Cultivating diversity and food quality. Proceedings of Diversifood EU Forum, Brussels, 11 April 2018

To tackle this issue, Diversifood team organised a forum with policy makers and stakeholders on the 11th of April 2018, in Brussels. Diversifood’s aim is to share results and key lessons including new approaches for the management of cultivated biodiversity, for plant breeding for sustainable farming systems, and new relationships among actors of food systems. In the afternoon, there was time for discussion, knowledge sharing, collecting feedback and extending current policies to include cultivating diversity and food quality (for FP9, CAP 2020, The outputs of this workshop will feed Diversifood’s final recommendations. The forum was kindly hosted by the European Committee of the Regions (Rue Belliard/Belliardstraat 101, 1040 Brussels)

Sraffa and Leontief Revisited: Mathematical Methods and Models of a Circular Economy

The new book SRAFFA AND LEONTIEF REVISITED: Mathematical methods and models of a circular economy is dedicated to Wassiliy Leontief’s concepts of Input-Output Analysis and to the algebraic properties of Piero Sraffa's seminal models described consequently by matrix algebra and the Perron-Frobenius Theorem. The academic editor Walter de Gruyter-Oldenbourg, has published this monography in January 2020 in English language.Мета роботи – дати інформацію про нову книгу «Повернення до Сраффи та Леонтьєва. Математичні методи і моделі кругової економіки». Ця монографія була видана в січні 2020 англійською мовою німецьким науковим видавництвом Вальтер де Гройтер (Walter de Gruyter-Oldenbourg).Цель работы – дать представление о новой книге «Возвращение к Сраффе и Леонтьеву. Математические методы и модели круговой экономики». Эта монография была издана в январе 2020 на английском языке немецким научным издательством Вальтер де Гройтер (Walter de Gruyter-Oldenbourg)

A Re-Examination of Global Suppression of RNA Interference by HIV-1

The nature of the interaction between replicating HIV-1 and the cellular RNAi pathway has been controversial, but it is clear that it can be complex and multifaceted. It has been proposed that the interaction is bi-directional, whereby cellular silencing pathways can restrict HIV-1 replication, and in turn, HIV-1 can suppress silencing pathways. Overall suppression of RNAi has been suggested to occur via direct binding and inhibition of Dicer by the HIV-1 Tat protein or through sequestration of TRBP, a Dicer co-factor, by the structured TAR element of HIV-1 transcripts. The role of Tat as an inhibitor of Dicer has been questioned and our results support and extend the conclusion that Tat does not inhibit RNAi that is mediated by either exogenous or endogenous miRNAs. Similarly, we find no suppression of silencing pathways in cells with replicating virus, suggesting that viral products such as the TAR RNA elements also do not reduce the efficacy of cellular RNA silencing. However, knockdown of Dicer does allow increased viral replication and this occurs at a post-transcriptional level. These results support the idea that although individual miRNAs can act to restrict HIV-1 replication, the virus does not counter these effects through a global suppression of RNAi synthesis or processing

Molecular control of HIV-1 postintegration latency: implications for the development of new therapeutic strategies

The persistence of HIV-1 latent reservoirs represents a major barrier to virus eradication in infected patients under HAART since interruption of the treatment inevitably leads to a rebound of plasma viremia. Latency establishes early after infection notably (but not only) in resting memory CD4+ T cells and involves numerous host and viral trans-acting proteins, as well as processes such as transcriptional interference, RNA silencing, epigenetic modifications and chromatin organization. In order to eliminate latent reservoirs, new strategies are envisaged and consist of reactivating HIV-1 transcription in latently-infected cells, while maintaining HAART in order to prevent de novo infection. The difficulty lies in the fact that a single residual latently-infected cell can in theory rekindle the infection. Here, we review our current understanding of the molecular mechanisms involved in the establishment and maintenance of HIV-1 latency and in the transcriptional reactivation from latency. We highlight the potential of new therapeutic strategies based on this understanding of latency. Combinations of various compounds used simultaneously allow for the targeting of transcriptional repression at multiple levels and can facilitate the escape from latency and the clearance of viral reservoirs. We describe the current advantages and limitations of immune T-cell activators, inducers of the NF-κB signaling pathway, and inhibitors of deacetylases and histone- and DNA- methyltransferases, used alone or in combinations. While a solution will not be achieved by tomorrow, the battle against HIV-1 latent reservoirs is well- underway

Human cellular restriction factors that target HIV-1 replication

Recent findings have highlighted roles played by innate cellular factors in restricting intracellular viral replication. In this review, we discuss in brief the activities of apolipoprotein B mRNA-editing enzyme 3G (APOBEC3G), bone marrow stromal cell antigen 2 (BST-2), cyclophilin A, tripartite motif protein 5 alpha (Trim5α), and cellular microRNAs as examples of host restriction factors that target HIV-1. We point to countermeasures encoded by HIV-1 for moderating the potency of these cellular restriction functions