Serologic evidence of avian influenza virus infections among Nigerian agricultural workers

Okoye, J. O. A.; Eze, Didacus Chukwuemeka; Krueger, Whitney S.; Heil, Gary L.; Friary, John A.; Gray, Gregory C.

doi:10.1002/jmv.23520

Cited by 31 publications

(32 citation statements)

References 25 publications

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“…In this group, one bird that never shed detectable virus had low HI levels. (Blair et al, 2013;Huang et al, 2013;Liu et al, 2009;Okoye et al, 2013;Pawar et al, 2012;Uyeki et al, 2012;Zhou et al, 2014). On days 4 and 6 p.i., three DI quail per group were euthanized and lung samples were collected for virus titration.…”

Section: Effects Of Ferret-adapted Mutations On H9 Iavsmentioning

confidence: 98%

Replication and transmission of mammalian-adapted H9 subtype influenza virus in pigs and quail

Obadan

Kimble

Rajão

et al. 2015

Journal of General Virology

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Influenza A virus is a major pathogen of birds, swine and humans. Strains can jump between species in a process often requiring mutations and reassortment, resulting in outbreaks and, potentially, pandemics. H9N2 avian influenza is predominant in poultry across Asia and occasionally infects humans and swine. Pandemic H1N1 (H1N1pdm) is endemic in humans and swine and has a history of reassortment in pigs. Previous studies have shown the compatibility of H9N2 and H1N1pdm for reassortment in ferrets, a model for human infection and transmission. Here, the effects of ferret adaptation of H9 surface gene segments on the infectivity and transmission in at-risk natural hosts, specifically swine and quail, were analysed. Reassortant H9N1 and H9N2 viruses, carrying seven or six gene segments from H1N1pdm, showed infectivity and transmissibility in swine, unlike the wholly avian H9N2 virus with ferretadapted surface genes. In quail, only the reassortant H9N2 with the six internal gene segments from the H1N1pdm strain was able to infect and transmit, although less efficiently than the wholly avian H9N2 virus with ferret-adapted surface genes. These results highlight that ferretadapted mutations on the haemagglutinin of H9 subtype virus do not restrict the ability of the virus to infect swine and quail, and that the ability to transmit in these species depends on the context of the whole virus. As such, this study emphasizes the threat that H9N2 reassortant viruses pose to humans and agricultural species and the importance of the genetic constellation of the virus to its ability to replicate and transmit in natural hosts of influenza.

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Section: Effects Of Ferret-adapted Mutations On H9 Iavsmentioning

confidence: 98%

Replication and transmission of mammalian-adapted H9 subtype influenza virus in pigs and quail

Obadan

Kimble

Rajão

et al. 2015

Journal of General Virology

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“…During the same period, a newly emergent avian H10N8 virus, also with six H9N2-like internal genes, was reported to cause fatal human infections in China (4). In the meantime, H9N2 viruses continued to cause human infections in China and other countries based on etiological and serological evidence (5)(6)(7)(8)(9)(10)(11)(12). We recently found that avian H9N2 viruses have undergone significant genetic evolution, especially in their internal genes, to form a predominant genotype (G57), which in turn provided the internal genes to multiple new subtypes, including H7N9 and H10N8 viruses (13).…”

mentioning

confidence: 99%

Prevailing PA Mutation K356R in Avian Influenza H9N2 Virus Increases Mammalian Replication and Pathogenicity

Zhang

Gao

et al. 2016

J Virol

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Adaptation of the viral polymerase complex comprising PB1, PB2, and PA is necessary for efficient influenza A virus replication in new host species. We found that PA mutation K356R (PA-K356R) has become predominant since 2014 in avian H9N2 viruses in China as with seasonal human H1N1 viruses. The same mutation is also found in most human isolates of emergent avian H7N9 and H10N8 viruses whose six internal gene segments are derived from the H9N2 virus. We further demonstrated the mammalian adaptive functionality of the PA-K356R mutation. Avian H9N2 virus with the PA-K356R mutation in human A549 cells showed increased nuclear accumulation of PA and increased viral polymerase activity that resulted in elevated levels of viral transcription and virus output. The same mutant virus in mice also enhanced virus replication and caused lethal infection. In addition, combined mutation of PA-K356R and PB2-E627K, a well-known mammalian adaptive marker, in the H9N2 virus showed further cooperative increases in virus production and severity of infection in vitro and in vivo. In summary, PA-K356R behaves as a novel mammalian tropism mutation, which, along with other mutations such as PB2-E627K, might render avian H9N2 viruses adapted for human infection. IMPORTANCE Mutations of the polymerase complex (PB1, PB2, and PA) of influenza A virus are necessary for viral adaptation to new hosts.This study reports a novel and predominant mammalian adaptive mutation, PA-K356R, in avian H9N2 viruses and human isolates of emergent H7N9 and H10N8 viruses. We found that PA-356R in H9N2 viruses causes significant increases in virus replication and severity of infection in human cells and mice and that PA-K356R cooperates with the PB2-E627K mutation, a wellcharacterized human adaptive marker, to exacerbate mammalian infection in vitro and in vivo. Therefore, the PA-K356R mutation is a significant adaptation in H9N2 viruses and related H7N9 and H10N8 reassortants toward human infectivity. The emergence of new pandemic influenza A viruses requires overcoming barriers to cross-species transmission from animal reservoirs to human populations. Influenza viruses of the H9N2 subtype and their reassortants circulating in poultry are a potential source of pandemic viruses and hence represent a significant public health threat (1). Since spring 2013, a novel avian H7N9 reassortant with six internal genes of the H9N2 virus had caused three major outbreaks in humans throughout China (2, 3). During the same period, a newly emergent avian H10N8 virus, also with six H9N2-like internal genes, was reported to cause fatal human infections in China (4). In the meantime, H9N2 viruses continued to cause human infections in China and other countries based on etiological and serological evidence (5-12). We recently found that avian H9N2 viruses have undergone significant genetic evolution, especially in their internal genes, to form a predominant genotype (G57), which in turn provided the internal genes to multiple new subtypes, including H7N9 and H10N8 viru...

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“…Gray et al also found neutralising antibodies to H6N2 and H7N2 influenza virus in the same study, but the prevalences were not significantly different between the exposed group and non-exposed controls (1.4 vs 4.0% and 5.5 vs 0%) [63]. Five other studies failed to find serological evidence of H6 or H7 exposure [18,63,80,102,117]. Only one-cross sectional study looked at H7N9 exposure, finding a seroprevalence of 6.3% in poultry workers in Guangdong, China, and a significantly lower percentage in non-exposed controls (0%) [110].…”

Section: Resultsmentioning

confidence: 95%

“…Gray et al found a significant difference in the seroprevalence of H5N2 antibodies in a swine- and poultry-exposed rural population from Iowa, United States, vs unexposed controls from the same region (8.8 vs 0%) [63]. Okoye et al found H5N2 antibodies in poultry-exposed and -unexposed groups from Nigeria (0.3 vs 1.8%), however, this difference was not significant [63,102]. Moreover, two studies executed in Romania and Vietnam found no antibodies in either group [18,91].…”

Section: Resultsmentioning

confidence: 99%

Weighing serological evidence of human exposure to animal influenza viruses − a literature review

2016

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Assessing influenza A virus strains circulating in animals and their potential to cross the species barrier and cause human infections is important to improve human influenza surveillance and preparedness. We reviewed studies describing serological evidence of human exposure to animal influenza viruses. Comparing serological data is difficult due to a lack of standardisation in study designs and in laboratory methods used in published reports. Therefore, we designed a scoring system to assess and weigh specificity of obtained serology results in the selected articles. Many studies report reliable evidence of antibodies to swine influenza viruses among persons occupationally exposed to pigs. Most avian influenza studies target H5, H7 and H9 subtypes and most serological evidence of human exposure to avian influenza viruses is reported for these subtypes. Avian influenza studies receiving a low grade in this review often reported higher seroprevalences in humans compared with studies with a high grade. Official surveillance systems mainly focus on avian H5 and H7 viruses. Swine influenza viruses and avian subtypes other than H5 and H7 (emphasising H9) should be additionally included in official surveillance systems. Surveillance efforts should also be directed towards understudied geographical areas, such as Africa and South America.

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Serologic evidence of avian influenza virus infections among Nigerian agricultural workers

Cited by 31 publications

References 25 publications

Replication and transmission of mammalian-adapted H9 subtype influenza virus in pigs and quail

Replication and transmission of mammalian-adapted H9 subtype influenza virus in pigs and quail

Prevailing PA Mutation K356R in Avian Influenza H9N2 Virus Increases Mammalian Replication and Pathogenicity

Weighing serological evidence of human exposure to animal influenza viruses − a literature review

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