As CXCL10 is known to have an important immunobiological function in the organism, which received a great deal of attention in recent years, we focused further studies on this chemokine. Thus, we analyzed whether NiV-infection induces production of CXCL10 in vivo, using the hamster animal model, which closely reproduces human infection and induces lethal outcome starting from day 5 p.i. [17] . Hamsters were infected by NiV and sacrificed on a daily basis for analysis of RNA in different organs (Fig. 4) . The baseline expression of CXCL10 was observed in all organs and increased during the course of infection, particularly in brain and kidney. In lung and spleen the level of CXCL10 initially increased, but decreased on the last day that preceded lethal outcome of the infection. The most rapid and highest induction of CXCL10 mRNA expression was observed in the spleen (16 times more than the baseline expression, already 24 h p.i.), which may correlate with the abundance of cells capable of secreting CXCL10 in the spleen (leukocytes, endothelial cells and splenic stromal cells [18] . The highest NiV replication was observed in lungs of infected hamsters. The level of CXCL10 expression significantly correlated to the level of NiV N expression in analysed organs (p,0.001), suggesting that production of this chemokine closely follows the NIV replication.