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Fig. 1 | Retrovirology

Fig. 1

From: Restriction factors in human retrovirus infections and the unprecedented case of CIITA as link of intrinsic and adaptive immunity against HTLV-1

Fig. 1

Possible mechanisms of CIITA-mediated inhibition of Tax-1-mediated and Tax-2-mediated LTR transactivation. a CIITA-Tax-1 association may impair in various ways Tax-1-mediated proviral transcription. aI In the absence of CIITA, Tax-1 promotes proviral genome transcription by inducing the formation of a multiprotein complex containing CREB, CBP and PCAF on the viral LTR promoter. aII In presence of CIITA, Tax-1 is bound by the MHC class II transactivator, preventing the physical formation and assembling of the multiprotein complex on the viral promoter, resulting in inhibition of LTR transcription. aIII Alternatively, Tax-1 in presence of CIITA can still be recruited on the viral LTR promoter with an assembled multiprotein complex which however is still not functional likely because the binding of Tax-1 to PCAF is inefficient due to steric hinderance generated by the Tax-1-CIITA interaction and/or PCAF-CIITA interaction. b In absence of CIITA, Tax-2 may bind endogenous NF-Y transcription factor but this binding is not sufficient to inhibit activation of HTLV-2 LTR and consequent proviral transcription (bI). In presence of CIITA, the NF-Y-CIITA complex strongly increases the affinity of NF-Y for Tax-2 thus recruiting Tax-2 and displacing it from the HTLV-2 LTR promoter. As a consequence, inhibition of HTLV-2 LTR transcription occurs (bII)

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