the RTCA system can provide dynamic monitoring of nearly all of the cells present in the wells without the label molecules. By this means, a wide range of noninvasive, label-free cell-based assays can be performed, such as monitoring of cytotoxicity and cell death, stem cell proliferation, RNA interference, virus-mediated cytopathogenicity, etc.. Here, we report the use of the RTCA system as a tool for quantifying 2009 H1N1 virus-induced CPE in Madin-Darby canine kidney cells in real time. As a proof of concept, this format was used to measure neutralizing antibodies in pre- and post-immune serum from 21 healthy individuals who had received the 2009 H1N1 vaccination; the data were then compared with those obtained by hemagglutination inhibition tests. With the emergence of the 2009 influenza pandemic, development of an effective vaccine became critical for the prevention and clearance of influenza virus infections. To evaluate seasonal or pandemic candidate vaccines, a sensitive, specific, and reproducible serological method is necessary to measure the antibody response elicited with a candidate vaccine against wildtype viruses. In this study, we developed a novel real-time method for measuring virus-induced CPE and evaluating the efficacy of neutralizing antibodies using electronic impedance biosensorbased RTCA technology. The RTCA system is based on integrated microelectronic sensor arrays, is non-invasive, and provides kinetic data regarding the dynamic nature of the cellular response to certain challenges, such as drug treatments, growth factor stimulation, analysis of cytotoxic composite components, and virus-induced cytopathogenesis. In this report, this new assay was used to monitor cytolysis induced by H1N1 viral proliferation. Virus-induced CPE kinetic curves could be used to differentiate between different infectious amounts of the same strain as well as to distinguish the infection kinetics of different H1N1 strains. The two strains, SH37T and SH143T, were isolated respectively from two hospitalized patients in SHAPHC received diagnostic of 2009 H1N1 infection at May 2009. While the clinical patterns were essentially similar, these strains revealed different kinetics of viral infection. The time points for both the onset of CPE and complete cell death of SH143Tinfected cells were delayed about 10 hours compared with those of SH37T-infected cells. Because an identical viral load was used, SH37T appeared to have a greater infectivity than SH143T. Therefore, the RTCA system can provide an indicator of virus capacity of replication and infectivity on MDCK cell culture. It was deserved to utilize complementary genetic approaches to define the role of specific viral genes and proteins underlying the phenotypes.