The Schindler Lab

@agschindler.bsky.social

Research group @unituebingen.bsky.social. Interested in viral immune modulation and development of broad-spectrum antivirals | Group account

HIV-1 Vpr does more than degrade cellular proteins! Johanna and Carlos dug deeper and found that Vpr activates the transcription factor NFAT to reprogram T cells. Nearly half of Vpr-deregulated genes were NFAT-controlled, and NFAT inhibition eased Vpr-induced G2 arrest and reduced HIV-1 replication.

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Coming back from the 50th anniversary of #cshretro. Johanna presented two of her PhD projects and represented our group in discussions throughout the week. A great opportunity to share research and connect with the international retrovirology community!

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Congratulations to our former student Sophia Kieferle on being awarded the MoBBEL price by the biochemists in Tübingen for her master thesis! She investigated Spike expression and release in primary cells upon BioNTech Corona vaccine treatment. Wishing her continued success!🚀

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📢A real multitasker: in our latest #Review we are summarizing the variety of #HIV-1 Vpr functions in primary CD4+ T cells https://www.mdpi.com/1999-4915/16/3/420

HIV-1 Vpr Functions in Primary CD4+ T Cells

HIV-1 encodes four accesory proteins in addition to its structural and regulatory genes. Uniquely amongst them, Vpr is abundantly present within virions, meaning it is poised to exert various biological effects on the host cell upon delivery. In this way, Vpr contributes towards the establishment of a successful infection, as evidenced by the extent to which HIV-1 depends on this factor to achieve full pathogenicity in vivo. Although HIV infects various cell types in the host organism, CD4+ T cells are preferentially targeted since they are highly permissive towards productive infection, concomitantly bringing about the hallmark immune dysfunction that accompanies HIV-1 spread. The last several decades have seen unprecedented progress in unraveling the activities Vpr possesses in the host cell at the molecular scale, increasingly underscoring the importance of this viral component. Nevertheless, it remains controversial whether some of these advances bear in vivo relevance, since commonly employed cellular models significantly differ from primary T lymphocytes. One prominent example is the “established” ability of Vpr to induce G2 cell cycle arrest, with enigmatic physiological relevance in infected primary T lymphocytes. The objective of this review is to present these discoveries in their biological context to illustrate the mechanisms whereby Vpr supports HIV-1 infection in CD4+ T cells, whilst identifying findings that require validation in physiologically relevant models.

mdpi.com