Virulence of an H5N8 highly pathogenic avian influenza is enhanced by the amino acid substitutions PB2 E627K and HA A149V

Wu, Haibo; Peng, Xiuming; Lu, Rufeng; Xu, Lixin; Liu, Fumin; Cheng, Linfang; Lu, Xiangyun; Yao, Hang‐Ping; Wu, Nanping

doi:10.1016/j.meegid.2017.07.026

Cited by 10 publications

(15 citation statements)

References 44 publications

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“…The viruses were titrated using HA of 1% chicken red blood cells (RBCs) before the HI assay was performed [33]. Control negative and positive sera were treated with receptor destroying enzyme (RDE) and inactivated at 56°C for 30 min [28].…”

Section: Haemagglutination Inhibition (Hi) Assaymentioning

confidence: 99%

“…The virus-antibody mixture was then added to confluent MDCK monolayers in 96-well plates and supplemented with 2 µg/ml TPCK-trypsin (Worthington) and incubated for 72 h at 37°C. Each sample consisted of four replicates, and the mAbs titres required to reduce virus replication by 50% were determined by an HA assay [33], following the Reed and Muench method [26].…”

Section: Virus Microneutralization (Mn) Assaymentioning

confidence: 99%

“…Then mixtures were inoculated into 11-day-old embryonated chicken eggs. The allantoic fluid was harvested and tested using an HA assay [33]. The positive allantoic fluid was again mixed with mAbs and passaged in eggs as described previously.…”

Section: Generation Of Antibody Escape Mutantsmentioning

confidence: 99%

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Generation of neutralizing and non-neutralizing monoclonal antibodies against H7N9 influenza virus

Yang

Xiao

et al. 2020

Emerging Microbes & Infections

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The H7N9 viruses have been circulating for six years. The insertion of a polybasic cleavage site in the haemagglutinin (HA) protein of H7N9 has resulted in the emergence of a highly pathogenic (HP) avian influenza virus. Currently, there are limited studies on neutralizing monoclonal antibodies(mAbs) against HP H7N9 AIVs. In this study, mice were immunized with inactivated H7N9 vaccine of A/ZJU01/PR8/2013 to produce murine mAbs. Finally, two murine mAbs against the HA of low pathogenic (LP) virus were produced and characterized. Characterization included determining mAbs binding breadth and affinity, in vitro neutralization capacity, and potential in vivo protection. Two of these mAbs, 1H10 and 2D1, have been identified to have therapeutic and prophylactic efficacy against the HP strain in mouse passive transfer-viral challenge experiments. The mAb 1H10 was most efficacious, even if the treatment-time was as late as 72 h post-infection, or the therapeutic dose was as low as 1 mg/kg; and it was confirmed to have haemagglutination inhibition and neutralizing activity on both LP-and HP-H7N9 strains. Further study indicated that the protection provided by 2D1 was mediated by antibody-dependent cellular cytotoxicity. The mAbs described here provide promising results and merit further development into potential antiviral therapeutics for H7N9 infection.

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Section: Haemagglutination Inhibition (Hi) Assaymentioning

confidence: 99%

Section: Virus Microneutralization (Mn) Assaymentioning

confidence: 99%

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Generation of neutralizing and non-neutralizing monoclonal antibodies against H7N9 influenza virus

Yang

Xiao

et al. 2020

Emerging Microbes & Infections

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“…5,10,11 Mutations facilitating adaptation of avian influenza viruses for the infection of mammalian hosts consist of individual or limited sets of point mutations in specific gene segments like PB2 (L89V, E627K, D701N) and hemagglutinin (HA) (A149V) and NS1 (P42S). [11][12][13][14][15][16][17][18][19][20][21][22][23] Thus, while influenza A(H5N8) poses limited zoonotic transmission risk, given its evolutionary history and relatively simple genetic adaptations required for potential mammalian infection, it could pose a potential pandemic risk.…”

Section: Introductionmentioning

confidence: 99%

“…While this mutation was not observed in any samples, sample 0416 sequenced in this study had a minority viral population (22%) that possessed the D701E mutation. All WCP A(H5N8) samples sequenced possessed the NS (P42S) and PB2 (L89V) mutations noted as markers of mammalian adaptation 12,13,15,16,23. However, the presence of these adaptation markers alone may not be sufficient to enable adaptation as no human infections with influenza A(H5N8) strains were detected or reported in South Africa or elsewhere.Our surveillance activities have found no human H5N8 infection, and sequence analyses have also shown no clear impression of influenza A(H5N8) adaptation for mammalian infection.…”

mentioning

confidence: 99%

Human surveillance and phylogeny of highly pathogenic avian influenza A(H5N8) during an outbreak in poultry in South Africa, 2017

Valley‐Omar

Cloete

Pieterse

et al. 2020

Influenza Resp Viruses

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Background: In June 2017, an outbreak of the highly pathogenic avian influenza A(H5N8) was detected in commercial poultry farms in South Africa, which rapidly spread to all nine South African provinces. Objectives:We conducted active surveillance for the transmission of influenza A(H5N8) to humans working with infected birds during the South African outbreak.Methods: Influenza A(H5N8)-positive veterinary specimens were used to evaluate the ability of real-time PCR-based assays to detect contemporary avian influenza A(H5N8) strains. Whole genome sequences were generated from these specimens by next-generation sequencing for phylogenetic characterization and screening for mammalian-adaptive mutations.Results: Human respiratory samples from 74 individuals meeting our case definition, all tested negative for avian influenza A(H5) by real-time PCR, but 2 (3%) were positive for human influenza A(H3N2). 54% (40/74) reported wearing personal protective equipment including overalls, boots, gloves, masks, and goggles. 94% (59/63) of veterinary specimens positive for H5N8 were detected on an influenza A(H5) assay for human diagnostics. A commercial H5N8 assay detected H5 in only 6% (3/48) and N8 in 92% (44/48). Thirteen (13/25; 52%) A(H5N8) genomes generated from veterinary specimens clustered in a single monophyletic clade. These sequences contained the NS (P42S) and PB2 (L89V) mutations noted as markers of mammalian adaptation. Conclusions:Diagnostic assays were able to detect and characterize influenza A(H5N8) viruses, but poor performance is reported for a commercial assay. Absence of influenza A(H5N8) in humans with occupational exposure and no clear impression | 267 VALLEY-OMAR Et AL.

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Improved pathogenicity of H9N2 subtype of avian influenza virus induced by mutations occurred after serial adaptations in mice

Zhang

Yang

Shi

et al. 2021

Microbial Pathogenesis

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Virulence of an H5N8 highly pathogenic avian influenza is enhanced by the amino acid substitutions PB2 E627K and HA A149V

Cited by 10 publications

References 44 publications

Generation of neutralizing and non-neutralizing monoclonal antibodies against H7N9 influenza virus

Generation of neutralizing and non-neutralizing monoclonal antibodies against H7N9 influenza virus

Human surveillance and phylogeny of highly pathogenic avian influenza A(H5N8) during an outbreak in poultry in South Africa, 2017

Improved pathogenicity of H9N2 subtype of avian influenza virus induced by mutations occurred after serial adaptations in mice

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