To investigate whether the results observed with PR/8 can be extended to contemporary human influenza virus infection, we performed a time-course experiment using a H3N2 virus NY/238, a influenza virus rescued by reverse genetics technology based on a swab sample from a patient from New York during the winter of 2005 [23] . Consistent with the results from PR/8 infection, human AM do not support a productive NY/238 infection as verified by no increase in infectious viral particles released from infected culture as measured by plaque assay (data not shown). As shown in Figure 4A , NY/238 infection markedly stimulated CXCL10 mRNA, NY/238 virus also triggered an early increase in the expression of RIG-I and IFNA1 genes and increased mRNA levels of antiviral gene ISG56 and CCL chemokine CCL5. Inoculation with the same amount of UV-inactivated NY/238 virus was able to stimulate an IFNA1 and CXCL10 response. However, the response was smaller than that observed with live virus. Unlike PR/8, NY/238 virus did not induce a significant increase in TLR7 mRNA ( Figure 4A) . At the protein level, NY/238 virus induced a similar response as PR/8 virus in terms of cytokine and IFN production ( Figure 4B ). Consistent with the finding with PR/ 8, viral replication was required for most chemokine and cytokine response and but was not requisite for CXCL10 release.