Yuwarat MonteeraratSaori SakabeSomying NgamurulertSirawat SrichatraphimukWasana JiamtomKridsada ChaichuenArunee ThitithanyanontParichart PermpikulTaweesak SongsermPilaipan PuthavathanaChairul A. NidomLe Quynh MaiKiyoko Iwatsuki-HorimotoYoshihiro KawaokaPrasert AuewarakulMahidol UniversityInstitute of Medical Science The University of TokyoKasetsart UniversityAirlannga UniversityNational Institute of Hygiene and Epidemiology HanoiUniversity of Wisconsin Madison, School of Veterinary MedicineJapan Science and Technology Agency2018-09-242018-09-242010-06-09Archives of Virology. Vol.155, No.8 (2010), 1273-1279030486082-s2.0-77955174869https://repository.li.mahidol.ac.th/handle/123456789/29218The highly pathogenic avian influenza virus H5N1 is known to induce high level of tumor necrosis factor α (TNF-α) from primary macrophages. However, it is still unclear whether current H5N1 strains also induce high TNF-α production, as most of the data were derived from extinct clade 0 H5N1 strain. Here, we show that current clade 1 and 2 H5N1 strains induce variable levels of TNF-α that are not necessarily higher than those induced by seasonal influenza viruses. The result suggests that hyper-induction of TNF-α in human macrophages is not always associated with a highly pathogenic phenotype. We further tested the contribution of the NS gene segment from H5N1 isolates to TNF-α induction by using reverse genetics. While NS conferred some variation in TNF-α induction when incorporated into an H1N1 virus genetic background, it did not affect TNF-α induction in an H5N1 virus genetic background, suggesting that other viral genes are involved. © 2010 Springer-Verlag.Mahidol UniversityImmunology and MicrobiologyArticleSCOPUS10.1007/s00705-010-0716-y