ライフサイエンスコーパス: swine influenza virus

1 modon hispidus) are susceptible to avian and swine influenza viruses.

2 nd might reassort with currently circulating swine influenza viruses.

3 l cells which is characteristic for virulent swine influenza viruses.

4 es and antigenically distinct from reference swine influenza viruses.

5 As a positive control, an H3N2 swine influenza virus A was used.

6 lb09]), with that of the 1918-like classical swine influenza virus (A/swine/Iowa/1930 [IA30]) in the

7 y shown to enhance the replication of a 1976 swine influenza virus also significantly improved the re

8 th the reconstructed 1918 virus, a 1976 H1N1 swine influenza virus, and a highly pathogenic H5N1 viru

9 uman H1N1 influenza A virus strains, several swine influenza viruses, and influenza B viruses but wer

10 uenza viruses, unlike other human, avian and swine influenza viruses, are resistant to the antiviral

11 stages of the European avian-like (EA) H1N1 swine influenza virus as it transitioned from avian to s

12 logic factors that limit the transmission of swine influenza viruses between humans are unresolved.

13 virus reassortment, as avian, human, and/or swine influenza viruses can infect swine and reassort, a

14 large-scale genomic characterization of 290 swine influenza viruses collected from 14 European count

15 y (typically found in avian and classic H1N1 swine influenza viruses), conferring binding to human- a

16 CD8(+) T-cell epitopes in NP of human versus swine influenza virus, consistent with the idea that the

17 The results suggest swine influenza viruses containing both a stabilized HA

18 Novel triple-reassortant H3N2 swine influenza virus emerged in 1998 and spread rapidly

19 ses--containing genes from avian, human, and swine influenza viruses--emerged and became enzootic amo

20 enting the avian-like precursor virus and EA swine influenza viruses from 1979-1983, 1984-1987 and 19

21 ttle known about the host barriers that keep swine influenza viruses from entering the human populati

22 we examine the innate antiviral response to swine influenza virus in primary and immortalized swine

23 se data highlight the increased diversity of swine influenza viruses in the United States and would i

24 n that infection in humans with the pandemic swine influenza virus induces antibodies with specificit

25 fluenza subtypes by mixing avian, human, and swine influenza viruses is possible.

26 For swine influenza viruses isolated in 2009-2016, gamma-cla

27 Before 1998, swine influenza virus isolates in the United States were

28 e its absence from some animal (particularly swine) influenza virus isolates, variable expression in

29 nes can be recombined from human, avian, and swine influenza viruses, leading to triple reassortants.

30 We report that swine influenza virus-like substitutions T200A and E227A

31 recursor strains from the triple-reassortant swine influenza virus lineage, which cause only sporadic

32 Due to their attenuation, NS1-mutated swine influenza viruses might have a great potential as

33 However, when transferred into avian and swine influenza viruses, only partial ts and attenuation

34 , and nonstructural genes being of classical swine influenza virus origin, and the PA and PB2 polymer

35 In 2009, a swine influenza virus (pH1N1) jumped to humans and sprea

36 The recent flu epidemic caused by an H1N1 swine influenza virus presents an opportunity to examine

37 Biosystems 7500 Fast platform, using the CDC swine influenza virus real-time RT-PCR detection panel (

38 Critically, both human and swine influenza viruses replicated in the immortalized c

39 Swine influenza virus (SIV) can cause respiratory illnes

40 Swine influenza virus (SIV) H3N2 with triple reassorted

41 1-F2 protein of triple-reassortant (TR) H3N2 swine influenza virus (SIV) in pigs and turkeys.

42 raction between Mycoplasma hyopneumoniae and swine influenza virus (SIV) in the induction of pneumoni

43 dentifying a student with triple-reassortant swine influenza virus (SIV) infection and pig exposure a

44 ole of the NS1 protein in the virulence of a swine influenza virus (SIV) isolate in pigs by using rev

45 The Eurasian avian-like (EA) H1N1 swine influenza virus (SIV) possesses the capacity to in

46 ation of a so-called triple reassortant (TR) swine influenza virus (SIV).

47 Swine influenza viruses (SIV) have been shown to sporadi

48 Swine influenza viruses (SIV) naturally infect pigs and

49 Triple reassortant swine influenza viruses (SIVs) and 2009 pandemic H1N1 (p

50 Since the introduction of H3N2 swine influenza viruses (SIVs) into U.S. swine in 1998,

51 in A/New Caledonia/20/1999 and 2009 pandemic swine influenza virus strain A/California/04/2009.

52 rotected completely against lethal avian and swine influenza virus strains in mice, and induced robus

53 Therefore, we chose a H1N1 swine influenza virus, Sw/OH/24366/07 (SwIV), which has

54 Swine influenza virus (SwIV) is one of the important zoo

55 We identified 34 swine influenza viruses (termed rH3N2p) with the same co

56 to a representative human triple-reassortant swine influenza virus that has circulated in pigs in the

57 all proposed to have been caused by avian or swine influenza viruses that acquired virulence factors

58 e epitopes in parallel lineages of human and swine influenza viruses that have been diverging since r

59 tinin receptor-binding specificity of the EA swine influenza viruses-that is, from recognition of bot

60 Here we use comparisons of human and swine influenza viruses to rigorously demonstrate that h

61 Unlike classical swine influenza virus, TR SIV produces a full-length PB1

62 A new H1N1 triple-reassortant "swine" influenza virus was recently described in individ

63 ing a panel of 28 distinct human, avian, and swine influenza viruses, we found that only a small subs

64 ls which recovered from exposure to virulent swine influenza virus were completely resistant to infec

65 onstrate here that an engineered reassortant swine influenza virus, with the same gene constellation