Viral contaminations are a serious threat for animal cell cultures and may lead to false results in research, development, and virus screening, to viral contaminations in the biologicals derived from the contaminated cultures and finally to an infection of the treated patient. Fortunately due to rigorous testing of the animals used as the source of explants, the production of ascites or the passage of cells, of raw materials, of the cell strains and cell lines in use, and finally of bulk and the final product can prevent potentially dangerous viral contaminations. Existing data demonstrate that contamination of cells and harvests by viruses can occur for products of biotechnology, and while the frequency may be low it is not zero. For instance, routine testing of cell lines of biotech interest revealed a contamination frequency with adventitious viruses of less than 1% (Moore, 1992) . However, the possibility of new emerging viruses and the permanently existing risk of contaminations by adventitious agents and viruses leads to the conclusion that the user of animal cells as well as the producer of biotech products by using animal cells have to be attentive to this possible threat and that they have to assure the absence of adventitious agents/viruses by any mean. Only then, animal cell technology biotech products can be used for the benefit of everyone. DENV Inhibits Type I IFN Production in Infected Cells by Cleaving Human STING Dengue virus (DENV) is a pathogen with a high impact on human health. It replicates in a wide range of cells involved in the immune response. To efficiently infect humans, DENV must evade or inhibit fundamental elements of the innate immune system, namely the type I interferon response. DENV circumvents the host immune response by expressing proteins that antagonize the cellular innate immunity. We have recently documented the inhibition of type I IFN production by the proteolytic activity of DENV NS2B3 protease complex in human monocyte derived dendritic cells (MDDCs). In the present report we identify the human adaptor molecule STING as a target of the NS2B3 protease complex. We characterize the mechanism of inhibition of type I IFN production in primary human MDDCs by this viral factor. Using different human and mouse primary cells lacking STING, we show enhanced DENV replication. Conversely, mutated versions of STING that cannot be cleaved by the DENV NS2B3 protease induced higher levels of type I IFN after infection with DENV. Additionally, we show that DENV NS2B3 is not able to degrade the mouse version of STING, a phenomenon that severely restricts the replication of DENV in mouse cells, suggesting that STING plays a key role in the inhibition of DENV infection and spread in mice. Viral infections have a vast impact on human health, resulting in hundreds of thousands of deaths yearly. To replicate and spread, these intracellular pathogens subvert the host cellular defense machinery. Dengue virus (DENV) is the most prevalent arbovirus in humans, and productively infects cells that are involved in the immune response, such as monocytes, B cells, macrophages and dendritic cells (DCs) among others [1, 2, 3, 4, 5] . Like most viruses, DENV has evolved in order to inhibit or evade different aspects of the innate immune system, the first line of human defense against microbes. DCs are antigen presenting cells (APCs) and some of the first cells that interact with the virus after the bite of an infected mosquito. Infection of these cells induces their activation, which results in their migration to the lymph nodes where the virus can infect other susceptible cells. The kinetics of infection of different cells in the immune system is not well documented, due to the lack of immune-competent mouse models for dengue disease. Nevertheless, in mice defective for type I IFN signaling, one of the most accepted current models for dengue disease, it has been shown that DCs and macrophages are productively infected by DENV [3, 4, 5, 6] reviewed in [7] .