Unravelling the pathobiological diversity of highly pathogenic avian influenza in birds
- Autores: Raul Sánchez González
- Directores de la Tesis: Antonio José Ramis Salva (dir. tes.), Natàlia Majó i Masferrer (dir. tes.)
- Lectura: En la Universitat Autònoma de Barcelona ( España ) en 2019
- Idioma: español
- Materias:
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- Resumen
Avian influenza (AI) is considered one of the most important viral diseases affecting the poultry industry and a continuous threat to human population and wildlife. To date, a direct comparison of the pathobiology of classical and Gs/GD H5 HPAIVs in avian species belonging to distinct taxonomic groups and breeds is lacking. In the present dissertation we systematically evaluated the differential pathobiological features of a highly pathogenic AI virus (HPAIV) belonging to a classical lineage (H7N1) and a HPAIV of Gs/GD H5 lineage (H5N8) in different breeds of chickens (Gallus gallus domesticus), domestic geese (Anser anser var. domestica) and pigeons (Columba livia var. domestica).
In Study I, the phylogenetic analyses of the H5N8 isolated in Spain in early 2017 indicated that belongs to clade 2.3.4.4 Group B of Gs/GD H5 lineage of HPAIVs, and presented high nucleotide identity with H5N8 HPAIVs previously isolated in Europe, Africa and Asia. The amino acid characterization revealed several amino acid substitutions associated to a phenotype in chickens, ducks and mammals, but the most common markers of human transmission and virulence were lacking. In Study II, both H7N1 and H5N8 HPAIVs were highly lethal for chickens, but H7N1 HPAIV is more virulent for chickens than H5N8 HPAIV based on the higher mortalities and shorter mean death time. The comparatively lower number of chickens inoculated with H5N8 HPAIV presenting cloacal excretion suggests that the horizontal transmission of this virus could be affected. The comparatively higher viral replication of H7N1 HPAIV in the brain of chickens inoculated with this virus suggest that the higher mortalities could be associated with the higher neurotropism of this strain. Local breeds were more susceptible to HPAIV infection than commercial breeds, demonstrating that local breeds do not necessarily present a higher resistance to HPAIVs. In Study III, all domestic geese inoculated with H5N8 HPAIV succumbed to infection, demonstrating that Gs/GD clade 2.3.4.4 H5N8 HPAIVs circulating in Europe in 2016/2017 acquired high virulence for this species. H5N8 HPAIV produced a systemic infection, and the birds likely died as a result of neurological dysfunction or multi-organ failure. The high excretion and the detection of AIV RNA in pool water indicate that this species could play an important role in the epidemiology of this virus. The lack of clinical signs but detection of viral RNA and the seroconversion demonstrate that several geese became subclinically infected with H7N1 HPAIV. Oral shedding was detected in several geese, suggesting that they may play a role in the epidemiology of classical lineages of H7 HPAIVs. In Study IV, H7N1 and H5N8 HPAIVs caused subclinical infections in pigeons, as demonstrated by the lack of clinical signs of disease but seroconversion and detection of viral shedding in several birds. One pigeon inoculated with H5N8 HPAIV presented severe nervous signs and presented severe microscopic lesions associated to widespread AIV antigen in the brain. Therefore, we demonstrate for the first time that Gs/GD clade 2.3.4.4 H5N8 HPAIVs could potentially cause lethal infections in pigeons by neurological dysfunction. The viral shedding in pigeons inoculated with H7N1 and H5N8 HPAIVs was low, but given the wide habitat use of this species, the biological implications of the viral shedding detected here should be further assessed.
Taken together, the present dissertation demonstrates that the clinico-pathological outcome and viral shedding after infection with HPAIVs varies largely depending on the virus and the host, highlighting the necessity to study the pathobiology of HPAIVs in different virus-host combinations. Considering the broad differences, this data also represents a start point to study viral and hosts factors associated with the observed results.
