scholarly journals In Vitro and in Vivo Inhibitory Effects of Disodium Cromoglycate on Influenza Virus Infection

2004 ◽  
Vol 27 (6) ◽  
pp. 825-830 ◽  
Author(s):  
Kazuya I. P. J. Hidari ◽  
Eisaku Tsujii ◽  
Jun Hiroi ◽  
Eriko Mano ◽  
Akihiko Miyatake ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Virus Infection ◽  
Influenza Virus Infection ◽  
Disodium Cromoglycate ◽  
Inhibitory Effects

scholarly journals Linear polysialoside outperforms dendritic analogs for inhibition of influenza virus infection in vitro and in vivo

Biomaterials ◽  
2017 ◽  
Vol 138 ◽  
pp. 22-34 ◽  
Author(s):  
Sumati Bhatia ◽  
Daniel Lauster ◽  
Markus Bardua ◽  
Kai Ludwig ◽  
Stefano Angioletti-Uberti ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Virus Infection ◽  
Influenza Virus Infection

scholarly journals In Vitro Evaluation of Synergistic Inhibitory Effects of Neuraminidase Inhibitors and Methylglyoxal Against Influenza Virus Infection

2015 ◽  
Vol 46 (1) ◽  
pp. 8-16 ◽  
Author(s):  
Siriwan Charyasriwong ◽  
Ken Watanabe ◽  
Ratika Rahmasari ◽  
Ayaka Matsunaga ◽  
Takahiro Haruyama ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Virus Infection ◽  
Influenza Virus Infection ◽  
Neuraminidase Inhibitors ◽  
Inhibitory Effects ◽  
In Vitro Evaluation

Activity of a Novel Fullerene-based Antiviral Against Influenza Virus Infection In Vitro and In Vivo

2010 ◽  
Vol 86 (1) ◽  
pp. A50-A51
Author(s):  
Vladimir Zarubaev ◽  
Pavel Anfimov ◽  
Anna Shtro ◽  
Lev Rasnetsov ◽  
Oleg Kiselev
Keyword(s):  
Influenza Virus ◽  
Virus Infection ◽  
Influenza Virus Infection

Taishan Pinus massoniana pollen polysaccharide inhibits H9N2 subtype influenza virus infection both in vitro and in vivo

2020 ◽  
Vol 248 ◽  
pp. 108803
Author(s):  
Hongqi Shang ◽  
Zhou Sha ◽  
Huan Wang ◽  
Yongqiang Miao ◽  
Xiangyun Niu ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Virus Infection ◽  
Influenza Virus Infection ◽  
Pinus Massoniana ◽  
H9n2 Subtype

scholarly journals Differential Response of Respiratory Dendritic Cell Subsets to Influenza Virus Infection

2008 ◽  
Vol 82 (10) ◽  
pp. 4908-4919 ◽  
Author(s):  
Xueli Hao ◽  
Taeg S. Kim ◽  
Thomas J. Braciale
Keyword(s):  
Influenza Virus ◽  
Virus Infection ◽  
Influenza Virus Infection ◽  
Chemokine Production ◽  
Susceptibility To Infection ◽  
Infection Pattern ◽  
Ligand Expression ◽  
Tract Infections

ABSTRACT Dendritic cells (DC) are believed to play an important role in the initiation of innate and adaptive immune responses to infection, including respiratory tract infections, where respiratory DC (RDC) perform this role. In this report, we examined the susceptibilities of isolated murine RDC to influenza virus infection in vitro and the effect of the multiplicity of infection (MOI) on costimulatory ligand upregulation and inflammatory cytokine/chemokine production after infection. We found that the efficiency of influenza virus infection of RDC increased with increasing MOIs. Furthermore, distinct subpopulations of RDC differed in their susceptibilities to influenza virus infection and in the magnitude/tempo of costimulatory ligand expression. Additional characterization of the CD11c-positive (CD11c+) RDC revealed that the identifiable subsets of RDC differed in susceptibility to infection, with CD11c+ CD103+ DC exhibiting the greatest susceptibility, CD11c+ CD11bhi DC exhibiting intermediate susceptibility, and CD11c+ B220+ plasmacytoid DC (pDC) exhibiting the least susceptibility to infection. A companion analysis of the in vivo susceptibilities of these RDC subsets to influenza virus revealed a corresponding infection pattern. The three RDC subsets displayed different patterns of cytokine/chemokine production in response to influenza virus infection in vitro: pDC were the predominant producers of most cytokines examined, while CD103+ DC and CD11bhi DC produced elevated levels of the murine chemokine CXCL1 (KC), interleukin 12p40, and RANTES in response to influenza virus infection. Our results indicate that RDC are targets of influenza virus infection and that distinct RDC subsets differ in their susceptibilities and responses to infection.

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