Pathogenicity of avian influenza virus H5N1 2007 isolates from Pakistan

Afzal, Farhan; Saeed, Ali; Sharif, Muhammad; Ayub, Najma; Hassan, Sara

doi:10.1016/s2221-1691(12)60192-0

Cited by 4 publications

(3 citation statements)

References 11 publications

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“…For CK/BE/1940/19, a high ICPI of 1.73 was measured. Although few ICPI data are available for AIV, ICPI scores for LPAIV were reported to be ≤ 0.73 [ 59 ], while HPAI viruses had indices of at least 1.36 and higher [ 60 , 61 ]. In this respect, the LPAIV CK/BE/1940/19 behaves like an HPAIV.…”

Section: Discussionmentioning

confidence: 99%

Neuraminidase-associated plasminogen recruitment enables systemic spread of natural avian Influenza viruses H3N1

et al. 2021

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Repeated outbreaks due to H3N1 low pathogenicity avian influenza viruses (LPAIV) in Belgium were associated with unusually high mortality in chicken in 2019. Those events caused considerable economic losses and prompted restriction measures normally implemented for eradicating high pathogenicity avian influenza viruses (HPAIV). Initial pathology investigations and infection studies suggested this virus to be able to replicate systemically, being very atypical for H3 LPAIV. Here, we investigate the pathogenesis of this H3N1 virus and propose a mechanism explaining its unusual systemic replication capability. By intravenous and intracerebral inoculation in chicken, we demonstrate systemic spread of this virus, extending to the central nervous system. Endoproteolytic viral hemagglutinin (HA) protein activation by either tissue-restricted serine peptidases or ubiquitous subtilisin-like proteases is the functional hallmark distinguishing (H5 or H7) LPAIV from HPAIV. However, luciferase reporter assays show that HA cleavage in case of the H3N1 strain in contrast to the HPAIV is not processed by intracellular proteases. Yet the H3N1 virus replicates efficiently in cell culture without trypsin, unlike LPAIVs. Moreover, this trypsin-independent virus replication is inhibited by 6-aminohexanoic acid, a plasmin inhibitor. Correspondingly, in silico analysis indicates that plasminogen is recruitable by the viral neuraminidase for proteolytic activation due to the loss of a strongly conserved N-glycosylation site at position 130. This mutation was shown responsible for plasminogen recruitment and neurovirulence of the mouse brain-passaged laboratory strain A/WSN/33 (H1N1). In conclusion, our findings provide good evidence in natural chicken strains for N1 neuraminidase-operated recruitment of plasminogen, enabling systemic replication leading to an unusual high pathogenicity phenotype. Such a gain of function in naturally occurring AIVs representing an established human influenza HA-subtype raises concerns over potential zoonotic threats.

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Section: Discussionmentioning

confidence: 99%

Neuraminidase-associated plasminogen recruitment enables systemic spread of natural avian Influenza viruses H3N1

et al. 2021

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“…The treatment of this kind of virus is mainly symptomatic treatment in modern medicine. Despite of the occurrence of many broad-spectrum antivirus agents and vaccine, this kind of infection can hardly be radically cured for the high variability and drug resistance of virus [11][12][13][14] . In the treatment of these diseases, traditional Chinese medicine focuses on the relationship between virus, organism and medicine rather than the virus itself.…”

Section: Discussionmentioning

confidence: 99%

Effect of the Haoqinqingdan decoction on damp-heat syndrome in rats with influenza viral pneumonia

Zhang¹,

Chen²,

Li³

et al. 2013

Asian Pacific Journal of Tropical Medicine

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“…In the past, intracerebral injection of AI viruses in day‐old chicks was performed to determine the pathogenicity of the virus (e.g. Afzal et al., ). However, the intracerebral pathogenicity index is not recommended any longer by the OIE ().…”

Section: Appendix F – Ai Introduction Non‐wild Bird Pathwaysmentioning

confidence: 99%