Project description:To elucidate the expression changes of host genes of SPF chickens infected with fowl adenovirus-4 at 48 hours post-infection. The hearts of SPF chickens infected with fowl adenovirus-4 were collected and high throughout sequenced. Compared with the control group, there were 1797 differentially expressed genes were obtained in the infection group, including 1082 up-regulated genes and 715 down-regulated genes.
Project description:With the purpose to elucidate the expression changes of host genes of SPF chickens infected with duck-origin H7N9 subtype avian influenza virus at 24 hours post-infection(hpi) and fowl adenovirus-4 at 48 dpi. The spleens of SPF chickens infected with duck-origin H7N9 subtype avian influenza virus and fowl adenovirus-4 were collected and high throughout sequenced. Compared with the control group, there were 2426 differentially expressed genes were obtained in the duck-origin H7N9 subtype avian influenza virus group, including 913 up-regulated genes and 1513 down-regulated genes, and there were 1534 differentially expressed genes were obtained in the fowl adenovirus-4 group, including 632 up-regulated genes and 902 down-regulated genes.
Project description:Fowl adenoviruses (FAdVs) are widely distributed in poultry populations around the world, and many diseases are associated with FAdV infection in chickens. This study documented the first characterization of coinfection with fowl adenovirus serotypes 1 and 4 (FAdV-1 and -4) associated with hydropericardium hepatitis syndrome (HHS) in Chinese layer flocks, revealing a novel viral cooperation mechanism. Two novel strains (CH/SX/201805-1 and -4) were identified and isolated, with whole-genome sequencing showing CH/SX/201805-1 clustering with FAdV-1 (99.7% identity to FAdV-A-61/11z), whereas CH/SX/201805-4 displayed characteristic ORF19/27/29 deletions mirroring emergent Chinese FAdV-4 variants. Experimental coinfection in SPF chickens resulted in 87.5% mortality, which was 16.7% greater than that resulting from infection alone, with exacerbated pathology. In vitro coinfection experiments demonstrated concurrent viral replication within same LMH cells, a previously unreported phenomenon, where FAdV-1 increased FAdV-4 replication efficiency 21-fold (P<0.001). Transcriptomic profiling revealed heat shock protein A2 (HSPA2) as the most differentially expressed gene, which was upregulated 2.8-fold during coinfection compared with infection with FAdV-4 alone. Functional validation through HSPA2 knockdown reduced FAdV-4 replication, establishing that FAdV-1 potentiates FAdV-4 through HSPA2-mediated host modulation. These findings provide the first evidence of HSPA2-dependent interserotype synergy in avian adenoviruses and can be used to develop a cellular model for FAdV coinfection studies. These insights redefine the understanding of FAdV pathogenesis and create new avenues for targeted intervention strategies against emerging poultry adenoviral coinfections.
