Large atom number dual-species magneto-optical trap for fermionic 6Li and 40K atoms

We present the design, implementation and characterization of a dual-species magneto-optical trap (MOT) for fermionic 6Li and 40K atoms with large atom numbers. The MOT simultaneously contains 5.2x10^9 6Li-atoms and 8.0x10^9 40K-atoms, which are continuously loaded by a Zeeman slower for 6Li and a 2D-MOT for 40K. The atom sources induce capture rates of 1.2x10^9 6Li-atoms/s and 1.4x10^9 40K-atoms/s. Trap losses due to light-induced interspecies collisions of ~65% were observed and could be minimized to ~10% by using low magnetic field gradients and low light powers in the repumping light of both atomic species. The described system represents the starting point for the production of a large-atom number quantum degenerate Fermi-Fermi mixture

The murine cytomegalovirus M35 protein antagonizes type I IFN induction downstream of pattern recognition receptors by targeting NF-κB mediated transcription.

The herpesvirus cytomegalovirus can cause severe morbidity in immunosuppressed people and poses a much greater global problem in the context of congenital infections than the Zika virus. To establish infection, cytomegalovirus needs to modulate the antiviral immune response of its host. One of the first lines of defense against viral infections is the type I interferon response which is activated by cellular sensors called pattern recognition receptors. These receptors sense viral entry and rapidly induce the transcription of type I interferons, which are instrumental for the induction of an antiviral state in infected and surrounding cells. We have identified the first viral protein encoded by murine cytomegalovirus, the M35 protein, that counteracts type I interferon transcription downstream of multiple pattern recognition receptors. We found that this viral countermeasure occurs shortly after viral entry into the host cell, as M35 is delivered with the viral particle. M35 then localizes to the nucleus where it modulates NF-κB-mediated transcription. In vivo, murine cytomegalovirus deficient of the M35 protein replicates to lower levels in spleen and liver and cannot establish a productive infection in the salivary glands, which is a key site of viral transmission, highlighting the important role of M35 for the establishment of infection. Our study provides novel insights into the complex interaction between cytomegalovirus and the innate immune response of its host