Key result
The Adenovirus Group C RID complex inhibits TNF-induced activation of NF-kB and AP-1 by downregulating surface levels of TNF receptor 1.
The adenovirus RID complex evades host immune responses by downregulating surface TNFR1, thereby inhibiting TNF-induced NF-kappaB and AP-1 signaling.
Provides mechanistic insight into adenovirus TNF evasion; leaves open relevance to human antiviral strategies.
Adenoviruses employ multiple genes to inhibit the host antiviral responses. There is increasing evidence that these immunoregulatory genes may function either during lytic or latent infection. Adenovirus early transcription region 3 (E3) encodes at least seven proteins, five of which block the acquired or innate immune response. Previous findings from this laboratory demonstrated that the E3 proteins 10.4K and 14.5K, which form a complex in the plasma membrane, inhibit tumor necrosis factor (TNF)-induced activation of NF-kappaB and the synthesis of chemokines. To determine the mechanism of inhibition of these pathways by the adenovirus E3 10.4K/14.5K proteins, we have examined the effects of this viral complex on the inhibition of AP-1 and NF-kappaB activation by TNF and found a reduction in assembly of the TNF receptor 1 (TNFR1) signaling complex at the plasma membrane accompanied by downregulation of surface levels of TNFR1.
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Fessler et al. (2004) studied Adenovirus infection / TNF signaling. Adenovirus Group C RID complex (Ad/RID) vs. Ad/null or mock infection was evaluated on Cell surface levels of TNFR1 and activation of NF-kB/AP-1. The Adenovirus Group C RID complex inhibits TNF-induced activation of NF-kB and AP-1 by downregulating surface levels of TNF receptor 1.
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