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Ruth Serra-Moreno, Ph.D.

Contact Information

Phone Numbers

Office: (585) 273-3622

Research Labs

Faculty Appointments


Professional Background

I obtained my Bachelors degree of Science with a major in Biology in 2003 from the University of Barcelona, Spain. I obtained my PhD in Microbiology with suma cum laude and the European doctorate mention in 2007, also at the University of Barcelona. My thesis dissertation was awarded with the Outstanding doctorate award. My graduate studies focused on understanding how viruses infecting bacteria (bacteriophages) affect the pathogenicity of the bacterial strains they infect.

In 2008, I started my post-doctoral studies at Harvard Medical School, where I focused my work on HIV and its ability to circumvent innate immune barriers. In 2012, I successfully competed in an international search for a non-tenured faculty position (Instructor, independent group leader) at Harvard Medical School, when I started my independent research program on HIV and innate immunity. In 2014, I accepted a tenure-track faculty position as an Assistant Professor at Texas Tech University. In September 2020, I accepted a faculty position as an Associate Professor in the Department of Microbiology and Immunology at URMC.

My research program focuses on understanding how HIV and relative lentiviruses as well as coronaviruses hijack cellular faros for their advantage as well as what innate barriers these viruses need to circumvent in order to establish a successful infection


The Serra-Moreno lab studies the mechanisms by which human pathogens such as Human Immunodeficiency Virus (HIV), its close relative Simian Immunodeficiency Virus (SIV), and SARS-CoV-2 (the causative agent of COVID-19) circumvent the barriers of the innate immunity in their respective hosts and cause disease. Current projects in the lab are investigating the interplay between these human pathogens and the cellular factors Tetherin/BST2, SERINC5, BCA2 and autophagy.

Human immunodeficiency virus (HIV) is the causative agent of acquired immunodeficiency syndrome (AIDS), a disease that has caused 36 million deaths. Although current treatments are effective at keeping HIV to undetectable levels, they are unable to eliminate this virus from infected cells. Therefore, there is a critical need to find strategies to eradicate HIV. The research program in the Serra-Moreno lab focuses on understanding how HIV overcomes the innate immune barriers in its target cells to establish a chronic infection, with the goal of using this information to find new avenues for therapeutic intervention.

Coronaviruses have gained much attention recently due to the COVID-19 pandemic, caused by a novel coronavirus, SARS-CoV-2. SARS-CoV-2 shares 80% identity with SARS-CoV, an eradicated virus that emerged in the human population in 2002, after its transmission from bats. Both SARS-CoV and SARS-CoV-2 infect epithelial cells in the gastric and respiratory tract. However, SARS-CoV-2 is much more pathogenic, very stable, with many person-to-person transmissions, which can occur even before individuals exhibit any symptoms. The absence of symptoms during the dissemination phase has significantly complicated the implementation of contingency measures to avoid the global spread of SARS-CoV-2. At this moment, the only measures to prevent the transmission of the virus are social distancing and physical barriers: goggles, face masks and gloves. Therefore, there is a critical need to investigate the infectivity and pathogenicity features of SARS-CoV-2, so we can develop strategies to halt its propagation. Our lab is currently investigating the role of autophagy as a source of double membrane vesicles to create viroplasms, membrane factories for genome replication. We are also investigating the role of the antiviral factors BST2/Tetherin and SERINC5 in the restriction of SARS-CoV-2 as well as the countermeasures this virus has evolved to antagonize these cellular defenses.


Post-doctoral Training & Residency

02/15/2008 - 12/31/2011
Harvard Medical School


Journal Articles

Castro-Gonzalez S, Shi Y, Colomer-Lluch M, Song Y, Mowery K, Almodovar S, Bansal A, Kirchhoff F, Sparrer K, Liang C, Serra-Moreno R. "HIV-1 Nef counteracts autophagy restriction by enhancing the association between BECN1 and its inhibitor BCL2 in a PRKN-dependent manner." Autophagy.. 2020 Feb 25; :1-25. Epub 2020 Feb 25.

Castro-Gonzalez, S.; Shi, Y.; Colomer-Lluch, M.; Song, Y.; Mowery, K.; Almodovar, S.; Bansal, A.; Kirchhoff, F.; Sparrer, K.; Liang, C.; Serra-Moreno, R.;. "HIV-1 Nef counteracts autophagy restriction by enhancing the association between BECN1 and its inhibitor BCL2 in a PRKN-dependent manner" . 2020; : 1-25.

Colomer-Lluch, M.; Castro-Gonzalez, S.; Serra-Moreno, R.;. "Ubiquitination and SUMOylation in HIV Infection: Friends and Foes" . 2020; 35: 159-194.