First Immunological Clue Why Some H1N1 Victims Get Very Ill or Die

[indigo girl]

http://www.eurekalert.org/pub_releases/2009-12/uhn-fic121509.php

If the dreaded cytokine storm could be prevented, this could potentially save the lives of many swine infected as well as bird flu infected cases of influenza. That really would be quite amazing.

The study analyzed different levels of regulating molecules for 20 hospitalized patients, 15 outpatients and 15 control subjects in 10 Spanish hospitals during the first pandemic wave in July and August 2009. Researchers from the Hospital Clinico Universitario de Valladolid in Spain and the University Health Network found high levels of a molecule called interleukin 17 in the blood of severe H1N1 patients, and low levels in patients with the mild form of the disease.

Interleukin 17 is produced by the body and is important in the normal regulation of white blood cells which fight infection and disease. In certain circumstances, the molecule becomes "out of control", leading to inflammation and autoimmune diseases. The research paper titled, "Th1 and Th17 hypercytokinemia as early host response signature in severe pandemic influenza" is published in the December issue of the Journal of Critical Care.

"In rare cases, the virus causes lung infections requiring patients to be treated in hospital. By targeting or blocking TH17 in the future, we could potentially reduce the amount of inflammation in the lungs and speed up recovery," says Dr. David Kelvin, the leader of the Canadian team, Head of the Experimental Therapeutics Division, Toronto General Hospital Research Institute, University Health Network and Professor of Immunology, University of Toronto. Dr. Kelvin added that the clinical applications of this work is still many years away.

(hat tip pfi/monotreme)

[kids]

Interesting considering that 2 months ago the CDC wasn't endorsing the idea that cytokine storm was a a factor in novel H1N1 deaths. Some of us didn't see how it could be anything else.

[indigo girl]

A link to the full study is here: http://ccforum.com/content/pdf/cc8208.pdf

Of note is the percentage of perfectly healthy people that developed severe disease. Hopefully, studies such as this one will tell us why, and how to prevent this from happening.

Introduction

The emergence of the new pandemic variant of influenza virus (nvH1N1) has brought renewed attention to the strategies for prevention, treatment and minimization of the social and human costs of the influenza disease. [1] [2] [3] [4] [5] The great majority of nvH1N1 infections are mild and self-limiting in nature. [6] [7][8] Nevertheless, a small percentage of the patients require hospitalization and specialized attention in Intensive Care Units (ICUs). [9] [10] [11] [12] Many severe cases occur in healthy young adults, an age group rarely seriously affected by seasonal influenza. [9] [10] [11] [12, 13] [14] While pregnancy and metabolic conditions (including obesity and diabetes) have been identified as risk factors for severe nvH1N1 disease, 40-50% of fatal cases have no documented underlying medical condition. [11] [12] [14] The new virus causes more severe pathological lesions in the lungs of infected mice, ferrets and non-human primates than seasonal human H1N1 virus [15]. The role of host immune responses in clearance of nvH1N1 or the role, if any, of host immune responses in contributing to severe respiratory pathogenesis of nvH1N1 infections is not known at this time. We have previously identified specific host immune response chemokine and cytokine signatures in severe and mild SARS CoV, H5N1 and Respiratory Syncytial Virus infections. In these studies, early host immune responses are characterized by the expression of systemic levels of chemokines, such as CXCL10, indicative of innate anti viral responses [16-18] [19]. Severe and mild SARS and RSV illness could further be defined by chemokine and cytokine signatures involved in the development of adaptive immunity.