Transcriptional analysis of the innate immune response of ducks to different species-of-origin low pathogenic H7 avian influenza viruses

Highly pathogenic avian influenza viruses (HPAIV) emerge from low pathogenic avian influenza viruses (LPAIV) through the introduction of basic amino acids at the hemagglutinin (HA) cleavage site. Following viral evolution, the newly formed HPAIV likely represents a minority variant within the index host, predominantly infected with the LPAIV precursor. Using reverse-genetics engineered H5N8 viruses differing solely at the HA cleavage, we tested the hypothesis that the interaction between the minority HPAIV and the majority LPAIV could modulate the risk of HPAIV emergence and that the nature of the interaction could depend on the host species. In chickens, we observed that the H5N8 LP increased H5N8 HP replication and pathogenesis. By contrast, the H5N8 LP antagonized H5N8 HP replication and pathogenesis in ducks. Ducks mounted a more potent antiviral innate immune response than chickens against the H5N8 LP , which correlated with H5N8 HP inhibition. Our results provide evidence that HPAIV may be more likely to emerge in chickens than in ducks because of differences in the host response to HPAIV and LPAIV co-infections.

Download Full-text

Host Innate Immune Response of Geese Infected with Clade 2.3.4.4 H5N6 Highly Pathogenic Avian Influenza Viruses

Microorganisms ◽

10.3390/microorganisms8020224 ◽

2020 ◽

Vol 8 (2) ◽

pp. 224

Author(s):

Siyu Wu ◽

Jianni Huang ◽

Qiwen Huang ◽

Junsheng Zhang ◽

Jing Liu ◽

...

Keyword(s):

Immune Response ◽

Avian Influenza ◽

Innate Immune Response ◽

High Mortality ◽

Highly Pathogenic Avian Influenza ◽

Southern China ◽

Influenza Viruses ◽

Innate Immune ◽

Highly Pathogenic ◽

Pathogenic Avian Influenza

Since 2014, highly pathogenic avian influenza (HPAI) H5N6 viruses have circulated in waterfowls and caused human infections in China, posing significant threats to the poultry industry and the public health. However, the genetics, pathogenicity and innate immune response of H5N6 HPAIVs in geese remain largely unknown. In this study, we analyzed the genetic characteristic of the two H5N6 viruses (GS38 and DK09) isolated from apparently healthy domestic goose and duck in live poultry markets (LPMs) of Southern China in 2016. Phylogenetic analysis showed that the HA genes of the two H5N6 viruses belonged to clade 2.3.4.4 and were clustered into the MIX-like group. The MIX-like group viruses have circulated in regions such as China, Japan, Korea, and Vietnam. The NA genes of the two H5N6 viruses were classified into the Eurasian sublineage. The internal genes including PB2, PB1, PA, NP, M, and NS of the two H5N6 viruses derived from the MIX-like. Therefore, our results suggested that the two H5N6 viruses were reassortants of the H5N1 and H6N6 viruses and likely derived from the same ancestor. Additionally, we evaluated the pathogenicity and transmission of the two H5N6 viruses in domestic geese. Results showed that both the two viruses caused serious clinical symptoms in all inoculated geese and led to high mortality in these birds. Both the two viruses were transmitted efficiently to contact geese and caused lethal infection in these birds. Furthermore, we found that mRNA of pattern recognition receptors (PRRs), interferons (IFNs), and stimulated genes (ISGs) exhibited different levels of activation in the lungs and spleens of the two H5N6 viruses-inoculated geese though did not protect these birds from H5N6 HPAIVs infection. Our results suggested that the clade 2.3.4.4 waterfowl-origin H5N6 HPAIVs isolated from LPMs of Southern China could cause high mortality in geese and innate immune-related genes were involved in the geese innate immune response to H5N6 HPAIVs infection. Therefore, we should pay more attention to the evolution, pathogenic variations of these viruses and enhance virological surveillance of clade 2.3.4.4 H5N6 HPAIVs in waterfowls in China.

Download Full-text

Emerging avian influenza infections: Current understanding of innate immune response and molecular pathogenesis

International Reviews of Immunology ◽

10.1080/08830185.2017.1291640 ◽

2017 ◽

Vol 36 (2) ◽

pp. 89-107 ◽

Cited By ~ 6

Author(s):

Anamika Mishra ◽

Periyasamy Vijayakumar ◽

Ashwin Ashok Raut

Keyword(s):

Immune Response ◽

Avian Influenza ◽

Innate Immune Response ◽

Innate Immune ◽

Molecular Pathogenesis ◽

Current Understanding

Download Full-text

Piglet innate immune response to Streptococcus suis colonization is modulated by the virulence of the strain

Veterinary Research ◽

10.1186/s13567-021-01013-w ◽

2021 ◽

Vol 52 (1) ◽

Author(s):

Carlos Neila-Ibáñez ◽

Louise Brogaard ◽

Lola Pailler-García ◽

Jorge Martínez ◽

Joaquim Segalés ◽

...

Keyword(s):

Immune Response ◽

Innate Immune Response ◽

Clinical Signs ◽

Systemic Infection ◽

Streptococcus Suis ◽

Innate Immune ◽

Transcriptional Analysis ◽

Local Inflammatory Response ◽

Virulence Potential ◽

Nasal Swabs

AbstractStreptococcus suis is a zoonotic pathogen of swine involved in arthritis, polyserositis, and meningitis. Colonization of piglets by S. suis is very common and occurs early in life. The clinical outcome of infection is influenced by the virulence of the S. suis strains and the immunity of the animals. Here, the role of innate immunity was studied in cesarean-derived colostrum-deprived piglets inoculated intranasally with either virulent S. suis strain 10 (S10) or non-virulent S. suis strain T15. Colonization of the inoculated piglets was confirmed at the end of the study by PCR and immunohistochemistry. Fever (≥40.5 °C) was more prevalent in piglets inoculated with S10 compared to T15 at 4 h after inoculation. During the 3 days of monitoring, no other major clinical signs were detected. Accordingly, only small changes in transcription of genes associated with the antibacterial innate immune response were observed at systemic sites, with S10 inducing an earlier response than T15 in blood. Local inflammatory response to the inoculation, evaluated by transcriptional analysis of selected genes in nasal swabs, was more sustained in piglets inoculated with the virulent S10, as demonstrated by transcription of inflammation-related genes, such as IL1B, IL1A, and IRF7. In contrast, most of the gene expression changes in trachea, lungs, and associated lymph nodes were observed in response to the non-virulent T15 strain. Thus, S. suis colonization in the absence of systemic infection induces an innate immune response in piglets that appears to be related to the virulence potential of the colonizing strain.

Download Full-text