Table S1 Associations of polymorphisms involved in the phagocyte-immune related response against Aspergil-lus. 1 Models adjusted for age, gender, hematological malignancy, HSCT, neutropenia (defined as absolute neutrophil count ,500 cells/mm3 for a period of more than 10 days), GVHD and corticoid therapy use (.0.3 mg/Kg/day). { Assuming a recessive model of inheritance. Abbreviations: OR, odds ratio; CI, confidence interval. Differences in samples numbers are due to failures in genotyping. (DOC)  Lethal Nipah Virus Infection Induces Rapid Overexpression of CXCL10 Nipah virus (NiV) is a recently emerged zoonotic Paramyxovirus that causes regular outbreaks in East Asia with mortality rate exceeding 75%. Major cellular targets of NiV infection are endothelial cells and neurons. To better understand virus-host interaction, we analyzed the transcriptome profile of NiV infection in primary human umbilical vein endothelial cells. We further assessed some of the obtained results by in vitro and in vivo methods in a hamster model and in brain samples from NiV-infected patients. We found that NiV infection strongly induces genes involved in interferon response in endothelial cells. Among the top ten upregulated genes, we identified the chemokine CXCL10 (interferon-induced protein 10, IP-10), an important chemoattractant involved in the generation of inflammatory immune response and neurotoxicity. In NiV-infected hamsters, which develop pathology similar to what is seen in humans, expression of CXCL10 mRNA was induced in different organs with kinetics that followed NiV replication. Finally, we showed intense staining for CXCL10 in the brain of patients who succumbed to lethal NiV infection during the outbreak in Malaysia, confirming induction of this chemokine in fatal human infections. This study sheds new light on NiV pathogenesis, indicating the role of CXCL10 during the course of infection and suggests that this chemokine may serve as a potential new marker for lethal NiV encephalitis. Nipah virus (NiV) is a recently emerged zoonotic pathogen of the family Paramyxoviridae that is distinguished by its ability to cause fatal disease in both animals and humans. NiV along with Hendra virus (HeV) comprise the new genus Henipavirus (reviewed in [1] ). NiV was first identified during an outbreak of severe encephalitis in Malaysia and Singapore in 1998-99, with pigs serving as the intermediate amplifying host [2] . Since 1998 NiV has caused regular outbreaks, primarily in Bangladesh and India, with the most recent occurrences at the beginning of 2011 [3] . In the majority of subsequent spillover events, the mortality rate among humans has been higher (,75%) along with evidence of multiple rounds of person-to-person transmission [4, 5, 6] .