NDLI: COMMD1/Murr1 Reinforces HIV-1 Latent Infection through IκB-α Stabilization

Content Provider	PubMed Central
Author	Taura, Manabu Kudo, Eriko Kariya, Ryusho Goto, Hiroki Matsuda, Kouki Hattori, Shinichiro Vaeteewoottacharn, Kulthida Mcdonald, Fiona Ann, Suico Mary Shuto, Tsuyoshi Kai, Hirofumi Okada, Seiji
Editor	Kirchhoff, F.
Copyright Year	2015
Abstract	The transcription factor NF-κB is important for HIV-1 transcription initiation in primary HIV-1 infection and reactivation in latently HIV-1-infected cells. However, comparative analysis of the regulation and function of NF-κB in latently HIV-1-infected cells has not been done. Here we show that the expression of IκB-α, an endogenous inhibitor of NF-κB, is enhanced by latent HIV-1 infection via induction of the host-derived factor COMMD1/Murr1 in myeloid cells but not in lymphoid cells by using four sets of latently HIV-1-infected cells and the respective parental cells. IκB-α protein was stabilized by COMMD1, which attenuated NF-κB signaling during Toll-like receptor ligand and tumor necrosis factor alpha treatment and enhanced HIV-1 latency in latently HIV-1-infected cells. Activation of the phosphoinositol 3-kinase (PI3K)–JAK pathway is involved in COMMD1 induction in latently HIV-1-infected cells. Our findings indicate that COMMD1 induction is the NF-κB inhibition mechanism in latently HIV-1-infected cells that contributes to innate immune deficiency and reinforces HIV-1 latency. Thus, COMMD1 might be a double-edged sword that is beneficial in primary infection but not beneficial in latent infection when HIV-1 eradication is considered.
Related Links	http://dx.doi.org/10.1128/jvi.03105-14
Ending Page	2658
Page Count	16
Starting Page	2643
File Format	PDF
ISSN	0022538X
e-ISSN	10985514
Journal	Journal of Virology
Issue Number	5
Volume Number	89
Language	English
Publisher	American Society for Microbiology
Publisher Date	2015-03-01
Access Restriction	Open
Rights Holder	American Society for Microbiology
Subject Keyword	Immunology Virology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Virology Immunology Microbiology Insect Science

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