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1 intracellular signaling cascade activated by antiviral antibody.
2 , hypergammaglobulinemia, and high levels of antiviral antibody.
3 tralizing or cross-reactive non-neutralizing antiviral antibodies.
4 e HIV-1 envelope, with the goal of eliciting antiviral antibodies.
5 virus infection and defects in production of antiviral antibodies.
6 ship between antigenicity and sensitivity to antiviral antibodies.
7 ed for innate B cell-stimulating factors and antiviral antibodies.
8 nsfection, coincident with the appearance of antiviral antibodies.
9 ence, and inflammatory markers and increased antiviral antibodies.
10 r, they became beneficial in the presence of antiviral antibody (Ab).
11 ecrudescence is prevented by the transfer of antiviral antibody (Ab).
12  and to isolate several broadly neutralizing antiviral antibodies against highly variable pathogens s
13                    Our results indicate that antiviral antibodies against SARS-CoV-2 did not decline
14                                Prevalence of antiviral antibodies agreed with known infection rates f
15                                              Antiviral antibody also enables ADV to infect macrophage
16  This virus is amenable to the evaluation of antiviral antibodies and small-molecule inhibitors and t
17 titis B virus (HBV) is completely cleared by antiviral antibodies and specific cytotoxic T lymphocyte
18 -hBUGT, there was a marked inhibition of the antiviral antibody and Ad-specific cytotoxic T lymphocyt
19 een baseline IgE levels and the magnitude of antiviral antibody and CD4(+) T-cell responses was obser
20  with hypergammaglobulinemia, high levels of antiviral antibody and circulating immune complexes, and
21                                              Antiviral antibody and interferon-gamma have major roles
22 in PKCtheta+/+ and PKCtheta-/- mice, whereas antiviral antibody and T-helper cell cytokine production
23  treatments that diminish viral replication (antiviral antibody) and pulmonary inflammation (anti-inf
24  titer at the time of peak lesion formation, antiviral antibodies, and cellular immune responses.
25 pated in germinal center reactions, produced antiviral antibodies, and underwent immunoglobulin class
26 e a general strategy to boost the potency of antiviral antibodies, and, because membrane affinity is
27                                        While antiviral antibodies are protective, those targeting int
28 orphological evidence of the localization of antiviral antibodies at anatomical sites relevant to suc
29         C4d, sC5b-9, and C5a correlated with antiviral antibodies, but not with viral load.
30 tameric gH complex is the primary target for antiviral antibodies by vaccination.
31 and viral neutralization, but in rare cases, antiviral antibodies can promote disease progression.
32                                  Preexisting antiviral antibodies decreased after transplant in the p
33 roducing S and MHVR, because fusion-blocking antiviral antibodies did not prevent it.
34 d to demonstrate a novel approach to deliver antiviral antibody fragments with paratransgenic ISVs.
35 or prespecified sets of pro-inflammatory and antiviral/antibody gene transcripts.
36                                     Although antiviral antibodies generally confer protective functio
37                   No intervention, including antiviral antibodies, had an important impact on any out
38 ccurate quantitation of chiropteran maternal antiviral antibody half-life, provide fundamental baseli
39                Following reports of elevated antiviral antibodies in MS patient sera and viral DNA de
40 ty for evaluation of the efficacies of novel antiviral antibodies in protecting and restoring placent
41 ections are characterized by the presence of antiviral antibodies in the cerebral spinal fluid (CSF),
42 ective efficacy of purified vaccine-elicited antiviral antibodies in this model, even in the absence
43 ata directly demonstrate a critical role for antiviral antibody in protecting from the selective outg
44 early control of CNS virus replication, that antiviral antibody is critical for clearance from the br
45 nscutaneous vaccination but elicited similar antiviral antibody levels and T-cell responses in both t
46 king regarding the infectious virus load and antiviral antibody levels in the nasal tract.
47  does not correlate with the cross-sectional antiviral antibody levels per se but, rather, with the d
48                                              Antiviral antibodies limit B19 infection in vivo; howeve
49                    Herein, we tested whether antiviral antibody-mediated suppression of virus replica
50           To determine if passively acquired antiviral antibodies modulate virus transmission and dis
51                      Expression of APRIL and antiviral antibodies of IgA and IgM but not IgG isotype
52 ion has guided the development of engineered antiviral antibodies optimized for maximal effector acti
53                                        While antiviral antibody plays a key role in resistance to acu
54                                              Antiviral antibody production during respiratory syncyti
55 eased plasma cell maturation, and negligible antiviral antibody production.
56 trol sera did not demonstrate differences in antiviral antibody profiles.
57 ce cell-mediated responses but no detectable antiviral antibodies, protected a fraction of cats again
58 ncreased expression of both inflammatory and antiviral/antibody-related genes in response to the TSST
59                            Understanding the antiviral antibody repertoire induced during HCMV infect
60                              Decreased serum antiviral antibody repertoire is predictive of decompens
61 restriction is a key selective event for the antiviral antibody response and is probably important fo
62 levels of virus replication and undetectable antiviral antibody response and required sequence change
63                                          The antiviral antibody response to HCMV infection is complex
64 the magnitude of this effector cell-mediated antiviral antibody response was inversely associated wit
65 ation and undetectable or weak and transient antiviral antibody response.
66  hematologic malignancy develop a measurable antiviral antibody response.
67 t epitope specificities contributes to HIV-1 antiviral antibody responses and is important to induce
68 effectiveness is complicated by induction of antiviral antibody responses and rapid host clearance of
69             These observations indicate that antiviral antibody responses are critical in maintaining
70 dily with a half-life of 8-15 years, whereas antiviral antibody responses are maintained for up to 75
71 , strength, and kinetics of epitope-specific antiviral antibody responses in vaccine trials with a si
72  A vaccine capable of stimulating protective antiviral antibody responses is needed to curtail the gl
73                                              Antiviral antibody responses remained stable between 1-7
74 responses that declined slowly over time and antiviral antibody responses that remained stable for de
75                                              Antiviral antibody responses were remarkably stable, wit
76 infected but had a delayed viremia, enhanced antiviral antibody responses, and a slower disease cours
77 fected, the immunized animals mounted better antiviral antibody responses, controlled virus levels mo
78  envelope glycoproteins do not elicit strong antiviral antibody responses, particularly against prima
79 ferentiation of Ag-primed CD4(+) T cells and antiviral antibody responses.
80  reflects an adaptation to facilitate strong antiviral antibody responses.
81 rsisted in inoculated rabbits despite higher antiviral antibody responses.
82 uals with a high likelihood of having strong antiviral antibody responses.
83 ry S. pneumoniae infection exaggerates early antiviral antibody-secreting cell formation, and at late
84     Functional studies with human monoclonal antiviral antibodies showed that conformational epitopes
85       Current serological assays that detect antiviral antibodies suffer from low sensitivity and hig
86                            No elimination of antiviral antibodies tested was seen.
87              As indicated by the isotypes of antiviral antibodies, the T-B dipeptide preferentially i
88 nsmission, as measured by plasma viremia and antiviral antibodies, through 10 weeks postchallenge.
89  complete adjuvant was able to induce strong antiviral antibody titers and a high frequency of specif
90 5 who were tested (91.1%) were seropositive; antiviral antibody titers assayed by two pan-Ig assays i
91 ouse genotype, virus persistence in the CNS, antiviral antibody titers, mortality, and the severity o
92 ion promoted MHC class I expression, reduced antiviral antibody titers, promoted viral persistence, a
93  infections were defined as having no or low antiviral antibody titers.
94 ipants undergoing blepharoplasty to quantify antiviral antibody titers.
95 strated that vaccination elicited functional antiviral antibodies to multiple neutralizing sites in r
96  viral genome can further bypass circulating antiviral antibodies to reach the tumour and initiate re
97 g IFN-I autoantibodies from plasmas, leaving antiviral antibodies unaffected.
98 etween viral infections and T1D by profiling antiviral antibodies using a high-throughput immunoprote
99 throughput method to comprehensively analyze antiviral antibodies using immunoprecipitation and massi
100 s (n = 58) were investigated for intrathecal antiviral antibodies, using a phage display library expr
101 m dilution is most appropriate for screening antiviral antibody, using a positive-to-negative ratio o
102                                  IgM and IgG antiviral antibodies were detected in the serum of the d
103                 Antigen-specific B cells and antiviral antibodies were essential for the accelerated
104                                              Antiviral antibodies were not observed postvaccination.
105  newborns that had transplacentally acquired antiviral antibodies were protected against mucosal SIV
106     HRES-1/p28 is a target of cross-reactive antiviral antibodies, whereas HRES-1/Rab4 regulates the
107 and the challenging precedent of correlating antiviral antibodies with disease association, these ant

 
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