scholarly journals Avian Influenza Surveillance in the Danube Delta Using Sentinel Geese and Ducks

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Alexandru Coman ◽  
Daniel Narcis Maftei ◽  
Razvan M. Chereches ◽  
Elena Zavrotchi ◽  
Paul Bria ◽  
...  

Highly pathogenic avian influenza (HPAI) H5N1 virus incursions from migrating birds have occurred multiple times in Romania since 2005. Beginning in September 2008 through April 2013, seasonal sentinel surveillance for avian influenza A viruses (AIVs) using domestic geese (Anser cygnoides) and ducks (Anas platyrhynchos) in the Danube Delta was established by placing 15 geese and 5 ducks at seven sites. Tracheal and cloacal swabs, and sera collections (starting in 2009) were taken monthly. We studied a total of 580 domestic birds and collected 5,520 cloacal and tracheal swabs from each and 2,760 sera samples. All swabs were studied with real-time reverse transcription polymerase chain reaction (rRT-PCR) for evidence of AIV. Serological samples were studied with hemagglutination inhibition assays against avian H5, H7, and H9 influenza viruses. From 2009 to 2013, 47 swab specimens from Cot Candura, Enisala, and Saon screened positive for AIV; further subtyping demonstrated that 14 ducks and 20 geese had cloacal evidence of H5N3 carriage. Correspondingly, 4 to 12 weeks after these molecular detections, sentinel bird sera revealed elevated HI titers against H5 virus antigens. We posit that domestic bird surveillance is an effective method to conduct AIV surveillance among migrating birds in delta areas.

Viruses ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 212
Author(s):  
Josanne H. Verhagen ◽  
Ron A. M. Fouchier ◽  
Nicola Lewis

Highly pathogenic avian influenza (HPAI) outbreaks in wild birds and poultry are no longer a rare phenomenon in Europe. In the past 15 years, HPAI outbreaks—in particular those caused by H5 viruses derived from the A/Goose/Guangdong/1/1996 lineage that emerged in southeast Asia in 1996—have been occuring with increasing frequency in Europe. Between 2005 and 2020, at least ten HPAI H5 incursions were identified in Europe resulting in mass mortalities among poultry and wild birds. Until 2009, the HPAI H5 virus outbreaks in Europe were caused by HPAI H5N1 clade 2.2 viruses, while from 2014 onwards HPAI H5 clade 2.3.4.4 viruses dominated outbreaks, with abundant genetic reassortments yielding subtypes H5N1, H5N2, H5N3, H5N4, H5N5, H5N6 and H5N8. The majority of HPAI H5 virus detections in wild and domestic birds within Europe coincide with southwest/westward fall migration and large local waterbird aggregations during wintering. In this review we provide an overview of HPAI H5 virus epidemiology, ecology and evolution at the interface between poultry and wild birds based on 15 years of avian influenza virus surveillance in Europe, and assess future directions for HPAI virus research and surveillance, including the integration of whole genome sequencing, host identification and avian ecology into risk-based surveillance and analyses.


2017 ◽  
Vol 56 (4) ◽  
pp. 339
Author(s):  
C. S. KYRIAKIS (Κ. ΣΠ. ΚΥΡΙΑΚΗΣ) ◽  
K. Van REETH

The huge epizootics of highly pathogenic avian influenza (subtype H5N1) in Southeastern Asia over the last two years and especially the transmission of avian influenza viruses to humans have alerted the international scientific community. Many support that the threat of a new influenza pandemic appears greater today than ever before. During the 20th century, humanity has faced three pandemics, including the "Spanish flu" of 1918-19, which claimed over 20 to 40 million lives, and two less dramatic pandemics in 1957-58 and 1968-69. Influenza A viruses are single stranded RNA viruses belonging to the family Orthomyxoviridae. Their genome expresses only 10 proteins, most important of which are the two surface glycoproteins: haemagglutinin (HA) and neuraminidase (NA). So far, 16 different types of haemagglutinin (HI to Η16) and 9 of neuraminidase (Nl to N9) have been recognized. Influenza A viruses are grouped into "subtypes", according to the HA and NA surface proteins they bear (for example Η I N I , H5N2). Natural reservoirs of influenza A viruses are the wild aquatic birds (migratory waterfowl), from which all types of HA and NA have been isolated. It is important to mention that migratory waterfowl do not show clinical signs of disease, but shed the virus through their excretions.The host range of flu viruses includes domestic poultry, and mammalian species from aquatic mammals to horses, humans and swine. Because of their segmented single stranded RNA genome, influenza viruses have a very high mutation rate (genetic drift) and the possibility to undergo reassortment. Reassortment may occur when more than one virus co-infect the same cell, exchange genes and as a result, provide a totally new influenza virus (genetic shift). At least two subtypes of influenza A viruses are currendy endemic within the human population (H1N1 and H3N2), causing every year outbreaks of disease with very low mortality, especially in elders. Unlike these endemic viruses, pandemic viruses have a much higher morbidity, affecting people of all ages. Η I N I , H3N2 and H1N2 influenza viruses are currently circulating in the European and American swine population. Some of the swine influenza virus subtypes, namely Η I N I and H3N2, are thus similar to those of humans, but there are still important antigenic differences between them. Only rarely swine influenza viruses may be transmitted or cause disease to humans. Unlike mammalian influenza viruses, influenza viruses of domestic birds are grouped in two "pathotypes": low pathogenic avian influenza (LPAI) viruses, which cause localized infections and remain mild or subclinical, and highly pathogenic avian influenza (HPAI) viruses, which cause severe general infection with mortality up to 100% (fowl plague). The majority of avian influenza viruses are low pathogenic and only some, but not all, viruses of H5 and H7 subtypes are highly pathogenic. Occasionally low pathogenic Η5 or H7 viruses from wild birds transmit to poultry. Such viruses can undergo mutations in poultry as a result of which they may acquire a highly pathogenic phenotype. Until the recent avian influenza epizootics in Asia, the predominant theory for the creation of a pandemic virus supported that the pig was likely to act as an intermediate host for transmission of influenza viruses from birds to humans. The fact that genetic reassortment between human and avian viruses has also been shown to occur in pigs in nature, had led to the hypothesis that the pandemic viruses of 1957 and 1968 may have been generated through the pig. More recent data, however, come to question these theories and hypotheses: (a)the direct transmission of the H5N1 and H7N7 avian influenza viruses from birds to humans in Southeastern Asia and The Netherlands, and (b) the presence of cellular receptors recognized preferentially by the haemagglutinin of avian influenza viruses in the human conjunctiva and ciliated respiratory epithelial cells, which support that avian influenza viruses can be transmitted in toto (without reassortment) to and between humans or that humans can be the mixing vessel themselves. Furthermore, there is no solid scientific evidence to prove that any influenza virus reassortants, that have originated in swine, have posed a risk for humans. There are three criteria (conditions) an influenza virus must fulfill in order to be characterized as a pandemic virus: (a) it must be a new virus against which humans are immunologically naive, (b) it must be able to replicate in humans causing severe disease, and (c) it must be efficiendy transmitted among humans, causing wide outbreaks. So far the H5N1 influenza virus only fulfills the first and second condition, and even though it has been sporadically infecting humans for over two years, it has not yet been able to fully adapt to it's new host. Compared to the human population that may have been exposed to the H5N1 influenza virus in Asia, the number of patients and fatalities due to the H5N1 virus is very small. So far, it appears that swine do not play an important role in the epidemiology of this specific virus. Experimental infections of swine with highly pathogenic H5N1 virus have shown that it does not replicate extensively in pigs. Additionally, extensive serological investigations in the swine population of Viet Nam, indicated that the H5N1 virus merely spread to a very small number (~0.25%) of contact animals within the epizootic regions. Nevertheless, it is critical to continue monitor ring pigs and studying the behavior and spread of influenza viruses in these species.


2018 ◽  
Author(s):  
Marina Escalera-Zamudio ◽  
Michael Golden ◽  
Bernardo Gutiérrez ◽  
Julien Thézé ◽  
Jeremy Russell Keown ◽  
...  

ABSTRACTParallel molecular evolution and adaptation are important phenomena commonly observed in viruses. Here we exploit parallel molecular evolution to understand virulence evolution in avian influenza viruses (AIV). Highly-pathogenic AIVs independently evolve from low-pathogenic ancestors via acquisition of a polybasic cleavage sites (pCS). Why some AIV lineages but not others evolve in this way is unknown. We hypothesise that the parallel emergence of highly-pathogenic AIV may be facilitated by permissive or compensatory mutations occurring across the AIV genome. We combined phylogenetic, statistical and structural approaches to discover parallel mutations in AIV genomes associated with the highly-pathogenic phenotype. Parallel mutations were screened using a new statistical test of mutation-phenotype association and further evaluated in the contexts of positive selection and protein function. The mutational panel we present reveals new links between virulence evolution and other viral traits and raises the possibility of predicting aspects of AIV evolution.


2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Marina Escalera-Zamudio ◽  
Michael Golden ◽  
Bernardo Gutiérrez ◽  
Julien Thézé ◽  
Jeremy Russell Keown ◽  
...  

AbstractParallel molecular evolution and adaptation are important phenomena commonly observed in viruses. Here, we exploit parallel molecular evolution to understand virulence evolution in avian influenza viruses (AIV). Highly-pathogenic AIVs evolve independently from low-pathogenic ancestors via acquisition of polybasic cleavage sites. Why some AIV lineages but not others evolve in this way is unknown. We hypothesise that the parallel emergence of highly-pathogenic AIV may be facilitated by permissive or compensatory mutations occurring across the viral genome. We combine phylogenetic, statistical and structural approaches to discover parallel mutations in AIV genomes associated with the highly-pathogenic phenotype. Parallel mutations were screened using a statistical test of mutation-phenotype association and further evaluated in the contexts of positive selection and protein structure. Our resulting mutational panel may help to reveal new links between virulence evolution and other traits, and raises the possibility of predicting aspects of AIV evolution.


2009 ◽  
Vol 83 (9) ◽  
pp. 4205-4215 ◽  
Author(s):  
Jun Han Lee ◽  
Philippe Noriel Q. Pascua ◽  
Min-Suk Song ◽  
Yun Hee Baek ◽  
Chul-Joong Kim ◽  
...  

ABSTRACT Due to dual susceptibility to both human and avian influenza A viruses, pigs are believed to be effective intermediate hosts for the spread and production of new viruses with pandemic potential. In early 2008, two swine H5N2 viruses were isolated from our routine swine surveillance in Korea. The sequencing and phylogenetic analysis of surface proteins revealed that the Sw/Korea/C12/08 and Sw/Korea/C13/08 viruses were derived from avian influenza viruses of the Eurasian lineage. However, although the Sw/Korea/C12/08 isolate is an entirely avian-like virus, the Sw/Korea/C13/08 isolate is an avian-swine-like reassortant with the PB2, PA, NP, and M genes coming from a 2006 Korean swine H3N1-like virus. The molecular characterization of the two viruses indicated an absence of significant mutations that could be associated with virulence or binding affinity. However, animal experiments showed that the reassortant Sw/Korea/C13/08 virus was more adapted and was more readily transmitted than the purely avian-like virus in a swine experimental model but not in ferrets. Furthermore, seroprevalence in swine sera from 2006 to 2008 suggested that avian H5 viruses have been infecting swine since 2006. Although there are no known potential clinical implications of the avian-swine reassortant virus for pathogenicity in pigs or other species, including humans, at present, the efficient transmissibility of the swine-adapted H5N2 virus could facilitate virus spread and could be a potential model for pandemic, highly pathogenic avian influenza (e.g., H5N1 and H7N7) virus outbreaks or a pandemic strain itself.


Viruses ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 886
Author(s):  
Yuan Liang ◽  
Jakob N. Nissen ◽  
Jesper S. Krog ◽  
Solvej Ø. Breum ◽  
Ramona Trebbien ◽  
...  

Since late 2020, outbreaks of H5 highly pathogenic avian influenza (HPAI) viruses belonging to clade 2.3.4.4b have emerged in Europe. To investigate the evolutionary history of these viruses, we performed genetic characterization on the first HPAI viruses found in Denmark during the autumn of 2020. H5N8 viruses from 14 wild birds and poultry, as well as one H5N5 virus from a wild bird, were characterized by whole genome sequencing and phylogenetic analysis. The Danish H5N8 viruses were found to be genetically similar to each other and to contemporary European clade 2.3.4.4b H5N8 viruses, while the Danish H5N5 virus was shown to be a unique genotype from the H5N5 viruses that circulated at the same time in Russia, Germany, and Belgium. Genetic analyses of one of the H5N8 viruses revealed the presence of a substitution (PB2-M64T) that is highly conserved in human seasonal influenza A viruses. Our analyses showed that the late 2020 clade 2.3.4.4b HPAI H5N8 viruses were most likely new incursions introduced by migrating birds to overwintering sites in Europe, rather than the result of continued circulation of H5N8 viruses from previous introductions to Europe in 2016/2017 and early 2020.


2021 ◽  
Vol 9 (8) ◽  
pp. 1639
Author(s):  
Andrew T. Bisset ◽  
Gerard F. Hoyne

In 2020, several geographically isolated farms in Victoria, Australia, experienced an outbreak of highly pathogenic avian influenza (HPAI) virus H7N7 and low pathogenic avian influenza (LPAI) viruses H5N2 and H7N6. Effective containment and control measures ensured the eradication of these viruses but the event culminated in substantial loss of livestock and significant economic impact. The avian HPAI H7N7 virus generally does not infect humans; however, evidence shows the ocular pathway presents a favourable tissue tropism for human infection. Through antigenic drift, mutations in the H7N7 viral genome may increase virulence and pathogenicity in humans. The Victorian outbreak also detected LPAI H7N6 in emus at a commercial farm. Novel influenza A viruses can emerge by mixing different viral strains in a host susceptible to avian and human influenza strains. Studies show that emus are susceptible to infections from a wide range of influenza viral subtypes, including H5N1 and the pandemic H1N1. The emu’s internal organs and tissues express abundant cell surface sialic acid receptors that favour the attachment of avian and human influenza viruses, increasing the potential for internal genetic reassortment and the emergence of novel influenza A viruses. This review summarises the historical context of H7N7 in Australia, considers the potential for increased virulence and pathogenesis through mutations and draws attention to the emu as potentially an unrecognised viral mixing vessel.


eLife ◽  
2014 ◽  
Vol 3 ◽  
Author(s):  
Colin A Russell ◽  
Peter M Kasson ◽  
Ruben O Donis ◽  
Steven Riley ◽  
John Dunbar ◽  
...  

Assessing the pandemic risk posed by specific non-human influenza A viruses is an important goal in public health research. As influenza virus genome sequencing becomes cheaper, faster, and more readily available, the ability to predict pandemic potential from sequence data could transform pandemic influenza risk assessment capabilities. However, the complexities of the relationships between virus genotype and phenotype make such predictions extremely difficult. The integration of experimental work, computational tool development, and analysis of evolutionary pathways, together with refinements to influenza surveillance, has the potential to transform our ability to assess the risks posed to humans by non-human influenza viruses and lead to improved pandemic preparedness and response.


mBio ◽  
2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Huihui Kong ◽  
David F. Burke ◽  
Tiago Jose da Silva Lopes ◽  
Kosuke Takada ◽  
Masaki Imai ◽  
...  

ABSTRACT Since the emergence of highly pathogenic avian influenza viruses of the H5 subtype, the major viral antigen, hemagglutinin (HA), has undergone constant evolution, resulting in numerous genetic and antigenic (sub)clades. To explore the consequences of amino acid changes at sites that may affect the antigenicity of H5 viruses, we simultaneously mutated 17 amino acid positions of an H5 HA by using a synthetic gene library that, theoretically, encodes all combinations of the 20 amino acids at the 17 positions. All 251 mutant viruses sequenced possessed ≥13 amino acid substitutions in HA, demonstrating that the targeted sites can accommodate a substantial number of mutations. Selection with ferret sera raised against H5 viruses of different clades resulted in the isolation of 39 genotypes. Further analysis of seven variants demonstrated that they were antigenically different from the parental virus and replicated efficiently in mammalian cells. Our data demonstrate the substantial plasticity of the influenza virus H5 HA protein, which may lead to novel antigenic variants. IMPORTANCE The HA protein of influenza A viruses is the major viral antigen. In this study, we simultaneously introduced mutations at 17 amino acid positions of an H5 HA expected to affect antigenicity. Viruses with ≥13 amino acid changes in HA were viable, and some had altered antigenic properties. H5 HA can therefore accommodate many mutations in regions that affect antigenicity. The substantial plasticity of H5 HA may facilitate the emergence of novel antigenic variants.


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