Clauss Lab

The research lab of Matthias Clauss, PhD, is focused on vascular function and repair, which are involved in many diseases, in particular in those of the cardiopulmonary system. The research program in this lab is concerned with the mechanisms of vascular endothelial cell activation and aims to identify the links between aging, chronic inflammation and infection in blood vessel function and repair. A specific focus is on the regulation of proangiogenic endothelial progenitor cells (ECFC) and anti-angiogenic factors such as EMAP II.

Active Research

NIH funding including 1R01HL154859-02 (Clauss/ Potential Role of Extracellular Vesicles for the Development of HIV Comorbidities/ 1/2020-7/31/2024) 1R01HL152804-02 (MacLean/ Exploratory Research on HIV Contribution to Heart and Lung Comorbidities/ 4/1/2020-2/29/2024)

R21AG074179 (Wang/ The Role of COVID-19 Endothelial Cell Dysfunction and Hypercoagulability in the Development of Post-ICU Cognitive Impairment and Dementia/ 01/01/2022 - 12/31/2023)

  • HIV-1 Infection and Premature Aging

    HIV-1 infection can cause increased risk for cardiovascular and pulmonary diseases. In HIV-1 studies researchers, including in the Clauss lab, have identified an intracellular protein, HIV-Nef, as a likely candidate for cardiovascular and pulmonary disease development, even in the presence of anti-retroviral therapy. Noteworthy, these scientists were the first to demonstrate that HIV-Nef protein (!) levels in extracellular vesicles (EV) from un-treated patients are comparable to levels found in anti-retroviral drug treated patients (In collaboration with Homer L. Twigg III). Interestingly HIV-Nef can induce premature aging in endothelial cells, potentially explaining increased comorbidity risks in people living with HIV. In analogy to the ability of HIV-Nef to induce formation of toxic EVs, we hypothesize that long COVID-19 is caused by EV-associated inflammatory load (EVAIL) as summarized in our review article “Viral Bad News Sent by EVAIL".

  • Targeting the HIV-1 Resevoir

    Based on our published discovery that HIV-Nef protein is persistent in patients on successful antiretroviral therapy (Chelvanambi et al, AJRCMB 2018 and Circ.Res. 2019) we hypothesized that HIV-Nef is both released from and acting on latently HIV-infected cells in tissue reservoirs. Therefore, we are currently exploring therapeutic strategies to eliminate reservoirs of latently infected T cells. In focus of our efforts is pharmacological targeting of HIV-Nef (in collaboration with Thomas Smithgall and Andrew MacLean). We are hopeful that this approach when combined with others can lead to HIV eradication.

  • Pro-Apoptotic EMAP II, a Pulmonary Disease Accelerator

    Research on the pro-apoptotic EMAP II culminated in the development of a humanized EMAP II neutralizing antibody as therapeutic tool for treating pulmonary hypertension, cigarette smoke induced emphysema and Influenza-A-induced lung injury. Sponsored by three awards (DoD, NIH-SBIRphaseII and NIH-STTR; PI Clauss for Allinaire Therapeutics), this neutralizing monoclonal antibody was fully humanized, further affinity purified and tested in pulmonary disease models such as COPD and lung injury. In a new partnership with Chiesi Farmaceutici S.p.A., Allinaire Therapeutics  is currently advancing the humanized therapeutic anti-EMAP II antibody towards IND approval.

  • Premature Aging of Endothelial Stem Cells ECFC

    To understand the role of pro-inflammatory and infectious agents in premature aging of endothelial stem cells like progenitor cells (ECFC). The Clauss Lab team was the first to demonstrate that oxidative stress and cytokines cause premature aging (senescence) in these ECFC (Zhang et al., FASEB Journal 2009) and identified tmTNF as a  protective mechanism against this senescence (Green et al., Circulation Research 2016). 

Research Team Members

Vipin K. Verma (Postdoctoral Research Scientist): Vipin worked before at Vanderbilt University, TN, on proteins and signaling pathways that regulate cardiac injury and heart failure. At the University of Utah he studied cardiac structural and functional remodeling in end-stage heart failure patients, aging, and recovery after LVAD implantation. Currently, his focus is to identify the cargo composition and function of extracellular vesicles in HIV patients after combined antiretroviral therapy with the long term goal to reduced comorbidities in people living with HIV/AIDS. When not saving the world from diseases, Vipin uses cooking and cleaning as meditation.

Moraima E. Noda (PhD student): During her undergraduate studies Moraima worked in a microbiology and biochemistry lab for three years in which she performed protein purification, crystallization, and validation experiments as well as bacterial morphology studies. She became very interested in microbiology and subsequently joined the Clauss lab where she studies why HIV is causing premature aging.

four members of the clauss lab stand together in front of a poster at research conference
From left to right: Sarvesh Chelvanambi (previous PhD student with the Clauss lab, now Center for Interdisciplinary Cardiovascular Sciences, Harvard Medical School and 2022 AHA winner of the Elaine W. Raines Early Career Investigator Award competition), Matthias Clauss (PI), Vipin K. Verma, and Moraima E. Noda at AHA 2022.