Induction of proinflammatory cytokines in human macrophages by influenza A (H5N1) viruses: a mechanism for the unusual severity of human disease?

@article{Cheung2002InductionOP,
  title={Induction of proinflammatory cytokines in human macrophages by influenza A (H5N1) viruses: a mechanism for the unusual severity of human disease?},
  author={C Y Cheung and L. L. M. Poon and Asy Lau and Winsie Luk and Y. L. Lau and K. F. Shortridge and Siamon Gordon and Yi Guan and J. S. Malik Peiris},
  journal={The Lancet},
  year={2002},
  volume={360},
  pages={1831-1837}
}
View on Elsevier
doi.org
918 Citations
Highly Influential Citations
37
Background Citations
360
Methods Citations
30
Results Citations
41

918 Citations

Citation Type

Citation Type

Proinflammatory cytokine responses induced by influenza A (H5N1) viruses in primary human alveolar and bronchial epithelial cells
TLDR
The H5n1/97 and H5N1/04 subtype influenza A viruses are more potent inducers of proinflammatory cytokines and chemokines in primary human respiratory epithelial cells than subtype H1N1 virus, and it is suggested that this hyper-induction of cytokines may be relevant to the pathogenesis of human H4N1 disease.
Title Proinflammatory cytokine responses induced by influenza A ( H 5 N 1 ) viruses in primary human alveolar and bronchial epithelial cells
TLDR
The H5n1/97 and H5N1/04 subtype influenza A viruses are more potent inducers of proinflammatory cytokines and chemokines in primary human respiratory epithelial cells than subtype H1N1 virus, and it is suggested that this hyper-induction of cytokines may be relevant to the pathogenesis of human H4N1 disease.
Pro-inflammatory cytokine dysregulation is associated with novel avian influenza A (H7N9) virus in primary human macrophages.
TLDR
The overall profiles of cytokine and chemokine induction by the H7N9 influenza virus in an in vitro cell-culture model are identified and could provide potential therapeutic targets for the control of severe human H7n9 disease.
Differences in cytokine production in human macrophages and in virulence in mice are attributable to the acidic polymerase protein of highly pathogenic influenza A virus subtype H5N1.
TLDR
These results demonstrate that the PA gene of VN3028IIcl2 affects cytokine production in human macrophages and virulence in mice, and provide new insights into the cytokine-mediated pathogenesis of H5N1 infection in humans.
Systems-Level Comparison of Host-Responses Elicited by Avian H5N1 and Seasonal H1N1 Influenza Viruses in Primary Human Macrophages
TLDR
A network-based analysis suggests that the synergy between IFN-β and TNF-α results in an enhanced and sustained IFN and pro-inflammatory cytokine response at the early stage of viral infection that may contribute to the viral pathogenesis and this is of relevance to the design of novel therapeutic strategies for H5N1 induced respiratory disease.
Cytokine production by primary human macrophages infected with highly pathogenic H5N1 or pandemic H1N1 2009 influenza viruses.
TLDR
It is shown that high cytokine induction is not a universal feature of all H5N1 viruses, and a pandemic H1N1 virus induced higher levels of several cytokines compared with seasonal viruses and some H5n1 strains.
Profiles of cytokine and chemokine gene expression in human pulmonary epithelial cells induced by human and avian influenza viruses
TLDR
The results showed that H5N1 was more potent than H9N2 and H1N1 in inducing CXCL-10/IP-10, TNF-alpha and CCL-5/RANTES, and none of the avian subtypes examined could induce a persistent elevation of the immune-regulatory cytokine - TGF-β2.
Title Proinflammatory cytokine response and viral replication in mouse bone marrow derived macrophages infected with influenza H 1 N 1 and H 5 N 1 viruses
TLDR
In vitro cultures of mouse bone marrow derived macrophages from C57BL/6N mouse were developed to compare influenza A (H5N1 and H1N1) virus replication and pro-inflammatory cytokine and chemokine responses and there was not a clear differential TNF-a protein expression pattern.
Proinflammatory Cytokine Response and Viral Replication in Mouse Bone Marrow Derived Macrophages Infected with Influenza H1N1 and H5N1 Viruses
TLDR
In vitro cultures of mouse bone marrow derived macrophages from C57BL/6N mouse were developed to compare influenza A (H5N1 and H1N1) virus replication and pro-inflammatory cytokine and chemokine responses and the highly pathogenic influenza H5n1 virus was a more potent inducer of the chemokines.
Viral genetic determinants of H5N1 influenza viruses that contribute to cytokine dysregulation.
TLDR
The results suggest that the H5N1 polymerase gene segments, and to a lesser extent the NS gene segment, contribute to cytokine hyperinduction in human macrophages and that a putative H5 pandemic virus that may arise through genetic reassortment between H1N1 and one of the current seasonal influenza viruses may have a markedly altered cytokine phenotype.
...
...

References

SHOWING 1-10 OF 30 REFERENCES
Pathology of fatal human infection associated with avian influenza A H5N1 virus
TLDR
It is postulated that in fatal human infections with this avian subtype, initial virus replication in the respiratory tract triggers hypercytokinemia complicated by the reactive hemophagocytic syndrome.
Human influenza A H5N1 virus related to a highly pathogenic avian influenza virus
Lethal H5N1 influenza viruses escape host anti-viral cytokine responses
TLDR
It is shown that lethal H5N1 influenza virus, unlike other human, avian and swine influenza viruses, are resistant to the antiviral effects of interferons and tumor necrosis factor α, and the nonstructural (NS) gene of H5n1 viruses is associated with this resistance.
Susceptibility of mononuclear phagocytes to influenza A virus infection and possible role in the antiviral response
TLDR
The data show that monocytes and macrophages represent a primary target for an influenza A virus infection, and the mononuclear phagocyte response leads to a rapid proinflammatory reaction and an enhanced immigration of mon onuclear leukocytes, which may condition the infected host for the subsequent virus antigen‐specific defense.
Influenza A and sendai viruses induce differential chemokine gene expression and transcription factor activation in human macrophages.
TLDR
It is shown that during viral infections macrophages predominantly produce monocyte and Th1 cell attracting chemokines, emphasizing the role of IFN-alpha/beta in the development of Th1 immune responses.
Pathogenesis of Avian Influenza A (H5N1) Viruses in Ferrets
TLDR
It is demonstrated that both H5N1 viruses were highly virulent in the outbred ferret model, unlike the differential pathogenicity documented in inbred BALB/c mice.
Human influenza viruses activate an interferon-independent transcription of cellular antiviral genes: Outcome with influenza A virus is unique
TLDR
It is shown that influenza B virus induces the synthesis in human cells of several mature mRNAs encoded by genes containing an IFN-α/β-stimulated response element (ISRE), which constitutes an early antiviral response of cells against influenza A and B viruses.
Clinical features and rapid viral diagnosis of human disease associated with avian influenza A H5N1 virus
Local and systemic cytokine responses during experimental human influenza A virus infection. Relation to symptom formation and host defense.
TLDR
It is found that IL-6 and IFN-alpha levels in nasal lavage fluids peaked early (day 2) and correlated directly with viral titers, temperature, mucus production, and symptom scores, which implicate IL- 6 and IFn-alpha as key factors both in symptom formation and host defense in influenza.
Molecular Basis for High Virulence of Hong Kong H5N1 Influenza A Viruses
TLDR
Using reverse genetics, it is shown that a mutation at position 627 in the PB2 protein influenced the outcome of infection in mice, and high cleavability of the hemagglutinin glycoprotein was an essential requirement for lethal infection.
...
...