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

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.

A lack of antibody formation against inactivated influenza virus after aerosol vaccination in presence or absence of adjuvantia

“…Furthermore, in a previous experiment we performed aerosol inoculation with live H9N2 AIV (Reemers et al, 2009). In another study chickens were inoculated with virus via the intratracheal route and found similar immune responses and similar kinetics of the responses (Rebel et al, 2011).…”

Length Variations in the NA Stalk of an H7N1 Influenza Virus Have Opposite Effects on Viral Excretion in Chickens and Ducks

“…We observed no difference in the abilities of the insNA and wt viruses to induce cytokine transcription upon infection of the chicken lung epithelial cell line CLEC213 (6) (data not shown). Therefore, the differences observed in vivo could involve other cell types from the inflammatory response, including cells of myeloid origin and lymphocytes, activated or recruited locally in response to infection (22,28).…”

Serological survey of avian influenza virus infection of backyard chickens in Bosnia and Herzegovina

“…Causative pathogen is a virus that belongs to the family Orthomyxoviridae, genus Influenzavirus, type A. Avian influenza virus (AIV) can be divided in two groups: highly pathogenic avian influenza virus (HPAI) with 100% mortality rate and low pathogenic avian influenza virus (LPAI) that is often detected in wild birds (Rebel et al, 2011).…”

“…According to the literature data, domestic bird species that are predisposed to the AIV infection are chickens, turkeys and guinea fowls, while many species of wild birds are carriers of virus, especialy waterfowls and wild ducks (Rebel et al, 2011). Epidemics of AV were reported in Asia (China), North America (Mexico), Middle-Eastern countries, and recently in Europe -Netherlands, Belgium and Italy (De Jong et al, 2005;Perdue & Swayne, 2005;Bonfanti et al, 2014).…”