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Highly pathogenic or low pathogenic avian influenza virus subtype H7N1 infection in chicken lungs: small differences in general acute responses.

Rebel JM, Peeters B, Fijten H, Post J, Cornelissen J, Vervelde L - Vet. Res. (2011)

Bottom Line: No major difference between LPAI and HPAI infected birds in the induction of cytokines and interferons at mRNA level in lung tissue was found.In conclusion, the differences in lethality for chickens infected with LPAI or HPAI could be ascribed to difference in location of the virus.However similar amounts of viral RNA, similar cytokine mRNA levels, and similar influxes of CD8α+ and KUL01+ macrophages and DC were found between HPAI and LPAI in the lungs.A cytokine storm at mRNA level as described for mammals was not observed in the lungs of HPAI infected birds within 24 hpi.

View Article: PubMed Central - HTML - PubMed

Affiliation: Central Veterinary Institute, PO box 65, 8219 PH Lelystad, The Netherlands. Annemarie.Rebel@WUR.nl.

ABSTRACT
Avian influenza virus can be divided into two groups, highly pathogenic avian influenza virus (HPAI) and low pathogenic avian influenza virus (LPAI) based on their difference in virulence. To investigate if the difference in clinical outcome between LPAI and HPAI in chickens is due to immunological host responses in the lung within the first 24 hours post infection (hpi), chickens were infected with LPAI or HPAI of subtype H7N1. Virus was found in the caudal and cranial part of the lung. With LPAI, virus was localised around the intrapulmonary bronchus and secondary bronchi. In sharp contrast, HPAI was detected throughout the whole lung. However, based on viral RNA levels, no quantitative difference was observed between LPAI and HPAI infected birds. In infected areas of the lungs, an influx of CD8α+ cells as well as KUL01+ macrophages and dendritic cells (DC) occurred as fast as 8 hpi in both infected groups. No major difference between LPAI and HPAI infected birds in the induction of cytokines and interferons at mRNA level in lung tissue was found.In conclusion, the differences in lethality for chickens infected with LPAI or HPAI could be ascribed to difference in location of the virus. However similar amounts of viral RNA, similar cytokine mRNA levels, and similar influxes of CD8α+ and KUL01+ macrophages and DC were found between HPAI and LPAI in the lungs. A cytokine storm at mRNA level as described for mammals was not observed in the lungs of HPAI infected birds within 24 hpi.

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Related in: MedlinePlus

Scatter plot of the amount of viral RNA of individual birds in the lung at different time points post inoculation (hpi) with LPAI (open symbols) or HPAI (closed symbols). The horizontal line represents the mean of 6 individual birds. Viral RNA expression was determined using RT-PCR and data were expressed as EID50/g.
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Figure 2: Scatter plot of the amount of viral RNA of individual birds in the lung at different time points post inoculation (hpi) with LPAI (open symbols) or HPAI (closed symbols). The horizontal line represents the mean of 6 individual birds. Viral RNA expression was determined using RT-PCR and data were expressed as EID50/g.

Mentions: Viral RNA was detected in the lungs as early as 4 hpi and the amount of viral RNA increased significantly (F pr < 0.001) upto 24 hpi (Figure 2). In order to investigate the kinetics of the viral RNA in time between HPAI and LPAI infected birds we analysed the data with and without birds that had non-detectable level of viral RNA. When 4 of the 24 LPAI infected birds (2 birds at 4 hpi, 1 at 8 hpi and 1 at 24 hpi) with no detectable level of viral RNA were excluded from the analysis, no significant difference existed between the amount of viral RNA in the caudal lungs of LPAI and HPAI infected birds in time. When the birds with no detectable amount of viral RNA were included in the analysis differences did exist between HPAI and LPAI infected birds. For the cranial part a difference between HPAI and LPAI in time was found (F pr = 0.07), while at 24 h no significant difference existed between HPAI and LPAI. Viral RNA was not detected in the control animals. In the trachea viral RNA was detected from 4 hpi in similar amounts as in the lungs and the amounts increased in time (data not shown).


Highly pathogenic or low pathogenic avian influenza virus subtype H7N1 infection in chicken lungs: small differences in general acute responses.

Rebel JM, Peeters B, Fijten H, Post J, Cornelissen J, Vervelde L - Vet. Res. (2011)

Scatter plot of the amount of viral RNA of individual birds in the lung at different time points post inoculation (hpi) with LPAI (open symbols) or HPAI (closed symbols). The horizontal line represents the mean of 6 individual birds. Viral RNA expression was determined using RT-PCR and data were expressed as EID50/g.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3037890&req=5

Figure 2: Scatter plot of the amount of viral RNA of individual birds in the lung at different time points post inoculation (hpi) with LPAI (open symbols) or HPAI (closed symbols). The horizontal line represents the mean of 6 individual birds. Viral RNA expression was determined using RT-PCR and data were expressed as EID50/g.
Mentions: Viral RNA was detected in the lungs as early as 4 hpi and the amount of viral RNA increased significantly (F pr < 0.001) upto 24 hpi (Figure 2). In order to investigate the kinetics of the viral RNA in time between HPAI and LPAI infected birds we analysed the data with and without birds that had non-detectable level of viral RNA. When 4 of the 24 LPAI infected birds (2 birds at 4 hpi, 1 at 8 hpi and 1 at 24 hpi) with no detectable level of viral RNA were excluded from the analysis, no significant difference existed between the amount of viral RNA in the caudal lungs of LPAI and HPAI infected birds in time. When the birds with no detectable amount of viral RNA were included in the analysis differences did exist between HPAI and LPAI infected birds. For the cranial part a difference between HPAI and LPAI in time was found (F pr = 0.07), while at 24 h no significant difference existed between HPAI and LPAI. Viral RNA was not detected in the control animals. In the trachea viral RNA was detected from 4 hpi in similar amounts as in the lungs and the amounts increased in time (data not shown).

Bottom Line: No major difference between LPAI and HPAI infected birds in the induction of cytokines and interferons at mRNA level in lung tissue was found.In conclusion, the differences in lethality for chickens infected with LPAI or HPAI could be ascribed to difference in location of the virus.However similar amounts of viral RNA, similar cytokine mRNA levels, and similar influxes of CD8α+ and KUL01+ macrophages and DC were found between HPAI and LPAI in the lungs.A cytokine storm at mRNA level as described for mammals was not observed in the lungs of HPAI infected birds within 24 hpi.

View Article: PubMed Central - HTML - PubMed

Affiliation: Central Veterinary Institute, PO box 65, 8219 PH Lelystad, The Netherlands. Annemarie.Rebel@WUR.nl.

ABSTRACT
Avian influenza virus can be divided into two groups, highly pathogenic avian influenza virus (HPAI) and low pathogenic avian influenza virus (LPAI) based on their difference in virulence. To investigate if the difference in clinical outcome between LPAI and HPAI in chickens is due to immunological host responses in the lung within the first 24 hours post infection (hpi), chickens were infected with LPAI or HPAI of subtype H7N1. Virus was found in the caudal and cranial part of the lung. With LPAI, virus was localised around the intrapulmonary bronchus and secondary bronchi. In sharp contrast, HPAI was detected throughout the whole lung. However, based on viral RNA levels, no quantitative difference was observed between LPAI and HPAI infected birds. In infected areas of the lungs, an influx of CD8α+ cells as well as KUL01+ macrophages and dendritic cells (DC) occurred as fast as 8 hpi in both infected groups. No major difference between LPAI and HPAI infected birds in the induction of cytokines and interferons at mRNA level in lung tissue was found.In conclusion, the differences in lethality for chickens infected with LPAI or HPAI could be ascribed to difference in location of the virus. However similar amounts of viral RNA, similar cytokine mRNA levels, and similar influxes of CD8α+ and KUL01+ macrophages and DC were found between HPAI and LPAI in the lungs. A cytokine storm at mRNA level as described for mammals was not observed in the lungs of HPAI infected birds within 24 hpi.

Show MeSH
Related in: MedlinePlus