Global transcriptome analysis of H5N1 influenza virus-infected human cells

Abstract

BackgroundInfluenza A virus (IAV) belongs to the Orthomyxoviridae family. IAV causes a highly contagious respiratory disease in humans that exacts severe economic losses globally. The virus uses strategies developed to exploit and subvert cellular proteins and pathways to increase its own replication and to inhibit antiviral immune response.ResultsA/bar-headed goose/Qinghai/1/2005 (A/QH) was able to infect A549 and 293 T cells, with a high infection rate for A549 cells. To identify host cellular responses of human cells to influenza infection, differentially expressed genes (DEGs) between AIV-infected groups and uninfected controls were identified using RNA-sequencing. The DEGs were annotated by Gene Ontology and the Kyoto Encyclopedia of Genes and Genomes pathway analyses, which revealed that the DEGs were mainly linked to cellular function and metabolic processes, while the cellular function that is probably associated with host cellular response of human cells, including defense response to virus and protein modification. All the DEGs and pathways were possibly involved in the response to IAV invasion.ConclusionsThe global transcriptome analysis results revealed that sensitive genes and pathways of the cells were infected with the influenza virus and provided further evidence to investigate the complicated relationship between IAV and host cells.Electronic supplementary materialThe online version of this article (10.1186/s41065-019-0085-9) contains supplementary material, which is available to authorized users.

Robust induction of interferon and interferon-stimulated gene expression by influenza B/Yamagata lineage virus infection of A549 cells

“…The cells were proliferated on glass coverslips, infected with B-SH (MOI = 0.1) until a monolayer of cells spread to > 80% of the bottom of the culture glass coverslips, incubated for 1 h, and then the inoculum was displaced with DMEM for continued incubation at 37˚C, 5% CO 2 . Cells were collected at 0, 4, 8, and 12 h, and the specific steps of immunofluorescence assay, as described by Jing et al [7] and Cao et al [15].…”

“…In our previous reports, migratory birds could also carry and spread H5N1 A/QH virus, which is likely the reasons for human infections throughout China and Europe over the past several years. We tried to analyze and compare the common genes regulated by IAV and IBV infection in A549 cells, and we found that there were very few common genes, so the infection processes of these two viruses differ [15,[49][50][51]. Compared to B/Victoria, there were differences between the two strains, and individual specific strains can reflect idiosyncratic specific effects.…”

“…Existing studies describe the production of host cytokines, including IFNs, IFN-stimulated genes (ISGs), and proinflammatory cytokines against influenza virus infection, as integral parts of the process of the cellular antiviral response [10][11][12][13]. We have also reported that type I IFNs, ISGs, and proinflammatory cytokines can be induced by IBV virions at the early stage of virus infection [7,14].The interaction between influenza virus infection and the host anti-viral response has been investigated in depth [15,16], and the regulatory mechanism of IBV infection is also under investigation. Previous research has already shown that IBV ribonucleoprotein rapidly activates TLR signaling pathways [14].…”

“…The interaction between influenza virus infection and the host anti-viral response has been investigated in depth [15,16], and the regulatory mechanism of IBV infection is also under investigation. Previous research has already shown that IBV ribonucleoprotein rapidly activates TLR signaling pathways [14].…”

Expansion of Single Cell Transcriptomics Data of SARS-CoV Infection in Human Bronchial Epithelial Cells to COVID-19

“…Previously, transcriptome analyses of host-pathogen interactions were conducted on the viral infections including herpesvirus [ 11 ], cytomegalovirus [ 12 , 13 ], influenza virus [ 14 ], human respiratory syncytial virus [ 15 ], measles virus [ 16 ], rubella virus [ 17 ], dengue virus [ 18 ], rabies virus [ 17 ], ebolavirus [ 19 , 20 ], and human immunodeficiency virus (HIV) [ 21 ]. Moreover, studding the transcriptome of Calu-3 cell line (human lung cancer cell line) after infection with severe acute respiratory syndrome coronavirus (SARS-CoV) revealed that recognition receptors and the interleukin 17 (IL-17) pathway were activated [ 22 ].…”