Maria João Amorim

Associate Professor

mjamorim@ucp.pt

Maria João Amorim

Associate Professor

Bio

Maria João Amorim

(from September 2022)

Biosketch

MJ Amorim graduated in Biochemistry at the University of Porto. Her work revolved around biochemistry (1998, Univ. Wageningen, NL), coacervation (1998-2000, ESB, Univ. Católica, PT), phase transitions (2000-2001, Nova Univ., PT), before being awarded a PhD in virology (2002-2007, Univ. of Cambridge, UK, mentored by Prof Paul Digard). After three postdocs in Virology and RNA Biology (NIMR in 2006-2007 and Depts. of Biochemistry in 2007-2009 & of Pathology in 2009-2012 at Univ. of Cambridge, UK), MJ Amorim became a group leader in virology at the Instituto Gulbenkian de Ciência in 2012. MJAmorim is, since September 2022, Group Leader and Vice-Director at the Católica Biomedical Research Center and Associated Professor at the Faculty of Medicine of the Universidade Católica Portuguesa.

*Cell Biology of Viral Infection*

The Amorim Lab investigates how viruses replicate inside their hosts and how organisms respond to viral infections with the goal to control viral challenges. Our main interest is to identify key host factors and pathways for viral replication, as well as virulence determinants impacting viral disease and find antiviral strategies to target them. Our recent work supports that targeting the material properties in biomolecular condensates is a feasible novel antiviral approach, meeting a critical need for alternatives to fight viral infection.

Links:

Google Scholar

ORCID

Personal webpage

Publications

Paper

A Metabolite-Based Resistance Mechanism Against Malaria

Maria João Amorim (with Andrés Fernando Muro). 2025. Science

Católica Medical School closed for holidays

Are vacations really a way to take care of ourselves? Or not so much? - Frederico Simões do Couto

Welcome Week 2025

Maria João Amorim

Maria João Amorim

Bio

A Metabolite-Based Resistance Mechanism Against Malaria

Bacteriocin-mediated prevention of secondary pneumococcal pneumonia by a human commensal Streptococcus mitis strain

Comparative study of humoral and cellular immunity against SARS-CoV-2 induced by different COVID-19 vaccine types

Deciphering respiratory viral infections by harnessing organ-on-chip technology to explore the gut-lung axis

Fast and flu-rious: How to prevent and treat emerging influenza A viruses

Fluorescence Loss After Photoactivation (FLAPh)

Functional redundancy in Oxa1-family insertases supports robust membrane insertion of influenza A virus M2 viroporin

Membrane association prevents premature degradation and mitigates inefficient biogenesis of suboptimal membrane proteins

Pre-existing IgG antibodies to HCoVs NL63 and OC43 spike increased during the pandemic and after COVID-19 vaccination

Understanding influenza

Beyond chemicals

Building an adverse outcome pathway network for COVID-19

Influenza A virus hemagglutinin remodels membranes into a vRNP clustering platform

Influenza A virus propagation requires the activation of the unfolded protein response and the accumulation of insoluble protein aggregates

ATG9A regulates the dissociation of recycling endosomes from microtubules to form liquid influenza A virus inclusions

Balance between maternal antiviral response and placental transfer of protection in gestational SARS-CoV-2 infection

CD8+ tissue-resident memory T-cell development depends on infection-matching regulatory T-cell types

Challenges in Imaging Analyses of Biomolecular Condensates in Cells Infected with Influenza A Virus

Defining basic rules for hardening influenza A virus liquid condensates

LP-25

ATG9A regulates dissociation of recycling endosomes from microtubules leading to formation of influenza A virus liquid condensates

Balance between maternal antiviral response and placental transfer of protection in gestational SARS-CoV-2 infection

Clinical Features Related to Severity and Mortality among COVID-19 Patients in a Pre-Vaccine Period in Luanda, Angola

COVID-19 through Adverse Outcome Pathways: Building networks to better understand the disease 3rd CIAO AOP Design Workshop

Gut as an Alternative Entry Route for SARS-CoV-2: Current Evidence and Uncertainties of Productive Enteric Infection in COVID-19

Mechanisms Leading to Gut Dysbiosis in COVID-19: Current Evidence and Uncertainties Based on Adverse Outcome Pathways

PI4P and BLOC-1 remodel endosomal membranes into tubules

PI4P and BLOC-1 remodel endosomal membranes into tubules

Rules for hardening influenza A virus liquid condensates

Saliva molecular testing bypassing RNA extraction is suitable for monitoring and diagnosing SARS-CoV-2 infection in children

Complement Decay-Accelerating Factor is a modulator of influenza A virus lung immunopathology

Enrichment of Zα domains at cytoplasmic stress granules is due to their innate ability to bind nucleic acids

Enrichment of Zα domains at cytoplasmic stress granules is due to their innate ability to bind to nucleic acids

Liquid Biomolecular Condensates and Viral Lifecycles: Review and Perspectives

Secretory IgA and T cells targeting SARS-CoV-2 spike protein are transferred to the breastmilk upon mRNA vaccination

Signatures in SARS-CoV-2 spike protein conferring escape to neutralizing antibodies

Understanding COVID-19 through adverse outcome pathways – 2nd CIAO AOP Design Workshop

Hybrid Gene Origination Creates Human-Virus Chimeric Proteins during Infection

Influenza A Virus Disturbs the Host Cell Protein Homeostasis by Inducing the Accumulation of Insoluble Proteins

A Comprehensive Review on the Interaction Between the Host GTPase Rab11 and Influenza A Virus

Influenza A virus ribonucleoproteins form liquid organelles at endoplasmic reticulum exit sites

Mutation S110L of H1N1 Influenza Virus Hemagglutinin: A Potent Determinant of Attenuation in the Mouse Model

Effects of mutations in the effector domain of influenza A virus NS1 protein

Influenza A Virus Ribonucleoproteins Form Liquid Organelles at Endoplasmic Reticulum Exit Sites

Clustering of Rab11 vesicles in influenza A virus infected cells creates hotspots containing the 8 viral ribonucleoproteins

Influenza A virus NS1 protein promotes efficient nuclear export of unspliced viral M1 mRNA

KIF13A mediates trafficking of influenza Avirus ribonucleoproteins

Using correlative light and electron microscopy to understand influenza A viral assembly

Influenza A virus ribonucleoproteins modulate host recycling by competing with Rab11 effectors

Recycling endosomes and viral infection

Exosome biogenesis, regulation, and function in viral infection

Nucleozin targets cytoplasmic trafficking of viral ribonucleoprotein-Rab11 complexes in influenza A virus infection

A Rab11-and Microtubule-Dependent Mechanism for Cytoplasmic Transport of Influenza A Virus Viral RNA

Global coordination of transcriptional control and mRNA decay during cellular differentiation

Rng3, a member of the UCS family of myosin co-chaperones, associates with myosin heavy chains cotranslationally

Nuclear export of influenza A virus mRNAs requires ongoing RNA polymerase II activity

Influenza A virus and the cell nucleus

Temperature sensitive influenza a virus genome replication results from low thermal stability of polymerase-cRNA complexes

'Genome gating'; polarized intranuclear trafficking of influenza virus RNPs

Increased amounts of the influenza virus nucleoprotein do not promote higher levels of viral genome replication

Lipid raft-dependent targeting of the influenza A virus nucleoprotein to the apical plasma membrane

Microcapsules with Chitosan for Delivering Small Proteins to the Intestine

Microparticles for delivering therapeutic peptides and proteins to the lumen of the small intestine

Microparticles for delivering therapeutic proteins and peptides to the small intestine

Novel structure and redox chemistry of the prosthetic groups of the iron-sulfur flavoprotein sulfide dehydrogenase from Pyrococcus furiosus; evidence for a [2Fe-2S] cluster with Asp(Cys)<inf>3</inf>ligands

Development of microparticles for peptides and proteins bioactive in the GI gut

Amino acids 484 and 494 of SARS-CoV-2 spike are hotspots of immune evasion affecting antibody but not ACE2 binding