tetano
Editor, Senior Moderator
Viruses. 2016 Feb 2;8(2). pii: E33. doi: 10.3390/v8020033.
[h=1]Pandemic Influenza A (H1N1) Virus Infection Increases Apoptosis and HIV-1 Replication in HIV-1 Infected Jurkat Cells.[/h] Wang X[SUP]1[/SUP], Tan J[SUP]2[/SUP], Biswas S[SUP]3[/SUP], Zhao J[SUP]4[/SUP], Devadas K[SUP]5[/SUP], Ye Z[SUP]6[/SUP], Hewlett I[SUP]7[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Influenza virus infection has a significant impact on public health, since it is a major cause of morbidity and mortality. It is not well-known whether influenza virus infection affects cell death and human immunodeficiency virus (HIV)-1 replication in HIV-1-infected patients. Using a lymphoma cell line, Jurkat, we examined the in vitro effects of pandemic influenza A (H1N1) virus (pH1N1) infection on cell death and HIV-1 RNA production in infected cells. We found that pH1N1 infection increased apoptotic cell death through Fas and Bax-mediated pathways in HIV-1-infected Jurkat cells. Infection with pH1N1 virus could promote HIV-1 RNA production by activating host transcription factors including nuclear factor kappa-light-chain-enhancer of activated B cells (NF-ĸB), nuclear factor of activated T-cells (NFAT) and activator protein 1 (AP-1) through mitogen-activated protein kinases (MAPK) pathways and T-cell antigen receptor (TCR)-related pathways. The replication of HIV-1 latent infection could be reactivated by pH1N1 infection through TCR and apoptotic pathways. These data indicate that HIV-1 replication can be activated by pH1N1 virus in HIV-1-infected cells resulting in induction of cell death through apoptotic pathways.
[h=4]KEYWORDS:[/h] CD4; HIV-1; apoptosis; pandemic influenza A (H1N1) virus; replication
PMID: 26848681 [PubMed - in process] Free full text
[h=1]Pandemic Influenza A (H1N1) Virus Infection Increases Apoptosis and HIV-1 Replication in HIV-1 Infected Jurkat Cells.[/h] Wang X[SUP]1[/SUP], Tan J[SUP]2[/SUP], Biswas S[SUP]3[/SUP], Zhao J[SUP]4[/SUP], Devadas K[SUP]5[/SUP], Ye Z[SUP]6[/SUP], Hewlett I[SUP]7[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Influenza virus infection has a significant impact on public health, since it is a major cause of morbidity and mortality. It is not well-known whether influenza virus infection affects cell death and human immunodeficiency virus (HIV)-1 replication in HIV-1-infected patients. Using a lymphoma cell line, Jurkat, we examined the in vitro effects of pandemic influenza A (H1N1) virus (pH1N1) infection on cell death and HIV-1 RNA production in infected cells. We found that pH1N1 infection increased apoptotic cell death through Fas and Bax-mediated pathways in HIV-1-infected Jurkat cells. Infection with pH1N1 virus could promote HIV-1 RNA production by activating host transcription factors including nuclear factor kappa-light-chain-enhancer of activated B cells (NF-ĸB), nuclear factor of activated T-cells (NFAT) and activator protein 1 (AP-1) through mitogen-activated protein kinases (MAPK) pathways and T-cell antigen receptor (TCR)-related pathways. The replication of HIV-1 latent infection could be reactivated by pH1N1 infection through TCR and apoptotic pathways. These data indicate that HIV-1 replication can be activated by pH1N1 virus in HIV-1-infected cells resulting in induction of cell death through apoptotic pathways.
[h=4]KEYWORDS:[/h] CD4; HIV-1; apoptosis; pandemic influenza A (H1N1) virus; replication
PMID: 26848681 [PubMed - in process] Free full text