Pathology of A(H5N8) (Clade 2.3.4.4) Virus in Experimentally Infected Chickens and Mice

Abstract

The emergence of novel highly pathogenic avian influenza viruses (HPAIVs) in migratory birds raises serious concerns as these viruses have the potential to spread during fall migration. We report the identification of novel HPAIV A(H5N8) clade 2.3.4.4 virus that was isolated from sick domestic duck at commercial farm during the second wave of spread that began in October and affected poultry (ducks; chiсkens) in several European regions of Russia and Western Siberia in 2016. The strain was highly lethal in experimental infection of chickens and mice with IVPI = 2.34 and MLD50 = 1.3log10⁡ EID50, accordingly. Inoculation of chickens with the HPAIV A/H5N8 demonstrated neuroinvasiveness, multiorgan failure, and death of chickens on the 3rd day post inoculation. Virus replicated in all collected organ samples in high viral titers with the highest titer in the brain (6.75±0.1 log10TCID50/ml). Effective virus replication was found in the following cells: neurons and glial cells of a brain; alveolar cells and macrophages of lungs; epithelial cells of a small intestine; hepatocytes and Kupffer cells of a liver; macrophages and endothelial cells of a spleen; and the tubular epithelial cells of kidneys. These findings advance our understanding of histopathological effect of A(H5N8) HPAIV infection.

Pathological and Molecular Characterization of H5 Avian Influenza Virus in Poultry Flocks from Egypt over a Ten-Year Period (2009–2019)

“…In addition, depletion of the lymphoid follicles and heterophilic cells infiltration was observed in the spleen, together with hemorrhagic foci and necrosis of the periellipsoid lymphocyte sheaths, which is consistent with several previous studies [ 43 , 48 , 51 ]. Regarding the liver, it showed multiple necrotic foci with leukocytic infiltration, which is in agreement with several previous reports where the liver showed severe congestion, hemorrhage, multifocal hepatic necrosis with fragmented nuclei of the hepatocytes, and infiltration of lymphocytes and macrophages in the periphery of portal triades [ 48 , 51 , 52 , 54 ]. Furthermore, the pancreas showed multifocal necrosis with vacuolation of acinar epithelium and infiltration of the mononuclear cells in the parenchyma, as reported elsewhere [ 48 , 51 , 55 ].…”

Comparative Virological and Pathogenic Characteristics of Avian Influenza H5N8 Viruses Detected in Wild Birds and Domestic Poultry in Egypt during the Winter of 2016/2017

“…The diminished severity of Egyptian H5N8 avian influenza viruses in mammals could be explained by the presence of only one (L75) of the two sites (L75 and Q69) required for PB2-F1 mitochondrial localization [42], the presence of S82 instead of L [38], and the presence of 68TQG70 instead of 68IVF70 cytotoxic sequence in PB1-F2 [19,38] in addition to the presence of the PB2 627E avian preference factors [43] and NP F464-L466 that cause a specific packaging defect affecting the incorporation of segments 3 and 5 [44]. Histopathological changes caused by different H5N8 strains support the previous reports elucidating the ability of the H5N8 virus to replicate well in different organs causing necrotic lesions [45,46]. However, inflammatory reactions varied significantly in different experiments and birds.…”

Lung transcriptional unresponsiveness and loss of early influenza virus control in infected neonates is prevented by intranasal Lactobacillus rhamnosus GG

“…At 3 and 6 DPI, neonates pre-treated with LGG had similar broncho-pneumonia and clinical severity scores, compared to neonatal animals given the sham treatment (Fig 3A and 3B). Although surprising, pathomorphological features do not always reflect disease severity or outcome during an early influenza infection [31].…”