Table 3 : Interaction between Cellular DUBs and viral oncoproteins.


Cellular DUB Virus   Viral protein   Function References
Cylindroma-tosis tumor suppressor (CYLD) Human papiloma virus- 16/18 (HPV)   E6   Inhibits CYLD-mediated deubiquitination of Iκκ-γ, TRAF2 and    TRAF-6
Activates NFκB signaling cascade.
Ubiquitinates CYLD and targets it for proteasomal degradation under     hypoxia.
[17]
Human T-cell leukemia virus type-1 (HTLV-1)   Tax   Constitutively phosphorylates and inactivates CYLD
Deubiquitinates and inactivates Tax for Iκκ’s activation.
[25]
USP 7/ HAUSP Herpes simplex virus type-1 (HSV-1)   ICP0   Tethers USP7 to the cytoplasm. and promotes TRAF6 and Iκκ-γ    deubiquitination.
Inhibits TLR-induced NFκB and JNK signaling cascade for cytokine     secretion.
[20]
Epstein Barr Virus (EBV)   EBNA1   Recruits USP7 to the Ori P of episomal viral DNA.
USP7 in association with GMPS deubiquitinates the    monoubiquitinated H2B on the FR-controlled promoters and    stimulates transcription.
[21]
Kaposi’s sarcoma associated Herpes virus (KSHV)   vIRF4   Interferes with the p53-MDM-USP7 axis.
Inhibits USP7 by acting as a pseudosubstrate and inhibiting its    catalytic activity.
[22]
USP11 HPV-16   E7   USP11 stabilizes and modulates the activity of E7 involved in cell     transformation. [19]
 
USP15 HPV-16, HPV-18   E6   USP15 deubiquitinates and stabilizes E6 to promote cellular     transformation. [18]

USP20 HTLV-1   Tax   USP20 deubiquitinates K-63 ubiquitinated Tax.
Inhibit Tax-mediated activation of Iκκ-γ.
USP20 also inactivate TRAF-6 (activated by Tax) to attenuate NFκB     signaling pathway.
[20]

A20 EBV   LMP1   LMP1 stimulates A20 activity.
A20 inhibits the LMP1 triggered NFκB signaling pathway.
A20 also reverses the LMP1-mediated K-63 ubiquitination and     activation of IRF7.
[23]

STAMBPL1 HTLV-1   Tax   STAMBPL1 protects Tax by translocating it to the cytoplasm from the     nucleus.
The cytoplasmic Tax interacts with Iκκ-γ to activate Iκκ and     consequently the NFκB pathway.
[24]

Kumar et al.Virology Discovery  2013 1:5DOI : 10.7243/2052-6202-1-5