Systemic Virus distribution and host responses in brain and intestine of chickens infected with low pathogenic and high pathogenic avian influenza virus

J. Post, D.W. Burt, J.B.W.J. Cornelissen, V.C.M. Broks, D. van Zoelen, B.P.H. Peeters, J.M.J. Rebel

Research output: Contribution to journalArticleAcademicpeer-review

24 Citations (Scopus)

Abstract

Background: Avian influenza virus (AIV) is classified into two pathotypes, low pathogenic (LP) and high pathogenic ( HP), based on virulence in chickens. Differences in pathogenicity between HPAIV and LPAIV might eventually be related to specific characteristics of strains, tissue tropism and host responses. Methods: To study differences in disease development between HPAIV and LPAIV, we examined the first appearance and eventual load of viral RNA in multiple organs as well as host responses in brain and intestine of chickens infected with two closely related H7N1 HPAIV or LPAIV strains. Results: Both H7N1 HPAIV and LPAIV spread systemically in chickens after a combined intranasal/intratracheal inoculation. In brain, large differences in viral RNA load and host gene expression were found between H7N1 HPAIV and LPAIV infected chickens. Chicken embryo brain cell culture studies revealed that both HPAIV and LPAIV could infect cultivated embryonic brain cells, but in accordance with the absence of the necessary proteases, replication of LPAIV was limited. Furthermore, TUNEL assay indicated apoptosis in brain of HPAIV infected chickens only. In intestine, where endoproteases that cleave HA of LPAIV are available, we found minimal differences in the amount of viral RNA and a large overlap in the transcriptional responses between HPAIV and LPAIV infected chickens. Interestingly, brain and ileum differed clearly in the cellular pathways that were regulated upon an AI infection. Conclusions: Although both H7N1 HPAIV and LPAIV RNA was detected in a broad range of tissues beyond the respiratory and gastrointestinal tract, our observations indicate that differences in pathogenicity and mortality between HPAIV and LPAIV could originate from differences in virus replication and the resulting host responses in vital organs like the brain.
Original languageEnglish
Article number61
Number of pages14
JournalVirology journal
Volume9
DOIs
Publication statusPublished - 2012

Fingerprint

Influenza in Birds
Orthomyxoviridae
Intestines
Chickens
Viruses
Brain
Viral RNA
Virulence
Viral Tropism
In Situ Nick-End Labeling
Virus Replication
Viral Load
Ileum
Respiratory System
Gastrointestinal Tract
Peptide Hydrolases
Embryonic Structures
Cell Culture Techniques
RNA
Apoptosis

Keywords

  • hemagglutinin cleavage site
  • membrane-fusion
  • pekin ducks
  • a viruses
  • h5n1
  • pathology
  • pathobiology
  • replication
  • chemokines
  • antibodies

Cite this

@article{b96d72aa808f459e8ec8a5b29337e70a,
title = "Systemic Virus distribution and host responses in brain and intestine of chickens infected with low pathogenic and high pathogenic avian influenza virus",
abstract = "Background: Avian influenza virus (AIV) is classified into two pathotypes, low pathogenic (LP) and high pathogenic ( HP), based on virulence in chickens. Differences in pathogenicity between HPAIV and LPAIV might eventually be related to specific characteristics of strains, tissue tropism and host responses. Methods: To study differences in disease development between HPAIV and LPAIV, we examined the first appearance and eventual load of viral RNA in multiple organs as well as host responses in brain and intestine of chickens infected with two closely related H7N1 HPAIV or LPAIV strains. Results: Both H7N1 HPAIV and LPAIV spread systemically in chickens after a combined intranasal/intratracheal inoculation. In brain, large differences in viral RNA load and host gene expression were found between H7N1 HPAIV and LPAIV infected chickens. Chicken embryo brain cell culture studies revealed that both HPAIV and LPAIV could infect cultivated embryonic brain cells, but in accordance with the absence of the necessary proteases, replication of LPAIV was limited. Furthermore, TUNEL assay indicated apoptosis in brain of HPAIV infected chickens only. In intestine, where endoproteases that cleave HA of LPAIV are available, we found minimal differences in the amount of viral RNA and a large overlap in the transcriptional responses between HPAIV and LPAIV infected chickens. Interestingly, brain and ileum differed clearly in the cellular pathways that were regulated upon an AI infection. Conclusions: Although both H7N1 HPAIV and LPAIV RNA was detected in a broad range of tissues beyond the respiratory and gastrointestinal tract, our observations indicate that differences in pathogenicity and mortality between HPAIV and LPAIV could originate from differences in virus replication and the resulting host responses in vital organs like the brain.",
keywords = "hemagglutinin cleavage site, membrane-fusion, pekin ducks, a viruses, h5n1, pathology, pathobiology, replication, chemokines, antibodies",
author = "J. Post and D.W. Burt and J.B.W.J. Cornelissen and V.C.M. Broks and {van Zoelen}, D. and B.P.H. Peeters and J.M.J. Rebel",
year = "2012",
doi = "10.1186/1743-422X-9-61",
language = "English",
volume = "9",
journal = "Virology journal",
issn = "1743-422X",
publisher = "Springer Verlag",

}

Systemic Virus distribution and host responses in brain and intestine of chickens infected with low pathogenic and high pathogenic avian influenza virus. / Post, J.; Burt, D.W.; Cornelissen, J.B.W.J.; Broks, V.C.M.; van Zoelen, D.; Peeters, B.P.H.; Rebel, J.M.J.

In: Virology journal, Vol. 9, 61, 2012.

Research output: Contribution to journalArticleAcademicpeer-review

TY - JOUR

T1 - Systemic Virus distribution and host responses in brain and intestine of chickens infected with low pathogenic and high pathogenic avian influenza virus

AU - Post, J.

AU - Burt, D.W.

AU - Cornelissen, J.B.W.J.

AU - Broks, V.C.M.

AU - van Zoelen, D.

AU - Peeters, B.P.H.

AU - Rebel, J.M.J.

PY - 2012

Y1 - 2012

N2 - Background: Avian influenza virus (AIV) is classified into two pathotypes, low pathogenic (LP) and high pathogenic ( HP), based on virulence in chickens. Differences in pathogenicity between HPAIV and LPAIV might eventually be related to specific characteristics of strains, tissue tropism and host responses. Methods: To study differences in disease development between HPAIV and LPAIV, we examined the first appearance and eventual load of viral RNA in multiple organs as well as host responses in brain and intestine of chickens infected with two closely related H7N1 HPAIV or LPAIV strains. Results: Both H7N1 HPAIV and LPAIV spread systemically in chickens after a combined intranasal/intratracheal inoculation. In brain, large differences in viral RNA load and host gene expression were found between H7N1 HPAIV and LPAIV infected chickens. Chicken embryo brain cell culture studies revealed that both HPAIV and LPAIV could infect cultivated embryonic brain cells, but in accordance with the absence of the necessary proteases, replication of LPAIV was limited. Furthermore, TUNEL assay indicated apoptosis in brain of HPAIV infected chickens only. In intestine, where endoproteases that cleave HA of LPAIV are available, we found minimal differences in the amount of viral RNA and a large overlap in the transcriptional responses between HPAIV and LPAIV infected chickens. Interestingly, brain and ileum differed clearly in the cellular pathways that were regulated upon an AI infection. Conclusions: Although both H7N1 HPAIV and LPAIV RNA was detected in a broad range of tissues beyond the respiratory and gastrointestinal tract, our observations indicate that differences in pathogenicity and mortality between HPAIV and LPAIV could originate from differences in virus replication and the resulting host responses in vital organs like the brain.

AB - Background: Avian influenza virus (AIV) is classified into two pathotypes, low pathogenic (LP) and high pathogenic ( HP), based on virulence in chickens. Differences in pathogenicity between HPAIV and LPAIV might eventually be related to specific characteristics of strains, tissue tropism and host responses. Methods: To study differences in disease development between HPAIV and LPAIV, we examined the first appearance and eventual load of viral RNA in multiple organs as well as host responses in brain and intestine of chickens infected with two closely related H7N1 HPAIV or LPAIV strains. Results: Both H7N1 HPAIV and LPAIV spread systemically in chickens after a combined intranasal/intratracheal inoculation. In brain, large differences in viral RNA load and host gene expression were found between H7N1 HPAIV and LPAIV infected chickens. Chicken embryo brain cell culture studies revealed that both HPAIV and LPAIV could infect cultivated embryonic brain cells, but in accordance with the absence of the necessary proteases, replication of LPAIV was limited. Furthermore, TUNEL assay indicated apoptosis in brain of HPAIV infected chickens only. In intestine, where endoproteases that cleave HA of LPAIV are available, we found minimal differences in the amount of viral RNA and a large overlap in the transcriptional responses between HPAIV and LPAIV infected chickens. Interestingly, brain and ileum differed clearly in the cellular pathways that were regulated upon an AI infection. Conclusions: Although both H7N1 HPAIV and LPAIV RNA was detected in a broad range of tissues beyond the respiratory and gastrointestinal tract, our observations indicate that differences in pathogenicity and mortality between HPAIV and LPAIV could originate from differences in virus replication and the resulting host responses in vital organs like the brain.

KW - hemagglutinin cleavage site

KW - membrane-fusion

KW - pekin ducks

KW - a viruses

KW - h5n1

KW - pathology

KW - pathobiology

KW - replication

KW - chemokines

KW - antibodies

U2 - 10.1186/1743-422X-9-61

DO - 10.1186/1743-422X-9-61

M3 - Article

VL - 9

JO - Virology journal

JF - Virology journal

SN - 1743-422X

M1 - 61

ER -