Clinical Course of Avian Influenza A(H5N1) in Patients at the Persahabatan Hospital, Jakarta, Indonesia, 2005–2008

Soepandi, Priyanti Zuswayudha; Burhan, Erlina; Mangunnegoro, Hadiarto; Nawas, Arifin; Aditama, Tjandra Yoga; Partakusuma, Lia Gardenia; Isbaniah, Fathiyah; Ikhsan, Mukhtar; Swidarmoko, Boedi; Sutiyoso, Agung; Malik, Suhud; Benamore, Rachel; Baird, J Kevin; Taylor, Walter

doi:10.1378/chest.09-2644

Cited by 25 publications

(25 citation statements)

References 41 publications

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“…Increased serum ferritin levels have been observed in some viral infections such as hepatitis C (13), H5N1 (14) and dengue fever (15); however, very high levels, as observed in our patients, are not a known feature of common viral infections. High serum ferritin levels are a feature of HLH.…”

Section: Discussioncontrasting

confidence: 56%

Very high serum ferritin levels in three newborns with Kawasaki-like illness

Nasir

Tatari

Hamdan

2012

Paediatrics &Amp; Child Health

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Section: Discussioncontrasting

confidence: 56%

Very high serum ferritin levels in three newborns with Kawasaki-like illness

Nasir

Tatari

Hamdan

2012

Paediatrics &Amp; Child Health

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“…This is probably due to dysregulated systemic inflammatory responses, which lead to poor clinical outcomes [35–37]. In our cohort, we observed that the rs4644 AA genotype was associated with the lower serum glucose levels, but no differences in serum leukocyte counts and CRP levels, both indicators for inflammation severity.…”

Section: Discussionmentioning

confidence: 59%

Galectin-3 and Its Genetic Variation rs4644 Modulate Enterovirus 71 Infection

Huang

Chen

et al. 2016

PLoS ONE

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Galectin-3, a chimeric type β-galactoside-binding protein, is known to modulate viral infection; however, its role in enterovirus 71 (EV71) infection has not been investigated. We generated galectin-3 null rhabdomyosarcoma (RD) cells and evaluated whether EV71 infection would be affected. In galectin-3 null cells, the released and intracellular EV71 viral loads were suppressed after 24 h of infection, and cell death rates were significantly lower, while cell proliferation remained unaltered. In addition, RD cells expressing a nonsynonymous genetic variant of galectin-3, rs4644 (LGALS3 +191C/A, P64H), produced lower virus titers than those with wild-type galectin-3 (C allele). To clarify whether the in vitro viral load reduction correlates with clinical severity, we enrolled children with laboratory-confirmed EV71 infection. Since hyperglycemia is an indicator of severe EV71 infection in children, 152 of 401 enrolled children had glucose examinations at admission, and 59 subjects had serum glucose levels ≥ 150 mg/dL. In comparison to the rs4644 AA genotype (2.2 ± 0.06 log10 mg/dL), serum glucose levels during EV71 infection were higher in patients with CC (2.4 ± 0.17 log10 mg/dL, p = 0.03) and CA (2.4 ± 0.15 log10 mg/dL, p = 0.02) genotypes, respectively. These findings suggest that the rs4644 AA genotype of galectin-3 might exert a protective effect. In summary, galectin-3 affects EV71 replication in our cellular model and its variant, rs4644, is associated with hyperglycemia in the clinical setting. The underlying mechanism and its potential therapeutic application warrant further investigation.

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“…Consistently, Keller et al showed an activation of the fibrinolytic system during non-pathogenic IAV infection in mice [15]. Remarkably, in humans increased production of D-dimer, a marker of fibrinolysis was found to be a risk factor for fatal outcome of H5N1 and pandemic H1N1 virus infections [24], [25]. Furthermore, IAV infections have been associated with bleeding medical disorders [26], [27].…”

Section: Discussionmentioning

confidence: 79%

Plasminogen Controls Inflammation and Pathogenesis of Influenza Virus Infections via Fibrinolysis

et al. 2013

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Detrimental inflammation of the lungs is a hallmark of severe influenza virus infections. Endothelial cells are the source of cytokine amplification, although mechanisms underlying this process are unknown. Here, using combined pharmacological and gene-deletion approaches, we show that plasminogen controls lung inflammation and pathogenesis of infections with influenza A/PR/8/34, highly pathogenic H5N1 and 2009 pandemic H1N1 viruses. Reduction of virus replication was not responsible for the observed effect. However, pharmacological depletion of fibrinogen, the main target of plasminogen reversed disease resistance of plasminogen-deficient mice or mice treated with an inhibitor of plasminogen-mediated fibrinolysis. Therefore, plasminogen contributes to the deleterious inflammation of the lungs and local fibrin clot formation may be implicated in host defense against influenza virus infections. Our studies suggest that the hemostatic system might be explored for novel treatments against influenza.

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Clinical Course of Avian Influenza A(H5N1) in Patients at the Persahabatan Hospital, Jakarta, Indonesia, 2005–2008

Cited by 25 publications

References 41 publications

Very high serum ferritin levels in three newborns with Kawasaki-like illness

Very high serum ferritin levels in three newborns with Kawasaki-like illness

Galectin-3 and Its Genetic Variation rs4644 Modulate Enterovirus 71 Infection

Plasminogen Controls Inflammation and Pathogenesis of Influenza Virus Infections via Fibrinolysis

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