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

2017 ◽  
Vol 36 (2) ◽  
pp. 89-107 ◽  
Author(s):  
Anamika Mishra ◽  
Periyasamy Vijayakumar ◽  
Ashwin Ashok Raut
PLoS ONE ◽  
2016 ◽  
Vol 11 (6) ◽  
pp. e0157816
Author(s):  
T. J. Hagenaars ◽  
E. A. J. Fischer ◽  
C. A. Jansen ◽  
J. M. J. Rebel ◽  
D. Spekreijse ◽  
...  

2020 ◽  
Vol 8 (2) ◽  
pp. 224
Author(s):  
Siyu Wu ◽  
Jianni Huang ◽  
Qiwen Huang ◽  
Junsheng Zhang ◽  
Jing Liu ◽  
...  

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.


2008 ◽  
Vol 225 (1) ◽  
pp. 68-84 ◽  
Author(s):  
Taronna R. Maines ◽  
Kristy J. Szretter ◽  
Lucy Perrone ◽  
Jessica A. Belser ◽  
Rick A. Bright ◽  
...  

2020 ◽  
Vol 11 ◽  
Author(s):  
Jacintha G. B. van Dijk ◽  
Josanne H. Verhagen ◽  
Arne Hegemann ◽  
Conny Tolf ◽  
Jenny Olofsson ◽  
...  

Domestic mallards (Anas platyrhynchos domesticus) are traditionally used as a model to investigate infection dynamics and immune responses to low pathogenic avian influenza viruses (LPAIVs) in free-living mallards. However, it is unclear whether the immune response of domestic birds reflects the response of their free-living counterparts naturally exposed to these viruses. We investigated the extent to which the innate humoral immune response was similar among (i) wild-type domestic mallards in primary and secondary infection with LPAIV H4N6 in a laboratory setting (laboratory mallards), (ii) wild-type domestic mallards naturally exposed to LPAIVs in a semi-natural setting (sentinel mallards), and (iii) free-living mallards naturally exposed to LPAIVs. We quantified innate humoral immune function by measuring non-specific natural antibodies (agglutination), complement activity (lysis), and the acute phase protein haptoglobin. We demonstrate that complement activity in the first 3 days after LPAIV exposure was higher in primary-exposed laboratory mallards than in sentinel and free-living mallards. LPAIV H4N6 likely activated the complement system and the acute phase response in primary-exposed laboratory mallards, as lysis was higher and haptoglobin lower at day 3 and 7 post-exposure compared to baseline immune function measured prior to exposure. There were no differences observed in natural antibody and haptoglobin concentrations among laboratory, sentinel, and free-living mallards in the first 3 days after LPAIV exposure. Our study demonstrates that, based on the three innate humoral immune parameters measured, domestic mallards seem an appropriate model to investigate innate immunology of their free-living counterparts, albeit the innate immune response of secondary-LPAIV exposed mallards is a better proxy for the innate immune response in pre-exposed free-living mallards than that of immunologically naïve mallards.


2021 ◽  
Author(s):  
Pierre Bessière ◽  
Thomas Figueroa ◽  
Amelia Coggon ◽  
Charlotte Foret-Lucas ◽  
Alexandre Houffschmitt ◽  
...  

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.


2011 ◽  
Vol 85 (9) ◽  
pp. 4421-4431 ◽  
Author(s):  
I. Ramos ◽  
D. Bernal-Rubio ◽  
N. Durham ◽  
A. Belicha-Villanueva ◽  
A. C. Lowen ◽  
...  

2020 ◽  
pp. IAI.00714-20

Rui Appelberg passed away suddenly on August 8th 2020. His research tremendously contributed to our current understanding on the crosstalk between mycobacteria species and the host innate immune response. He was an exceptional member of the microbiology and immunology community, he acted as Associate Editor of The Journal of Immunology and belonged to the Editorial Board of Infection and Immunity. Rui will be terribly missed. Collaborators, mentees and friends wrote him the following tribute.


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