Avian influenza A (H7N9) virus infections in humans across five epidemics in mainland China, 2013–2017

Hui, David Shu-Cheong; Lee, Nelson; Chan, Paul K.S.

doi:10.21037/jtd.2017.11.17

Cited by 9 publications

(6 citation statements)

References 23 publications

(26 reference statements)

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“…Influenza A virus (IAV) has been the cause of historical noxious pandemics, such as the Spanish flu 1918 H1N1, Asian flu H2N2 1957, Hong Kong H3N2 flu 1968, and more recently the pandemic of H1N1 2009 (Swine flu). Influenza also causes seasonal epidemics and outbreaks with high morbidity and mortality rates such as the 2015 H1N1 outbreak in India ( 1 , 2 ). The error-prone nature of the viral RNA polymerase (RdRP) and virus’ capacity for genetic re-assortment (antigenic drift and shift) result in the viral components’ susceptibility to mutations, allowing the viruses to evade the immune system and increases their resistance to control strategies.…”

Section: Introductionmentioning

confidence: 99%

Advancements in Host-Based Interventions for Influenza Treatment

et al. 2018

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Influenza is a major acute respiratory infection that causes mortality and morbidity worldwide. Two classes of conventional antivirals, M2 ion channel blockers and neuraminidase inhibitors, are mainstays in managing influenza disease to lessen symptoms while minimizing hospitalization and death in patients with severe influenza. However, the development of viral resistance to both drug classes has become a major public health concern. Vaccines are prophylaxis mainstays but are limited in efficacy due to the difficulty in matching predicted dominant viral strains to circulating strains. As such, other potential interventions are being explored. Since viruses rely on host cellular functions to replicate, recent therapeutic developments focus on targeting host factors involved in virus replication. Besides controlling virus replication, potential targets for drug development include controlling virus-induced host immune responses such as the recently suggested involvement of innate lymphoid cells and NADPH oxidases in influenza virus pathogenesis and immune cell metabolism. In this review, we will discuss the advancements in novel host-based interventions for treating influenza disease.

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Section: Introductionmentioning

confidence: 99%

Advancements in Host-Based Interventions for Influenza Treatment

et al. 2018

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“…The public health burden of these annual outbreaks is significant with up to 650,000 excess deaths estimated annually by the WHO from influenza infections [1]. In addition, a vast array of different IAV subtypes circulate in the natural reservoir population of wild aquatic birds and sporadically these avian IAVs can cross the host species barrier and result in infection of humans, often with high case fatality rates, such as H7N9 or H5N1 [2][3][4].…”

Section: Introductionmentioning

confidence: 99%

Mapping the interaction sites of Influenza A viruses and human complement Factor H

Rabeeah,

Billington,

Nal-Rogier

et al. 2023

Preprint

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The complement system is an innate immune mechanism against microbial infection. It involves a cascade of effector molecules that is activated via classical, lectin and alternative pathways. Consequently, many pathogens bind to or incorporate in their structures host negative regulators of the complement pathways as an evasion mechanism. Factor H (FH) is a negative regulator of the complement alternative pathway that protects self cells of the host from non-specific complement attack. Viruses including human influenza A viruses (IAVs) have been shown to bind to FH. Here we show that IAVs of both human and avian origin can bind directly to human FH and the interaction is mediated via the IAV surface glycoprotein haemagglutinin (HA). HA bound to common pathogen binding footprints on the FH structure, complement control protein modules, CCP 5-7 and CCP 15-20. The FH binding to H1 and H3 showed that the interaction overlapped with the receptor binding site of both HAs but the footprint was more extensive for the H3 HA than the H1 HA. The HA - FH interaction impeded the initial entry of H1N1 and H3N2 IAV strains but its impact on viral multicycle replication in human lung cells was strain specific. The H3N2 virus binding to cells was significantly inhibited by preincubation with FH, whereas there was no alteration in replicative rate and progeny virus release for human H1N1 or avian H9N2 and H5N3 IAV strains. We have mapped the interaction between IAV and FH, the significance of which for the virus or host is yet to be elucidated.

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“…Since the first human infection with avian H7N9 subtype influenza virus detected in early 2013, this novel virus has resulted in 1567 laboratory confirmed cases as of March 2nd, 2018 with a case‐fatality rate of 40% . Compared with the past four epidemic waves, the number of human cases during the fifth wave in 2016 to 2017 become higher than ever before . Among these waves, geographic expansion may be epidemiologically associated with the distribution of live poultry market, the density of human population or poultry movements .…”

Section: Introductionmentioning

confidence: 99%

“…the number of human cases during the fifth wave in 2016 to 2017 become higher than ever before. 3,4 Among these waves, geographic expansion may be epidemiologically associated with the distribution of live poultry market, the density of human population or poultry movements. 5 Up to now, no evidence implied that this virus can cause sustainable human-to-human transmission.…”

mentioning

confidence: 99%

Establishment of sandwich ELISA for detecting the H7 subtype influenza A virus

Ruan

Sun

Chen

et al. 2019

Journal of Medical Virology

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Avian H7N9 subtype influenza virus infects human with high case‐fatality rate since it emerged in 2013. Although the vaccination has been rapidly used in poultry due to the emergence of highly pathogenic strain, this virus remains prevalent in this region. Thus, rapid diagnosis both in poultry and human clinic is critically important for the control and prevention of H7N9 infection. In this study, a batch of H7 subtype‐specific monoclonal antibodies (mAbs) were developed and a pair of mAb, 2B6, and 5E9 were used to establish a double‐antibody sandwich enzyme‐linked immunosorbent assay (ELISA) to quantify H7 protein and detect influenza A virus baring H7 subtype HA. The lowest detection limit for the recombinant H7 protein was 10 ng/mL and 0.5 HAU/50 μL of A/Guangdong/17SF003/2016(H7N9), 2 HAU/50 μL of A/Netherlands/219/2003(H7N7) and A/Anhui/1/2013(H7N9) for live virus, respectively. The ELISA could not only detect the prevailing H7N9 virus, but also antigenic drift H7 subtype viruses, showing excellent sensitivity and high specificity. Hence, it could serve as a valuable approach to diagnose H7 subtype virus which showed great potential to cause pandemic, as well as antigen quantification.

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Avian influenza A (H7N9) virus infections in humans across five epidemics in mainland China, 2013–2017

Cited by 9 publications

References 23 publications

Advancements in Host-Based Interventions for Influenza Treatment

Advancements in Host-Based Interventions for Influenza Treatment

Mapping the interaction sites of Influenza A viruses and human complement Factor H

Establishment of sandwich ELISA for detecting the H7 subtype influenza A virus

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