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H7N9 virulent mutants detected in chickens in Chin

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    Posted: October 25 2017 at 8:39am
H7N9 virulent mutants detected in chickens in China pose an increased threat to humans

Abstract

Certain low pathogenic avian influenza viruses can mutate to highly pathogenic viruses when they circulate in domestic poultry, at which point they can cause devastating poultry diseases and severe economic damage. The H7N9 influenza viruses that emerged in 2013 in China had caused severe human infections and deaths. However, these viruses were nonlethal in poultry. It is unknown whether the H7N9 viruses can acquire additional mutations during their circulation in nature and become lethal to poultry and more dangerous for humans. Here, we evaluated the evolution of H7N9 viruses isolated from avian species between 2013 and 2017 in China and found 23 different genotypes, 7 of which were detected only in ducks and were genetically distinct from the other 16 genotypes that evolved from the 2013 H7N9 viruses. Importantly, some H7N9 viruses obtained an insertion of four amino acids in their hemagglutinin (HA) cleavage site and were lethal in chickens. The index strain was not lethal in mice or ferrets, but readily obtained the 627K or 701N mutation in its PB2 segment upon replication in ferrets, causing it to become highly lethal in mice and ferrets and to be transmitted efficiently in ferrets by respiratory droplet. H7N9 viruses bearing the HA insertion and PB2 627K mutation have been detected in humans in China. Our study indicates that the new H7N9 mutants are lethal to chickens and pose an increased threat to human health, and thus highlights the need to control and eradicate the H7N9 viruses to prevent a possible pandemic.

Introduction

Influenza viruses are negative-sense RNA viruses, whose genome comprises eight gene segments: basic polymerase 2 (PB2), basic polymerase 1 (PB1), acidic polymerase (PA), hemagglutinin (HA), nucleoprotein (NP), neuraminidase (NA), matrix (M), and nonstructural protein (NS). Each gene segment encodes one or two proteins. Influenza A viruses are categorized into different subtypes on the basis of antigenic differences in their two surface glycoproteins: HA and NA. Currently, 16 different HA and 9 different NA subtypes of influenza viruses have been detected in avian species, but only three subtypes, namely H1N1, H2N2, and H3N2, have caused influenza pandemics in humans1,2.

In the last two decades, avian influenza viruses of the H5N1 and H7N9 subtypes have continued to present challenges to the poultry industry and human health. The H5N1 highly pathogenic avian influenza viruses have caused infections and disease outbreaks among poultry and wild birds in over 60 countries around the world3,4, and have sporadically jumped to humans and caused severe disease and deaths5. Several studies have indicated that the H5N1 influenza viruses will become transmissible in mammals if they acquire more mutations in their HA protein that allow them to recognize human-type receptors and the mutation of lysine (K) at position 627 of their PB26,7,8, or if they reassort with human influenza viruses9.

H7N9 subtype viruses have caused severe human infections and deaths every year in China since they emerged in 201310. Epidemiology studies have shown that humans become infected mainly through exposure to virus-infected poultry or a contaminated environment11,12,13,14,15. Biologic studies on H7N9 viruses have revealed several important characters: (i) the viruses can replicate efficiently in chickens but do not cause disease in any avian species16; (ii) most of the viruses can bind human-type receptors16,17,18,19, mainly because they bear valine (V) at position 186 and leucine (L) at position 226 in their HA protein18 (H3 numbering used throughout), which is an important determinant for avian influenza virus to infect humans; and (iii) when the viruses replicate in humans, they can easily obtain the glutamic acid (E) to K mutation at position 627 (E627K) or aspartic acid (D) to asparagine (N) mutation at position 701 (D701N) in their PB210,11,16,20,21. These two mutations are known to increase the virulence and transmissibility of avian influenza viruses in mammals22,23,24,25,26,27. Indeed, the human H7N9 viruses are transmissible in ferrets, although their transmissibility varies among different strains16,17,28,29,30. The ability to bind to human-type receptors and transmit in mammals is an important indicator of the pandemic potential of the H7N9 viruses. However, because the H7N9 viruses showed low pathogenicity in poultry, strategies to eradicate them in poultry have not been successful in China, with the exception of the temporary closure of live poultry markets in cities where human cases were detected.

The low pathogenic H5 and H7 avian influenza viruses are predisposed to acquire more mutations when they circulate in gallinaceous poultry and subsequently become highly pathogenic for chickens and turkeys, as occurred of the H5N2 outbreak in the United States in 198331, the H5N2 outbreak in Mexico in 199532, and the H7N1 outbreak in Italy in 199933. It is unknown whether the H7N9 viruses can acquire additional mutations during their circulation in nature and become lethal to poultry. Therefore, close monitoring and evaluation of the H7N9 viruses have important implications for both animal and human public health. Here, we characterized H7N9 viruses isolated from avian species in China between 2013 and 2017.

Surveillance and genetic analysis of H7N9 avian influenza viruses

To monitor the evolution of the H7N9 viruses in poultry, we collected 112 593 samples from poultry markets, farms, wild bird habitats, and slaughterhouses in 24 provinces from July 2013 to January 2017, and inoculated the samples individually into 10-day-old embryonated chicken eggs for virus isolation. In total, 3 664 influenza viruses were detected from these samples, of which 293 strains of H7N9 viruses were isolated across 17 provinces (Supplementary information, Table S1). Six viruses were isolated from samples collected from chicken farms in Fujian, Guangdong, Jiangsu, and Zhejiang provinces; all of the other viruses were isolated from samples collected from live poultry markets (Supplementary information, Table S1).

To detect the key mutations that may significantly affect the biologic properties of the viruses, portions of the HA and PB2 genes of the 293 viruses were sequenced. We found that 280 and 266 of the 293 avian viruses bear 186V and 226L mutations, respectively, in their HA, but none of them bear the 627K or 701N mutations in their PB2 (Table 1). Importantly, 12 extra nucleotides (-aaacggactgcg-) encoding four amino acids (-KRTA-) in the cleavage site of HA were detected in seven viruses isolated from chickens in Guangdong province in 2017

For complete Study with full results, Tables, materials and methods, etc. see:   http://www.nature.com/cr/journal/vaop/ncurrent/full/cr2017129a.html
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Post Options Post Options   Thanks (0) Thanks(0)   Quote arirish Quote  Post ReplyReply Direct Link To This Post Posted: October 25 2017 at 8:49am
HARBIN, Oct. 25 (Xinhua) -- Chinese scientists studying the evolution of H7N9 influenza viruses have found that mutations of the virus pose increased threats to humans.

The findings were published on the website Cell Research on Tuesday.

The scientists spent four years doing the research, collecting more than 110,000 samples from poultry markets and slaughterhouses in over 20 provinces, Chen Hualan, director of the National Avian Influenza Reference Laboratory, told Xinhua.

They evaluated the evolution of H7N9 viruses isolated from avian species and found 23 different genotypes. Some of the viruses were not lethal in mice or ferrets, but, via replication in ferrets, mutated and became highly lethal. The viruses were easily spread amongst ferrets by breathing.

"Our study indicated that the new H7N9 mutations are lethal to chickens and pose an increased threat to humans, thus highlighting the need to control and eradicate H7N9 viruses to prevent a possible pandemic," Chen said.

H7N9 was first reported in humans in China in March 2013 and is most likely to cause an epidemic in winter and spring.

http://news.xinhuanet.com/english/2017-10/25/c_136704883.htm
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