Heterogeneity of Early Host Response to Infection with Four Low-Pathogenic H7 Viruses with a Different Evolutionary History in the Field

Abstract

Once low-pathogenic avian influenza viruses (LPAIVs) of the H5 and H7 subtypes from wild birds enter into poultry species, there is the possibility of them mutating into highly pathogenic avian influenza viruses (HPAIVs), resulting in severe epizootics with up to 100% mortality. This mutation from a LPAIV to HPAIV strain is the main cause of an AIV’s major economic impact on poultry production. Although AIVs are inextricably linked to their hosts in their evolutionary history, the contribution of host-related factors in the emergence of HPAI viruses has only been marginally explored so far. In this study, transcriptomic sequencing of tracheal tissue from chickens infected with four distinct LP H7 viruses, characterized by a different history of pathogenicity evolution in the field, was implemented. Despite the inoculation of a normalized infectious dose of viruses belonging to the same subtype (H7) and pathotype (LPAI), the use of animals of the same age, sex and species as well as the identification of a comparable viral load in the target samples, the analyses revealed a heterogeneity in the gene expression profile in response to infection with each of the H7 viruses administered.

Dual Host and Pathogen RNA-Seq Analysis Unravels Chicken Genes Potentially Involved in Resistance to Highly Pathogenic Avian Influenza Virus Infection

“…The outcome of HPAIV infection is a complex and multifactorial process where both the host innate immune response and the virus play an important role. The last years RNA-Seq have proved to be a powerful tool to characterize these complex processes in chickens against several pathogens ( 32 – 34 ). The aim of the present study was to characterize the early host and viral factors that determine the individual clinical outcome of HPAIV infected chickens.…”

Comparative Analysis of Different Inbred Chicken Lines Highlights How a Hereditary Inflammatory State Affects Susceptibility to Avian Influenza Virus

“…Hereditary differences in uninfected birds and differences in the kinetics of the cytokine and chemokine responses in MHC I inbred chicken lines have been reported previously after infection with IBV [ 50 ], infectious bursal disease virus [ 51 ], Eimeria maxima [ 52 ] and Campylobacter jejuni [ 53 ], as well as in vitro after the infection of macrophages with Marek’s disease virus [ 54 ]. Recently, the transcriptomic analysis of tracheal tissue from chickens infected with four distinct LP H7 viruses, characterised by different histories of pathogenicity evolution in the field, highlighted that the first line of defence against AIVs was initiated with a different magnitude to those viruses that switched from an LP to an HP genotype and phenotype in the field [ 55 ]. Therefore, not only the identification of genes involved in the resistance against viral infections but also the magnitude and kinetics of the responses should be taken into account, as many genes are differentially regulated in susceptible and resistant birds.…”

Transcriptome Profiling of Oncorhynchus mykiss Infected with Low or Highly Pathogenic Viral Hemorrhagic Septicemia Virus (VHSV)

“…Acod1 was also found among the over-expressed genes in a recent study on RNA-Seq conducted on avian influenza virus (Family Orthomixoviridae ). Interestingly, a transcriptional increase of acod1 was observed only in the groups infected with precursor strains of highly pathogenic avian influenza viruses [ 53 ].…”