HIV-1 and HIV-2 differentially regulate NF-κB activity during the late stages of the replication cycle through BST-2/tetherin antagonism

Dufrasne, F.E.; Dessilly, Géraldine; Lucchetti, Mara; Soumillion, Kate; Ngyuvula, Eleonore; Ruelle, Jean; Tafforeau, Lionel; Sanou, Mahamoudou; Kabamba-Mukadi, Benoît

doi:10.1101/2020.05.11.088385

Cited by 1 publication

(1 citation statement)

References 80 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is also known to reduce cytoplasmic concentration of NF-κB2 (p52)/p100 [83]. Viruses such as HIV-1 and HIV-2 are also known to modulate NF-κB signalling differentially at the late phase of their life cycle [85].…”

Section: Discussionmentioning

confidence: 99%

Modulation of cellular autophagy by genotype 1 hepatitis E virus ORF3 protein

Srivastava

Bhukya

Barman

et al. 2023

Journal of General Virology

View full text Add to dashboard Cite

Hepatitis E virus (HEV) egresses from infected hepatocytes as quasienveloped particles containing open reading frame 3 (ORF3) protein. HEV ORF3 (small phosphoprotein) interacts with host proteins to establish a favourable environment for virus replication. It is a functional viroporin that plays an important role during virus release. Our study provides evidence that pORF3 plays a pivotal role in inducing Beclin1-mediated autophagy that helps HEV-1 replication as well as its exit from cells. The ORF3 interacts with host proteins involved in regulation of transcriptional activity, immune response, cellular and molecular processes, and modulation of autophagy, by interacting with proteins, DAPK1, ATG2B, ATG16L2 and also several histone deacetylases (HDACs). For autophagy induction, the ORF3 utilizes non-canonical NF-κB2 pathway and sequesters p52NF-κB and HDAC2 to upregulate DAPK1 expression, leading to enhanced Beclin1 phosphorylation. By sequestering several HDACs, HEV may prevent histone deacetylation to maintain overall cellular transcription intact to promote cell survival. Our findings highlight a novel crosstalk between cell survival pathways participating in ORF3-mediated autophagy

show abstract

Section: Discussionmentioning

confidence: 99%