Dr. rer. nat. Roland Schwarzer

Curriculum Vitae

At a Glance

Title	Dr. rer. nat.
Name	Roland Schwarzer
Current Position	Group Leader
Institution	Institute for the Research on HIV & AIDS-associated Diseases, University Medicine Essen (UME), Essen, Germany
E-mail	roland.schwarzer@uk-essen.de
ORCID	0000-0002-7497-5180
LinkedIn	linkedin.com/in/roland-schwarzer
h-index	12 (Web of Science, Aug 2025)

Professional Experience

Jan 2021 – present Essen, Germany	Group Leader Institute for the Research on HIV and AIDS-associated Diseases
Jul 2019 – Dec 2020 San Francisco, CA	Scientist Gladstone Center for HIV Cure Research
Jul 2016 – Jul 2019 San Francisco, CA	Postdoctoral Fellow Gladstone Center for HIV Cure Research
Sep 2014 – Mar 2016 Rehovot, Israel	Postdoctoral Fellow Weizmann Institute of Science — Dept. of Biomolecular Sciences
Jan 2014 – Jul 2014 Berlin, Germany	Academic Staff Member Charité — Institute of Virology
Jul 2009 – Dec 2013 Berlin, Germany	Doctoral Candidate Humboldt University — Molecular Biophysics
May 2008 – May 2009 Berlin, Germany	Graduating Student Humboldt University — Molecular Biophysics

Education & Degrees

Jul 2009 – Jun 2013 Berlin, Germany	Dr. rer. nat., Experimental Biophysics Humboldt University
May 2008 – May 2009 Berlin, Germany	Diploma, Biophysics Humboldt University
Oct 2004 – Jul 2009 Berlin, Germany	Undergraduate Studies Humboldt University

Contributions to Science

My research career spans molecular biophysics, virology, and immunology, with a central focus on understanding and targeting the persistence of viral pathogens. Early biophysics work on viral protein–membrane organization set the stage for later studies of host–virus interfaces. I subsequently helped define cellular reservoirs of HIV, advance cure strategies, discover antiviral modalities, and illuminate Orthohantavirus glycoprotein/nucleocapsid dynamics. Together, this work integrates structural biology, cell biology, and translational virology to inform therapeutic strategies against persistent and emerging infections.

HIV Reservoirs in T Cells

We identified cellular phenotypes and microenvironmental axes that bias CD4⁺ T cells toward latency, including hypoxia–CD73/adenosine signaling and chemokine‑driven recruitment. These findings map concrete targets to prevent seeding and to expose latent reservoirs for cure strategies.

The hypoxia‑regulated ectonucleotidase CD73 is a host determinant of HIV latency. Cell Reports (2023)
Sperber HS; Raymond KA; Bouzidi MS; Ma T; Valdebenito S; Eugenin EA; Roan NR; Deeks SG; Winning S; Fandrey J; Schwarzer R; Pillai SK.
Tissue memory CD4⁺ T cells expressing IL‑7Rα (CD127) preferentially support latent HIV‑1 infection. PLoS Pathogens (2020)
Hsiao F; Frouard J; Gramatica A; Xie G; Telwatte S; Lee GQ; Roychoudhury P; Schwarzer R; Luo X; Yukl SA; Lee S; Hoh R; Deeks SG; Jones RB; Cavrois M; Greene WC; Roan NR.
CCL2: a chemokine potentially promoting early seeding of the latent HIV reservoir. mBio (2022)
Packard TA#; Schwarzer R#; Herzig E; Rao D; Luo X; Egedal JH; Hsiao F; Widera M; Hultquist JF; Grimmett ZW; Messer RJ; Krogan NJ; Deeks SG; Roan NR; Dittmer U; Hasenkrug KJ; Greene WC. (# equal contribution)

HIV Cure Approaches

We engineered adaptable effector platforms and explored pharmacologic levers to expose and eliminate latently infected cells. These studies provide translational proof‑of‑concepts for both latency reversal and targeted cell killing.

Reactivation of latent HIV‑1 by the glucocorticoid receptor modulator AZD9567. Journal of Virology (2025)
Fayyaz S; Lotke R; Haußmann I; Petersen M; Müller E; Schwarzer‑Sperber HS; Schwarzer R; Sauter D.
Attacking latent HIV with convertibleCAR‑T cells, a highly adaptable killing platform. Cell (2019)
Herzig E; Kim KC; Packard TA; Vardi N; Schwarzer R; Gramatica A; Deeks SG; Williams SR; Landgraf K; Killeen N; Martin DW; Weinberger LS; Greene WC.

Antivirals & Entry Inhibitors

We discovered and characterized antiviral activities ranging from membrane‑active proteins to small‑molecule entry blockers. This work spans HIV and coronaviruses and highlights tractable paths to broad‑spectrum inhibition.

The bovine seminal plasma protein PDC‑109 possesses pan‑antiviral activity. Viruses (2022)
Sperber HS; Sutter K; Müller K; Müller P; Schwarzer R.
Identification of nitrile‑containing isoquinoline‑related natural product derivatives as coronavirus entry inhibitors in silico and in vitro. Biomedicine & Pharmacotherapy (2024)
Shahhamzehei N; Abdelfatah S; Schwarzer‑Sperber HS; Sutter K; Yücer R; Bringmann G; Schwarzer R; Efferth T.

Viral Life Cycles & Host–Virus Interfaces

Using quantitative imaging and membrane biophysics, we defined how viral proteins traffic, oligomerize, and engage host structures. These insights clarify fusion, assembly, and spread across HIV‑1 and Orthohantaviruses.

The cholesterol‑binding motif of HIV‑1 gp41 regulates lateral sorting and oligomerization. Cell Microbiology (2014)
Schwarzer R; Levental I; Gramatica A; Scolari S; Buschmann V; Veit M; Herrmann A.
Self‑association and subcellular localization of Puumala hantavirus envelope proteins. Scientific Reports (2019)
Sperber HS; Welke RW; Petazzi RA; Bergmann R; Schade M; Shai Y; Chiantia S; Herrmann A; Schwarzer R.
Characterization of hantavirus N protein intracellular dynamics and localization. Viruses (2022)
Welke RW; Sperber HS; Bergmann R; Koikkarah A; Menke L; Sieben C; Krüger DH; Chiantia S; Herrmann A; Schwarzer R.

Activities in the Research System

2025 – 2028	DFG Research Grant, “Host-pathogen interactions in Hantavirus infections: a focus on cytoskeleton crosstalk” (Project number 524028135)
2025	DFG/TWAS Cooperation Visit Grant, “CRISPR activation to study miR‑128‑3p suppression of HIV transcription in Monocyte and T‑Cells”
2024 – 2027	DFG Research Grant, “Exploring hypoxia and purinergic signaling in HIV persistence” (Project number 533483360)

Schwarzer Lab

Mechanisms of Viral Persistence