1995
DOI: 10.1099/0022-1317-76-9-2381
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CD4 down-modulation by ganglioside and phorbol ester inhibits human herpesvirus 7 infection

Abstract: Recently, data demonstrating that CD4 is an essential component of the receptor for human herpesvirus 7 (HHV-7) as well as for human immunodeficiency virus have been accumulating. Since gangliosides and phorbol esters are known to induce selective down-modulation of cell surface CD4 expression, it might be expected that treatment with these agents would interfere with HHV-7 infection of CD4 + T cells. The present study, undertaken to verify this possibility, demonstrated that addition of monosialoganglioside-G… Show more

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Cited by 15 publications
(10 citation statements)
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“…CD8 ϩ T cell cross-reactivity in humans has been recently documented between nonhomologous viruses, including influenza A virus with hepatitis C virus (33). While no study documents T cell cross-reactivity between human ␣-herpesviruses (VZV and HSV), human CD4 ϩ T cell cross-reactivity has been detected between human ␤-herpesviruses, namely CMV, HHV-6, and HHV-7, although this is rare (34). In at least one IS subject (patient 1), T cell cross-reactivity seems unlikely, since four CD4 ϩ T cell clones isolated from this subject recognized four different epitopes from four different HSV-2 proteins.…”
Section: Discussionmentioning
confidence: 99%
“…CD8 ϩ T cell cross-reactivity in humans has been recently documented between nonhomologous viruses, including influenza A virus with hepatitis C virus (33). While no study documents T cell cross-reactivity between human ␣-herpesviruses (VZV and HSV), human CD4 ϩ T cell cross-reactivity has been detected between human ␤-herpesviruses, namely CMV, HHV-6, and HHV-7, although this is rare (34). In at least one IS subject (patient 1), T cell cross-reactivity seems unlikely, since four CD4 ϩ T cell clones isolated from this subject recognized four different epitopes from four different HSV-2 proteins.…”
Section: Discussionmentioning
confidence: 99%
“…Therefore, HHV-7 infection is possible in the presence of antibody to HHV-6. It is, however, not clear whether there is some modification of clinical symptoms due to the prior infection, because the cross-reactivity of cellular immunity has also been reported (Yasukawa et al, 1993).…”
Section: Discussionmentioning
confidence: 95%
“…Differences in suppressive effects on colony formation between HHV-6 and HHV-7 might partly be attributed to the difference in the tropism between these viruses [Lusso et al,1991]. Specifically, HHV-7 uses the CD4 molecule as a receptor for the entry to the host cells [Lusso et al, 1994;Yasukawa et al, 1995]. It is likely that the lack of effect of this virus on hematopoietic colony formation is due to the inability of the virus to infect hematopoietic progenitor cells.…”
Section: Discussionmentioning
confidence: 97%