Objective <p>The innate immune response of an infected host is an essential defense mechanism to fight influenza virus infections in the respiratory tract. This response is essential to limit virus replication and spread. However, an exacerbated response may cause severe immune-pathologies. Therefore, it is very important to better understand innate immune responses at the level of its molecular networks in the context of viral infections.</p> Data <p>We infected human lung adenocarcinoma (A549) and human monocytic (THP-1) cells with H3N2 influenza virus A virus and performed transcriptome analysis using next generation RNA sequencing at various times post infection. We report raw sequence data and normalized log<sub>2</sub> transformed gene expression values. This data will allow researchers in the field to identify differentially expressed genes and pathways between the two cell types and over times post infection. Furthermore, our data enables comparisons to molecular studies performed in humans and animal models in the context of respiratory viral infections.</p>

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The host response to influenza infections in human lung and macrophages cell lines

  • Carmen Aguilar,
  • Ruth Lydia Olga Lambertz,
  • Mark Heise,
  • Ana Eulalio,
  • Klaus Schughart

摘要

Objective

The innate immune response of an infected host is an essential defense mechanism to fight influenza virus infections in the respiratory tract. This response is essential to limit virus replication and spread. However, an exacerbated response may cause severe immune-pathologies. Therefore, it is very important to better understand innate immune responses at the level of its molecular networks in the context of viral infections.

Data

We infected human lung adenocarcinoma (A549) and human monocytic (THP-1) cells with H3N2 influenza virus A virus and performed transcriptome analysis using next generation RNA sequencing at various times post infection. We report raw sequence data and normalized log2 transformed gene expression values. This data will allow researchers in the field to identify differentially expressed genes and pathways between the two cell types and over times post infection. Furthermore, our data enables comparisons to molecular studies performed in humans and animal models in the context of respiratory viral infections.