIL receptors, inhibits the cytopathicity and replication of human CMV by a nonapopt
34 ion and nsP2 or nsP3 genes to further reduce cytopathicity and to become capable of persisting in cel
35 p between virus-mediated CD4(+) T-lymphocyte cytopathicity and viral coreceptor preference among vari
36 s (e.g., coreceptor usage, cell tropism, and cytopathicity) and is a major target of antiviral immune
37 hesis of viral nucleic acids and viral mRNA, cytopathicity, and release of progeny virions were asses
38 e molecular events that underlie Ebola virus cytopathicity are poorly understood.
39 re prepared and evaluated using a whole cell cytopathicity assay (XTT).
40  due to intrinsic differences in the in vivo cytopathicities between the two viruses.
41 ese results suggest that the primary mode of cytopathicity by laboratory-adapted molecular clones of
42                                              Cytopathicity by virion-delivered mutant Vpr protein cor
43 ersistent infection contrasts with the rapid cytopathicity caused by FV in vitro, suggesting a host d
44 roteins derived from MV strains with reduced cytopathicities confirm that the strength of H and F gly
45 mounting evidence suggests that direct viral cytopathicity contributes to this loss.
46                                          The cytopathicity defect of the mutants to the U937 cells wa
47 d self-association but dispensable for HIV-1 cytopathicity due to residual cell proliferation blockad
48  and a shared cellular link to infection and cytopathicity for distantly related lentiviruses that ca
49    However, the molecular mechanism of viral cytopathicity has not been satisfactorily elucidated.
50 t that HHV-6 may protect DC from HIV-induced cytopathicity in AIDS patients.
51 hibits rapid replication kinetics and marked cytopathicity in both human and chimpanzee peripheral bl
52  is involved in paracrine-mediated C. parvum cytopathicity in cholangiocytes, we also tested the pote
53 irus type 1 (HIV-1) evolves toward increased cytopathicity in conjunction with disease progression in
54 dence of coreceptor-independent increases in cytopathicity in isolates obtained either before corecep
55 nsible for a higher replication capacity and cytopathicity in primary CD4(+) T-cell cultures.
56               We studied the replication and cytopathicity in SCID-hu mice of R5 human immunodeficien
57 assays indicated that 4 inhibits HIV-induced cytopathicity in T lymphocytes with an EC50 of 28 muM, w
58 that viral replication can be uncoupled from cytopathicity in vitro and in vivo.
59 st relationships and potential mechanisms of cytopathicity in vivo in simian immunodeficiency virus (
60  properties also contributes to accelerating cytopathicity in vivo, we used human lymphoid tissue exp
61  that HIV-1 does not evolve toward increased cytopathicity independently of changes in coreceptor uti
62 -2 strains revealed similar, high degrees of cytopathicity induced by both HIV types.
63 tion, and the data suggest that direct viral cytopathicity is a major factor.
64                        By contrast, if viral cytopathicity is high relative to the replication rate o
65                                 If the viral cytopathicity is low relative to the rate of viral repli
66 udies demonstrate that primary HIV-1-induced cytopathicity is separable from syncytium formation and
67 line-94, a determinant of measles virus (MV) cytopathicity, is predicted to lie in a cylindrical cavi
68 conferred its rapid replication kinetics and cytopathicity mapped to the capsid- and nucleocapsid-enc
69  human lymphoid tissue explants to assay the cytopathicity of a panel of primary HIV-1 isolates deriv
70                                 Instead, the cytopathicity of all HIV-1 isolates was determined solel
71 (gp41C) is implicated in the replication and cytopathicity of HIV-1 [1].
72 igated the impact of coreceptor usage on the cytopathicity of HIV-2 and compared its pathogenic poten
73 toplasmic tail influence the replication and cytopathicity of SIVMne variants that evolve in the host
74 n previously shown to be responsible for the cytopathicity of Spl574, S82F.
75 t alter the in vitro replication kinetics or cytopathicity of the mutant viruses in T-cell lines.
76  of the two types of component depend on the cytopathicity of the virus relative to its rate of repli
77 ts severely depleted CD4(+) T cells, whereas cytopathicity of the virus that used CCR5 only in lympho
78  the efficiency of primary infection and the cytopathicity of virus for infected CD4-positive T cells
79 l envelope, might influence viral-associated cytopathicity or apoptosis [6].
80  transduction may influence viral-associated cytopathicity or apoptosis.
81 s CCR3, CCR8, BOB, and Bonzo did not augment cytopathicity or diminish sensitivity toward CXCR4 antag
82 th deletions, rather than being required for cytopathicity, play a role in protecting cells from CPE.
83 age plasma membrane paralleled virus-induced cytopathicity, podosome formation, and cellular fusion.
84 ein replicates efficiently, has an increased cytopathicity, possesses a greater infectivity per parti
85 hesis", argues that viral attributes such as cytopathicity, replicability, syncytiality, cell tropism
86                                         This cytopathicity resembles that of Spl574 MLV, a novel vari
87  not characterized by an intrinsically lower cytopathicity than HIV-1 strains.
88                              These exhibited cytopathicity to a keratinocyte cell line and mediated p
89 c mutants had a similar phenotype of reduced cytopathicity to the U937 cells, showed a 100-fold incre
90  that use CXCR4 or CCR5 exclusively; and (c) cytopathicity toward the general CD4(+) T cell populatio
91    Mutations in the hel genes led to reduced cytopathicity towards U937 cells, although the mutant st
92 IL-4 inhibited virus entry, replication, and cytopathicity under these conditions.
93 rs of cells and induced comparable levels of cytopathicity, viral production was considerably higher
94                     We also found that HIV-1 cytopathicity was undiminished by the absence of nef.
95                         The effect of Vpr on cytopathicity was unrelated to reported activities of Vp
96 molecular determinants of measles virus (MV) cytopathicity, we have characterized mutant viruses exhi
97 tion and host immunologic defense against FV cytopathicity, we quantified FV in tissues of healthy rh
98 V-1 clone resulted in a marked impairment of cytopathicity without affecting viral replication effici