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1 HPIV1 and HPIV2 are best known to cause croup while HPIV
3 version of human parainfluenza virus type 1 (HPIV1) bearing a stabilized attenuating mutation in the
8 (RSV) and human parainfluenza virus type 1 (HPIV1) to HPIV4 infect virtually all children by the age
9 imens (8 of 10 positive for HPIV serotype 1 [HPIV1], 9 of 10 positive for HPIV2, and 9 of 10 positive
10 V); human parainfluenza viruses 1, 2, and 3 (HPIV1, -2, and -3, respectively); and influenza A and B
11 (IFN) is induced following infection with an HPIV1 mutant expressing defective C proteins with an F17
12 nd immunogenic against the RSV F protein and HPIV1 in the hamster model and provided substantial prot
13 not express any of the four C proteins, and HPIV1-C(F170S), a less attenuated mutant that contains a
14 ranasal pediatric vaccine.IMPORTANCE RSV and HPIV1 are major viral causes of acute pediatric respirat
17 rapidly identifying mutations that attenuate HPIV1 and for generating live-attenuated HPIV1 vaccine c
18 In the present study, we sought to attenuate HPIV1 by the importation of one or more known attenuatin
19 Two recently characterized live attenuated HPIV1 vaccine candidates expressing mutant C proteins we
23 tion is compromised, as in the case of F170S HPIV1, the resulting PKR activation and reduction in vir
26 The RSV F gene was engineered to include HPIV1 transcription signals and inserted individually in
28 the anti-IFN and antiapoptosis activities of HPIV1 were separable: both activities are disabled in rH
29 er Sendai viruses (the murine counterpart of HPIV1) to noninvasively measure primary infection, immun
30 as a tool for the preclinical evaluation of HPIV1 vaccines, although how these in vitro data will co
32 Mutation or deletion of the C proteins of HPIV1 permitted the activation of over 2,000 cellular ge
33 ail (TMCT) domains substituted with those of HPIV1 F in an effort to direct packaging in the vector p
35 ent RSV/HPIV1 vaccine based on a recombinant HPIV1 vector, attenuated by a stabilized mutation, that
36 he preclinical development of a bivalent RSV/HPIV1 vaccine based on a recombinant HPIV1 vector, atten
37 actions, was used in this study to show that HPIV1 selectively infects ciliated cells within the HAE
40 were ablated by a F170S substitution in the HPIV1 C proteins (F170S) or by silencing the C open read
41 Unmodified EBOV GP was packaged into the HPIV1 particle, and the TMCT modification did not increa
42 MCT) domains were replaced with those of the HPIV1 F protein in an effort to enhance packaging into t
43 us titer, supporting the hypothesis that the HPIV1 C proteins are critical for the inhibition of the
48 ns a single point mutation in C and, like wt HPIV1, does not efficiently induce apoptosis, to examine
49 Infection with either mutant, but not WT HPIV1, induced a significant accumulation of intracellul
51 V1-P(C-) protected against challenge with wt HPIV1, its highly restricted replication in AGMs and in
52 ssion kinetics to examine how wild-type (wt) HPIV1 infection altered gene expression in human respira
53 We found that infection with wild-type (WT) HPIV1 suppressed the innate immune response in human air
54 replicated as efficiently as wild-type (wt) HPIV1, but its titer subsequently decreased coincident w
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