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Review
. 2002 Jul;70(7):3311-7.
doi: 10.1128/IAI.70.7.3311-3317.2002.

Host-pathogen interactions: subversion and utilization of the NF-kappa B pathway during infection

C M Tato  1 , C A Hunter
Affiliations
Review

Host-pathogen interactions: subversion and utilization of the NF-kappa B pathway during infection

C M Tato et al. Infect Immun. 2002 Jul.
No abstract available

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Figures

FIG. 1.
FIG. 1.
Pathogen-mediated inhibition of the NF-κB pathway. 1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2, Yersinia Yop proteins interfere with MAP3K and IKKβ to prevent phosphorylation of IκBα and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IκBα; 4, Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IκBα; 5, orthopoxviruses can either dephosphorylate IκBα or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IκB-like molecule to inhibit NF-κB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-κB to DNA; 9, T. gondii prevents nuclear translocation of NF-κB; 10, S. mansoni disrupts NF-κB binding to DNA in the nucleus.
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