Clinical Preparedness for Cytokine Storm Induced By the Highly Pathogenic H5N1 Influenza Virus

Ishikawa, Toshihisa

doi:10.4172/2153-0645.1000e131

Cited by 15 publications

(15 citation statements)

References 6 publications

(9 reference statements)

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“…It was previously shown that cytokine-, chemokine-, and IFN-related gene products induced by IAV infection control viral propagation ( Mukherjee et al, 2011 ; Ishikawa, 2012 ) and that specific IAVs (pandemic H1N1 1918 and H5N1-type highly pathogenic avian influenza virus) induce a strong over expression of such factors, causing a so called cytokine storm (CS). CS can lead to increased pathogenicity and severe disease in infected humans ( Ishikawa, 2012 ; Tisoncik et al, 2012 ; Ranaware et al, 2016 ). This was observed for infected airway epithelial cells supporting productive viral replication, as well as alveolar macrophages and dendritic cells, which do not support productive IAV infections ( Perrone et al, 2008 ; Gill et al, 2010 ).…”

Section: Resultsmentioning

confidence: 99%

“…As NS1 is the main viral factor controlling cellular innate immune response in order to promote viral replication ( Mukherjee et al, 2011 ; Ishikawa, 2012 ) we next examined (i) whether the growth advantage in A549 (human lung epithelia) cells conferred by the NS segment of PR8 might be associated with altered mRNA expression levels of antiviral acting cyto-/chemokines- and interferon-related cellular genes, and (ii) whether NS segment-specific effects would also be evident in dTHP-1 cells. These cells are human monocytic THP-1 cells, which were morphologically and functionally differentiated to non-productive macrophages ( Short et al, 2012 ).…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

NS Segment of a 1918 Influenza A Virus-Descendent Enhances Replication of H1N1pdm09 and Virus-Induced Cellular Immune Response in Mammalian and Avian Systems

et al. 2018

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The 2009 pandemic influenza A virus (IAV) H1N1 strain (H1N1pdm09) has widely spread and is circulating in humans and swine together with other human and avian IAVs. This fact raises the concern that reassortment between H1N1pdm09 and co-circulating viruses might lead to an increase of H1N1pdm09 pathogenicity in different susceptible host species. Herein, we explored the potential of different NS segments to enhance the replication dynamics, pathogenicity and host range of H1N1pdm09 strain A/Giessen/06/09 (Gi-wt). The NS segments were derived from (i) human H1N1- and H3N2 IAVs, (ii) highly pathogenic- (H5- or H7-subtypes) or (iii) low pathogenic avian influenza viruses (H7- or H9-subtypes). A significant increase of growth kinetics in A549 (human lung epithelia) and NPTr (porcine tracheal epithelia) cells was only noticed in vitro for the reassortant Gi-NS-PR8 carrying the NS segment of the 1918-descendent A/Puerto Rico/8/34 (PR8-wt, H1N1), whereas all other reassortants showed either reduced or comparable replication efficiencies. Analysis using ex vivo tracheal organ cultures of turkeys (TOC-Tu), a species susceptible to IAV H1N1 infection, demonstrated increased replication of Gi-NS-PR8 compared to Gi-wt. Also, Gi-NS-PR8 induced a markedly higher expression of immunoregulatory and pro-inflammatory cytokines, chemokines and interferon-stimulated genes in A549 cells, THP-1-derived macrophages (dHTP) and TOC-Tu. In vivo, Gi-NS-PR8 induced an earlier onset of mortality than Gi-wt in mice, whereas, 6-week-old chickens were found to be resistant to both viruses. These data suggest that the specific characteristics of the PR8 NS segments can impact on replication, virus induced cellular immune responses and pathogenicity of the H1N1pdm09 in different avian and mammalian host species.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

NS Segment of a 1918 Influenza A Virus-Descendent Enhances Replication of H1N1pdm09 and Virus-Induced Cellular Immune Response in Mammalian and Avian Systems

et al. 2018

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“…67 Hence, the early recognition of CS and the prompt treatment can improve the clinical outcome of the COVID-19 infection. 67,72 Several antiviral and anti-inflammatory drug therapies have been proposed for treating SARS-CoV-2 mediated CS, in order to decrease both the morbidity and mortality in COVID-19 patients, and a comprehensive review and critical appraisal of these therapies has been made in this review.…”

Section: Host Defense Against Sars-cov-2 Viral Interactionmentioning

confidence: 99%

Understanding COVID-19 Pandemic: Molecular Mechanisms and Potential Therapeutic Strategies. An Evidence-Based Review

Hanna¹,

Dalvi²,

Sălăgean³

et al. 2021

JIR

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“…Cytokine Storm (CS) is a lethal clinical condition, and it requires intensive care; since it is responsible for the high mortality rate in COVID-19 patients [26,27].…”

Section: Treatment Of Cytokine Stormmentioning

confidence: 99%

Cytokine Storm: A Suicidal Immune Response to Novel Corona Virus

Gohil¹,

Gohil²

2021

GJMR

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SARS-CoV-2 virus is responsible for the COVID-19 disease in patients. Only 15-20 % of COVID-19 patients have developed severe pulmonary symptoms and illness, which are fatal to patients. Hyper-immune response to the SARS-CoV-2 virus by the host’s immune system causes the release and over production of certain kinds of inflammatory mediators and cytokines. And it results in the cytokine storm. Cytokine storm produces the hyper inflammatory reaction, which deteriorates the cells and tissue. This type of immune response is host killing and suicidal response to the SARS-CoV-2 virus by the host. This suicidal response ultimately leads to lung damage, respiratory tract pneumonia, ARDS, multi-organ failure at a later stage and ultimately death. Hence, it needs to suppress the hyper-functioning of the immune system to inhibit the cytokine release and cytokine storm. Anti-inflammatory and immuno-modulatory drugs can be repurposed to manage the cytokine storm and hyper-immune response. Inhibition and management of the host’s suicidal immune response and cytokine storm, could be life-saving and reduce the mortality rate in COVID-19 patients.

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Clinical Preparedness for Cytokine Storm Induced By the Highly Pathogenic H5N1 Influenza Virus

Cited by 15 publications

References 6 publications

NS Segment of a 1918 Influenza A Virus-Descendent Enhances Replication of H1N1pdm09 and Virus-Induced Cellular Immune Response in Mammalian and Avian Systems

NS Segment of a 1918 Influenza A Virus-Descendent Enhances Replication of H1N1pdm09 and Virus-Induced Cellular Immune Response in Mammalian and Avian Systems

Understanding COVID-19 Pandemic: Molecular Mechanisms and Potential Therapeutic Strategies. An Evidence-Based Review

Cytokine Storm: A Suicidal Immune Response to Novel Corona Virus

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