Autoimmunity
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The immune mechanisms underlying the pathogenesis of severe pneumonia associated with the A/H1N1 virus are not well known. The objective of this study was to determine whether severe A/H1N1-associated pneumonia can be explained by the emergence of particular T-cell subsets and the cytokines/chemokines they produced, as well as distinct responses to infection. T-cell subset distribution and cytokine/chemokine levels in peripheral blood and bronchoalveolar lavage (BAL) were determined in patients with severe A/H1N1 infection, asymptomatic household contacts, and healthy controls. ⋯ Several inflammatory mediators are up-regulated in peripheral and lung samples from A/H1N1-infected patients who developed severe pneumonia. In addition, the A/H1N1 strain induces higher levels of pro-inflammatory cytokines and chemokines than the seasonal H1N1 strain. These findings suggest that it is possible to identify biomarkers of severe pneumonia and also suggest the therapeutic use of immunomodulatory drugs in patients with severe pneumonia associated with A/H1N1 infection.
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Review
The impact of genetic variability on liver disease in the Hispanic/Latin-American population.
Liver cirrhosis is within the top 10 causes of death in Latin-American countries and recent evidence suggests that Hispanics in the USA have a more aggressive course of many types of liver disease and show lower response to treatment of hepatitis C compared with other ethnic groups. Although environmental factors are very important, they do not appear to fully account for the observed ethnic differences in the incidence of cirrhosis and progression rates. Genome-wide association studies have been a powerful tool to identify genetic variants that directly confer susceptibility to liver disease. Here, we review the current knowledge on genetic variants associated with the most common types of liver disease that may contribute to ancestry-related differences in disease progression and mortality.