Abstract:
:Immune activation is a major characteristic of human immunodeficiency virus type 1 (HIV-1) infection and a strong prognostic factor for HIV-1 disease progression. The underlying mechanisms leading to immune activation in viremic HIV-1 infection, however, are not fully understood. Here we show that, following the initiation of highly active antiretroviral therapy, the immediate decline of immune activation is closely associated with the reduction of HIV-1 viremia, which suggests a direct contribution of HIV-1 itself to immune activation. To propose a mechanism, we demonstrate that the single-stranded RNA of HIV-1 encodes multiple uridine-rich Toll-like receptor 7/8 (TLR7/8) ligands that induce strong MyD88-dependent plasmacytoid dendritic cell and monocyte activation, as well as accessory cell-dependent T-cell activation. HIV-1-encoded TLR ligands may, therefore, directly contribute to the immune activation observed during viremic HIV-1 infection. These data provide an initial rationale for inhibiting the TLR pathway to directly reduce the chronic immune activation induced by HIV-1 and the associated immune pathogenesis.
journal_name
J Viroljournal_title
Journal of virologyauthors
Meier A,Alter G,Frahm N,Sidhu H,Li B,Bagchi A,Teigen N,Streeck H,Stellbrink HJ,Hellman J,van Lunzen J,Altfeld Mdoi
10.1128/JVI.00421-07subject
Has Abstractpub_date
2007-08-01 00:00:00pages
8180-91issue
15eissn
0022-538Xissn
1098-5514pii
JVI.00421-07journal_volume
81pub_type
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doi:10.1128/JVI.61.4.1244-1247.1987
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