Genetic determinants of resistance to highly pathogenic avian influenza in chickens

2019 ◽  
Vol 15 (2) ◽  
pp. 9-22
Author(s):  
Wioleta Drobik-Czwarno ◽  
Anna Wolc ◽  
Kornelia Kucharska ◽  
Elżbieta Martyniuk

Highly pathogenic avian influenza (HPAI) poses a huge threat to poultry production and also introduces an epidemiological risk in the human population. Thus far, HPAI has been controlled mainly through widespread implementation of biosecurity, and in the case of an outbreak, liquidation of flocks and establishment of protection zones. Alternative strategies for combating HPAI include the use of vaccines, genetic modification, and genetic selection for increased general and specific immunity in birds. These kinds of strategies often require identification of the genes involved in the immune response to the pathogen. Many genes have been identified as potentially associated with differences in the response to HPAI between poultry species and between individuals. Thus far, the most attention has been focused on genes taking part in regulating the innate immune response, which is responsible for preventing infection and limiting the replication and spread of the virus. The most commonly mentioned candidates for layer chickens include interferon-stimulated genes (ISGs) and RIG-I-like receptors. Proteins encoded by genes of the BTLN family, defensins, and proteins involved in apoptosis have also been associated with differences in the response to HPAI. Recent years have seen an increasing number of studies on the genetic determinants of individual differences in the response to HPAI in chickens. Data from HPAI outbreaks in the US in the spring of 2015 and Mexico in the years 2012-2016 have enabled a more precise analysis of this problem. A number of genes have been identified as associated with the immune response, but their specific role in determining the survival of birds requires further study. Preliminary results indicate that genetic determinants of resistance to HPAI are highly complex and can vary depending on the virus strain and the genetic line of birds.

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. These data provide experimental evidence that HPAIV may be more likely to emerge in chickens than in ducks and underscore the importance of within-host viral variants interactions in viral evolution. IMPORTANCE Highly pathogenic avian influenza viruses represent a threat to poultry production systems and to human health because of their impact on food security and because of their zoonotic potential. It is therefore crucial to better understand how these viruses emerge. Using a within-host competition model between highly and low pathogenic avian influenza viruses, we provide evidence that highly pathogenic avian influenza viruses could be more likely to emerge in chickens than in ducks. These results have important implications for highly pathogenic avian influenza virus emergence prevention and they underscore the importance of within-host viral variants interactions in virus evolution.


2021 ◽  
Vol 50 (Supplement_1) ◽  
Author(s):  
Dae-sung Yoo ◽  
Chun Byung Chul

Abstract Background Highly pathogenic avian influenza (HPAI), a zoonotic infectious disease, has been considered a severe threat to public health. The fundamental prevention and control strategy against HPAI includes minimizing the outbreaks of poultry holdings where the virus primarily spreads through animal trade and poultry production associated vehicle movement (PPVM). However, very few attempts have been made to elucidate the association between PPVM and HPAI transmission compared to studies on poultry trade. Therefore, our study aimed to elucidate the role of PPVM on HPAI transmission. Methods We performed network analysis using PPVM data based on a global positioning system (GPS), with phylogenetic information of the HPAI virus for reliable estimation. Moreover, the contribution of PPVM to HPAI infection was estimated by Bayesian inference. Results The network analysis revealed that the connection via PPVM between the same genetic group of infected premises (IPs) was more prevalent than that of different genotype IPs. Moreover, the similarity of farm poultry species and the overlapped integrators between inter-linked IPs was associated with potential transmission route formation. Additionally, the contribution of PPVM among phylogenetically clustered IPs was estimated to have 28.25% of HPAI infections in IPs on average. Conclusions HPAI control strategies including targeted movement restriction and standstill should be established against the HPAI transmission via PPVM. Key messages This is a solid and novel study depicting the need for combining epidemiological analysis with data regarding molecular epidemiology of pathogens.


2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Olatunde Babatunde Akanbi ◽  
Victor Olusegun Taiwo

Commercial layer-type, pullet, cockerel, and broiler chicken flocks infected with highly pathogenic avian influenza (HPAI) H5N1 in Nigeria between 2006 and 2008 were investigated for morbidity, mortality, and pathology. Of the one hundred and fifty-three (153) farms confirmed with HPAI infection, one hundred and twenty-seven (127) were layer-type farms, nine (9) were pullet and broiler farms each, and eight (8) were cockerel rearing farms. This study revealed the morbidity and mortality of a total of 939,620 commercial layer chickens, 16,421 pullets, 3,109 cockerels, and 6,433 broilers. Mortality rates were 11.11% in commercial layers, 26.84% in pullets, 45.51% in cockerels, and 73.92% in broilers in a total of eighteen (18) states and the Federal Capital Territory, Abuja. A total of 316 carcasses were examined of which 248 were commercial layer, 25 were pullet, 14 were cockerel, and 29 were broiler. Main clinical and pathologic findings were observed in the nervous, circulatory, respiratory, integumentary, musculoskeletal, hemopoietic, gastrointestinal, and reproductive systems and, occasionally, lesions were generally nonspecific and multisystemic. Lesions occurred more frequently, severely, and in most of the carcasses examined, irrespective of chicken type.


2021 ◽  
Vol 12 ◽  
Author(s):  
Albert Perlas ◽  
Jordi Argilaguet ◽  
Kateri Bertran ◽  
Raúl Sánchez-González ◽  
Miquel Nofrarías ◽  
...  

Highly pathogenic avian influenza viruses (HPAIVs) cause severe systemic disease and high mortality rates in chickens, leading to a huge economic impact in the poultry sector. However, some chickens are resistant to the disease. This study aimed at evaluating the mechanisms behind HPAIV disease resistance. Chickens of different breeds were challenged with H7N1 HPAIV or clade 2.3.4.4b H5N8 HPAIV, euthanized at 3 days post-inoculation (dpi), and classified as resistant or susceptible depending on the following criteria: chickens that presented i) clinical signs, ii) histopathological lesions, and iii) presence of HPAIV antigen in tissues were classified as susceptible, while chickens lacking all these criteria were classified as resistant. Once classified, we performed RNA-Seq from lung and spleen samples in order to compare the transcriptomic signatures between resistant and susceptible chickens. We identified minor transcriptomic changes in resistant chickens in contrast with huge alterations observed in susceptible chickens. Interestingly, six differentially expressed genes were downregulated in resistant birds and upregulated in susceptible birds. Some of these genes belong to the NF-kappa B and/or mitogen-activated protein kinase signaling pathways. Among these six genes, the serine protease-encoding gene PLAU was of particular interest, being the most significantly downregulated gene in resistant chickens. Expression levels of this protease were further validated by RT-qPCR in a larger number of experimentally infected chickens. Furthermore, HPAIV quasi-species populations were constructed using 3 dpi oral swabs. No substantial changes were found in the viral segments that interact with the innate immune response and with the host cell receptors, reinforcing the role of the immune system of the host in the clinical outcome. Altogether, our results suggest that an early inactivation of important host genes could prevent an exaggerated immune response and/or viral replication, conferring resistance to HPAIV in chickens.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Dae-Sung Yoo ◽  
Byung chul Chun ◽  
Younjung Kim ◽  
Kwang-Nyeong Lee ◽  
Oun-Kyoung Moon

AbstractHighly pathogenic avian influenza (HPAI) in poultry holdings commonly spreads through animal trade, and poultry production and health-associated vehicle (PPHaV) movement. To effectively control the spread of disease, it is essential that the contact structure via those movements among farms is thoroughly explored. However, few attempts have been made to scrutinize PPHaV movement compared to poultry trade. Therefore, our study aimed to elucidate the role of PPHaV movement on HPAI transmission. We performed network analysis using PPHaV movement data based on a global positioning system, with phylogenetic information of the isolates during the 2016–2017 HPAI H5N6 epidemic in the Republic of Korea. Moreover, the contribution of PPHaV movement to the spread of HPAI was estimated by Bayesian modeling. The network analysis revealed that there was the relationship between phylogenetic clusters and the contact network via PPHaV movement. Furthermore, the similarity of farm poultry species and the shared integrators between inter-linked infected premises (IPs) were associated with ties within the same phylogenetic clusters. Additionally, PPHaV movement among phylogenetically clustered IPs was estimated to contribute to approximately 30% of HPAI H5N6 infections in IPs on average. This study provides insight into how HPAI spread via PPHaV movement and scientific basis for control strategies.


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.


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