scholarly journals Huntingtin-Interacting Protein 1 Promotes Vpr-Induced G2 Arrest and HIV-1 Infection in Macrophages

Viruses ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 2308
Author(s):  
Tomoyuki Murakami ◽  
Ryosuke Matsuura ◽  
Nopporn Chutiwitoonchai ◽  
Masami Takei ◽  
Yoko Aida

Human immunodeficiency virus type 1 (HIV-1) modulates the host cell cycle. The HIV-1 accessory protein Vpr arrests the cell cycle at the G2 phase in dividing cells, and the ability of Vpr to induce G2 arrest is well conserved among primate lentiviruses. Additionally, Vpr-mediated G2 arrest likely correlates with enhanced HIV-1 infection in monocyte-derived macrophages. Here, we screened small-interfering RNA to reveal candidates that suppress Vpr-induced G2 arrest and identified Huntingtin-interacting protein 1 (HIP1) required for efficient G2 arrest. Interestingly, HIP1 was not essential for Vpr-induced DNA double-strand breaks, which are required for activation of the DNA-damage checkpoint and G2 arrest. Furthermore, HIP1 knockdown suppressed HIV-1 infection in monocyte-derived macrophages. This study identifies HIP1 as a factor promoting Vpr-induced G2 arrest and HIV-1 infection in macrophages.

2020 ◽  
Author(s):  
Tomoyuki Murakami ◽  
Nopporn Chutiwitoonchai ◽  
Masami Takei ◽  
Yoko Aida

Abstract Background: Human immunodeficiency virus type 1 (HIV-1) modulates the host cell cycle. The HIV-1 accessory protein Vpr arrests the cell cycle at G2 phase, which is important for efficient viral replication in dividing CD4+ T cells, because the transcriptional activity of the HIV-1 long terminal repeat is most active in G2 phase. Additionally, Vpr-mediated G2 arrest likely correlates with enhanced HIV-1 infection in monocyte-derived macrophages.Results: Here, we screened small-interfering RNA to reveal candidates that suppress Vpr-induced G2 arrest and identified Huntingtin-interacting protein 1 (HIP1) as both directly interacting with Vpr and required for efficient G2 arrest. Interestingly, HIP1 was not essential for Vpr-induced DNA double-strand breaks, which are required for activation of the DNA-damage checkpoint and G2 arrest. Furthermore, HIP1 knockdown suppressed HIV-1 infection in monocyte-derived macrophages.Conclusions: These results suggest that HIP1 operates in the downstream step(s) of DNA-damage induction to promote Vpr-induced G2 arrest and enhances HIV-1 infection in macrophages.


1998 ◽  
Vol 43 ◽  
pp. 157-157
Author(s):  
Delane Shingadia ◽  
Jian Cao ◽  
Mingzhong Chen ◽  
Chen Wang ◽  
Yuqi Zhao

2000 ◽  
Vol 275 (52) ◽  
pp. 41299-41308 ◽  
Author(s):  
Abigail S. Hackam ◽  
Ayman S. Yassa ◽  
Roshni Singaraja ◽  
Martina Metzler ◽  
Claire-Anne Gutekunst ◽  
...  

2007 ◽  
Vol 67 (18) ◽  
pp. 8923-8931 ◽  
Author(s):  
Sarah V. Bradley ◽  
Mitchell R. Smith ◽  
Teresa S. Hyun ◽  
Peter C. Lucas ◽  
Lina Li ◽  
...  

2008 ◽  
Vol 28 (3) ◽  
pp. 599-609 ◽  
Author(s):  
Justin N. Moores ◽  
Sophie Roy ◽  
Donald W. Nicholson ◽  
Brian E. Staveley

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