Abstract:
:We have previously demonstrated that wild-type herpes simplex virus type 1 (HSV-1), as well as nonreplicating UV-inactivated HSV-1, promptly activates the nuclear factor-kappaB (NF-kappaB) in U937 monocytoid cells and that glycoprotein D (gD) of HSV-1 is sufficient by itself to exert a similar effect. We then investigated the signaling pathway used by HSV-1 to initiate NF-kappaB activation and, particularly, whether our observation could be related to the capability of HSV-1-gD to directly stimulate NF-kappaB through its interaction with the herpes virus entry receptor A (HveA). Here we report that: (a) co-cultivation of U937 cells with an adherent cell line expressing wild-type gD on its surface led to increased NF-kappaB activation, while co-cultivation with the same adherent cell line expressing a mutated form of gD, lacking the capability to bind HveA, did not cause the same effect; (b) exposure to UV-inactivated HSV-1 induced the activation of NF-kappaB in HveA-expressing U937 and THP-1 cells, but not in non-HveA-expressing HEp-2 cells; and (c) activation of NF-kappaB in U937 and THP-1 cells exposed to soluble gD was inhibited by an antibody able to interfere with gD-HveA interaction. These results suggest that HSV-1-gD-HveA interaction initiates a signal transduction pathway leading to NF-kappaB activation.
journal_name
Ann N Y Acad Scijournal_title
Annals of the New York Academy of Sciencesauthors
Teresa Sciortino M,Medici MA,Marino-Merlo F,Zaccaria D,Giuffrè M,Venuti A,Grelli S,Mastino Adoi
10.1196/annals.1397.074subject
Has Abstractpub_date
2007-01-01 00:00:00pages
89-96eissn
0077-8923issn
1749-6632pii
1096/1/89journal_volume
1096pub_type
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