- 2012: Instructor. Department of Medicine. Harvard Medical School
- 2008: Postdoctoral Research Fellow. Department of Microbiology and Immunobiology. Harvard Medical School
- 2007: Ph.D. Microbiology. University of Barcelona. Spain
- 2005: M.S. Advanced Microbiology and Biotechnology. University of Barcelona. Spain
- 2003: B.S. Biology. University of Barcelona. Spain
The research in my lab is focused on understanding the mechanisms by which Human Immunodeficiency Virus (HIV), and its close relative Simian Immunodeficiency Virus (SIV) circumvent the barriers of the innate immunity in their respective hosts, and cause Acquired Immunodeficiency Syndrome (AIDS). We are particularly interested in the mechanisms by which HIV and SIV overcome restriction by Tetherin/BST2 and BCA2.
Tetherin is an integral membrane protein that traps nascent enveloped virions to the plasma membrane, thereby, impeding their release and spread. Whereas HIV-1 and HIV-2 use Vpu and Env, respectively, as countermeasures against human Tetherin, we have demonstrated that SIV uses the Nef accessory protein to overcome non-human primate Tetherin.
BCA2 (Breast-Cancer Associated gene 2) is a co-factor in the restriction imposed by
Tetherin. By interacting with Tetherin, BCA2 promotes the internalization and degradation
of tethered virions. However, we have recently demonstrated that BCA2 also has Tetherin-independent
antiviral activity. In particular, BCA2 promotes the lysosomal degradation of the
Gag polyproteins of different retroviruses –among them HIV– thus, impairing virus
assembly. Therefore, these observations provide an additional mechanism by which BCA2
would represent a promising factor for antiretroviral therapy against HIV. Our current
research aims at 1) investigating additional mechanisms of HIV restriction by Tetherin
and BCA2; 2) exploring the strategies used by HIV and SIV to circumvent these barriers;
and 3) studying the association between BCA2 and cancer. Therefore, these goals are
directly relevant in the development of novel antiretroviral drugs to enhance the
containment of HIV replication by the innate immunity.
- Nityanandam, R. and Serra-Moreno, R. 2014. BCA2/Rabring7 targets HIV-1 Gag for lysosomal degradation in a tetherin-independent manner. PLoS Pathogens. May 22;10(5):e1004151.
- Serra-Moreno, R*., Zimmermann, K., Stern, L.J., and Evans, D.T. 2013. Tetherin/BST-2 Antagonism by Nef Depends on a Direct Physical Interaction between Nef and Tetherin, and on Clathrin-mediated Endocytosis. PLoS Pathogens. July;9(7):e1003487. *corresponding author
- Serra-Moreno, R., and Evans D.T. 2012. Adaptation of Human and Simian Immunodeficiency Viruses for Resistance to Tetherin/BST-2. Current HIV Research. Jun;10(4):277-82.
- Serra-Moreno, R., Jia, B., Breed, M., Alvarez, X., and Evans, D.T. 2011. Compensatory changes in gp41 restore resistance to tetherin in a pathogenic nef-deleted SIV. Cell Host & Microbe. Jan 20; 9(1): 46-57.
- Evans, D.T., Serra-Moreno, R., Singh, R.K., and Guatelli, J.C. 2010. BST2/Tetherin: a new component of the innate response to enveloped viruses. Trends Microbiol. Sep 18(9): 388-396.
- Jia, B*., Serra-Moreno, R*., Neidermyer, W., Rahmberg, A., Mackey, J., Fofana, I.B., Johnson, W.E., Westmoreland, S., and Evans, D. 2009. Species-specificity Activity of SIV Nef and HIV-1 Vpu in Overcoming Restriction by Tetherin/BST2. PLoS Pathog. May;5(5):e1000429. Epub 2009 May 15. *Both authors collaborated equally in this work.
- Serra-Moreno R., Jofre J. and Muniesa M. 2008. The CI repressors of Shiga toxin-converting prophages are involved in coinfection of Escherichia coli strains, which causes a down regulation in the production of Shiga toxin 2. J Bacteriol. Jul;190(13):4722-35. Epub 2008 May
- Serra-Moreno R., Jofre J. and Muniesa M. 2007. Insertion site occupancy by stx2 bacteriophages depends on the locus availability of the host strain chromosome. J Bacteriol. Sep;189(18):6645-54. Epub 2007 Jul 20.
- Serra-Moreno R., Acosta S., Hernalsteens J.P., Jofre J. and Muniesa M. 2006. Use of the lambda Red recombinase system to produce recombinant prophages carrying antibiotic resistance genes. BMC Mol Biol. Sep 19;7:31