Human cytomegalovirus stimulates cellular IKK2 activity and requires the enzyme for productive replication.
Human cytomegalovirus (HCMV) exploits the host transcription factor NF-kappaB to enhance its own replication, dissemination, and reactivation from latency. Here we report that HCMV infection activates the upstream IkappaB kinase (IKK) complex and that its catalytic IKK2 subunit is required for HCMV-induced NF-kappaB activation, as well as the replication of different HCMV strains. These results indicate that IKK2 is essential for HCMV replication and emphasize the feasibility of blocking NF-kappaB activation as a way of inhibiting infection.
Department of Public Health and Microbiology, University of Torino, Turin, Italy.
Patrizia
P
Caposio
Michel
M
Dreano
Gianni
G
Garotta
Giorgio
G
Gribaudo
Santo
S
Landolfo
D002460:Cell Line; D003587:Cytomegalovirus / Q000472:pathogenicity* / Q000502:physiology; D005786:Gene Expression Regulation; D006801:Humans; D051550:I-kappa B Kinase; D016328:NF-kappa B / Q000378:metabolism; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism*; D015533:Transcriptional Activation; D014779:Virus Replication
D016328:NF-kappa B; D017346:Protein Serine-Threonine Kinases; C496559:CHUK protein, human; D051550:I-kappa B Kinase; C496560:IKBKB protein, human; C496565:IKBKE protein, human