Jutta Eisemann

TL;DR: DC-SIGN and DC-SIGNR enhance infection mediated by the glycoprotein of Marburg virus and the S protein of severe acute respiratory syndrome coronavirus and might promote viral dissemination.

TL;DR: It is shown that platelets express both the C-type lectin-like receptor 2 (CLEC-2) and low levels of DC-SIGN, indicating that these lectins are required for efficient HIV-1 binding to platelets and providing evidence that platelet-associated virus remains infectious and can escape degradation by platelets.

TL;DR: Results indicate that HSV-1-infected mature DCs are limited in their capacity to migrate to secondary lymphoid organs, the areas of antigen presentation and T-cell stimulation, thus inhibiting an antiviral immune response.

TL;DR: The results indicate that DC-SIGN is not an EBOV receptor but, rather, is an attachmentpromoting factor that boosts entry into B cell lines susceptible to low levels of E BOV GP-mediated infection.

TL;DR: It is shown that HSV-1 blocks IFN-gamma signaling in mDCs, which requires viral gene expression and involves the viral protein vhs.