in a recent article for critical care , bermejo - martin and colleagues   describe th1 and th17 hypercytokinemia as an early signature host response to severe infection by the pandemic variant of the influenza virus ( nvh1n1 ) . the nvh1n1 infection is usually self - limiting in nature , but some patients develop severe symptoms requiring hospitalization . the human host immune response to nvh1n1 infection is unknown at this time and studies on its contribution to disease pathogenesis are desperately needed to improve prevention and treatment strategies . by analyzing 29 cytokines and chemokines and the hemagglutination inhibition activity , bermejo - martin and colleagues   assessed the early host innate and adaptive immune responses in patients both mildly and severely infected with nvh1n1 . while infection with nvh1n1 induces a typical innate response in both mild and severe cases , severe infections with respiratory involvement are characterized by an early secretion of th17 and th1 cytokines . thus , hospitalized patients tend to show high systemic levels of mediators that stimulate th17 ( il-8 , il-9 , il-17 , il-6 ) and th1 responses ( ifn- , tnf- , il-15 , il-12p70 ) . based on this finding , this study was able to highlight similarities between the cytokine response to severe h1n1 infection and the pathogenesis of asthma and some autoimmune diseases . the th1 response is primarily involved with host immune defense against intracellular pathogens by activating cellular immunity . indeed , th1 cells produce ifn- and cytokines that are involved in monocyte / macrophage - mediated inflammatory responses . when the th1 response is exhaustively prolonged , it may result in host damage . moreover , other authors have reported that th1-dominated responses may be implicated in the pathogenesis of autoimmune disorders and chronic inflammatory diseases . bermejo - martin and colleagues   found il-15 , il-12p70 , and il-6 to be particularly elevated following severe nvh1n1 infection . the authors   also found a significant inverse relationship of il-6 and il-8 with the pressure of oxygen in arterial blood in severely infected patients . interestingly , previous studies had already reported high levels of specific proinflammatory cytokines and chemokines in severe sars coronavirus , h5n1 and respiratory syncytial virus infections [ 6 - 11 ] . th17 promotes inflammation by inducing various pro - inflammatory cytokines and chemokines , recruiting neutrophils , enhancing antibody production , and activating t cells . th17 cells secrete il-17 , il-17f , and il-22 , thereby inducing a massive tissue reaction . also , these cells secrete il-21 to communicate with the cells of the immune system . in addition , th17 cells have a well - known role in clearing pathogens during infections and inducing tissue inflammation in autoimmune disease . interestingly , the key role of il-17 and its receptor in the immunopathology of influenza infection in a mouse model has just recently been reported . taken together , these findings show that severe pandemic h1n1 infection is characterized by early elevation of key immune pro - inflammatory mediators participating in both th1 and th17 inflammatory responses . this pro - inflammatory response may be the cause of the severe respiratory symptoms caused by nvh1n1 infection . however , the authors also provide an alternative version of the story : th1 and th17 cytokines may reflect a vigorous antiviral host response necessary for viral clearance . this article   is the first that describes an association between severe influenza infection and a th17 response in humans . the researchers correctly bring up the fact that a better understanding of the immune response to the new h1n1 virus could contribute to the design of more effective therapies . similarly , the results of this study reinforce the importance of early treatment with antivirals in those patients with high risk factors , such as pregnancy , asthma , and obesity , among others , to avoid triggering unwanted inflammatory phenomena , which could explain the appearance of pneumonia in these patients . the results of this work also support the study of drugs that modulate the immune response in the treatment of this disease . moreover , the study of genetic polymorphisms of relevant genes involved in the development of th1 and th17 immune responses in severely infected patients could be of interest , since these polymorphisms could strongly influence gene expression . further studies would help to understand the harmful or beneficial roles that these cytokines play in the evolution of mild and severe nvh1n1 infection . but this report confirms that th1 and th17 responses are distinctive hallmarks of severe respiratory compromise following nvh1n1 infection . ifn : interferon gamma ; il : interleukin ; nvh1n1 : new variant of h1n1 influenza virus ; tnf : tumor necrosis factor . this work was supported by grants from instituto de salud carlos iii ( pi08/0738 ; uipy 1467/07 ) to sr . mg - f is supported by a grant of instituto de salud carlos iii ( cm09/00031 ) . mg - a is supported by a grant of instituto de salud carlos iii ( cm08/00101 ) .
the great majority of infections caused by the pandemic variant of the influenza virus ( nvh1n1 ) are self - limited , but a small percentage of patients develop severe symptoms requiring hospitalization . 
 bermejo - martin and colleagues have presented a pilot study describing the differences in the early immune response for patients both mildly and severely infected with nvh1n1 . 
 patients who develop severe symptoms after nvh1n1 infection showed th1 and th17 ' hypercytokinemia ' , compared to mildly infected patients and healthy controls . 
 the mediators involved with the th1 and th17 profiles are known to be involved in antiviral , pro - inflammatory and autoimmune responses . 
 this is the first work reporting the association of a pro - inflamatory immune response with a severe pandemic infection , although it is likely that more studies are needed to understand the detrimental or beneficial roles these cytokines play in the evolution of mild and severe nvh1n1 infection .