Host-Pathogen Interactions

Group Leader

Elsa Anes

PhD (1998) in Pharmacy (Microbiology), Universidade de Lisboa
Post-Doctoral Fellow, EMBL, Heidelberg, Germany
Associate Professor, Microbiology and Immunology, Faculdade de Farmácia, Universidade de Lisboa

The Research


Microbial pathogens have evolved unique ways to interact with their hosts. It is therefore not surprising that pathogens have evolved a large and diverse array of virulence factors well suited to interfere with or stimulate a variety of host-cell responses in order to invade, survive and replicate within their hosts. The understanding of how pathogens interact with their hosts is providing the basis for the development of novel therapeutic approaches as well as a number of very sophisticated tools for probing basic aspects of cellular physiology and immunology. We take a multidisciplinary approach in our studies involving molecular biology, biochemistry, cell biology, immunology and cell imaging. As a result, we are beginning to define not only the molecular details of the host pathogen interactions but also potential targets to be manipulated from the host and the pathogen sides. Furthermore with the tools available the group offers expertise to assess the anti-microbial activity of new compounds targeting namely Mycobacterium tuberculosis (Mtb), HIV, Influenza virus or Helicobacter pylori.


Host-Pathogen Interactions 1

Mtb controls cathepsins and their inhibitors, cystatins, at the level of gene expression in infected macrophages. The pathogen induced an overall downregulation of cathepsins gene expression (green) when compared with the macrophage infection of the non-pathogen M. smegmatis. A) Green GFP Mtb within macrophages (red: actin; blue: nucleus). B) Heatmap of qRT-PCR quantification of mRNA obtained from macrophages 24 h PI. C) M. smegmatis containing phagosomes colocalization with cathepsin H, a lysosomal enzyme upregulated during this mycobacteria infection (B).


Ongoing Projects

Source: FCT Investigator 2015 (IF/00414/2015)
Title: “Dissecting Mycobacterium tuberculosis complex cell wall structure and modifications: contribution to host immune recognition and drug resistance.”
PI: Maria J. Catalão
Period: 2017-2021

Source: ESCMID Research Grant 2018
Title: “Decoding the peptidoglycan patterns associated with b-lactams hypersusceptibility in drug-resistant Mycobacterium tuberculosis”.
PI: Maria J. Catalão
Period: 2018-2020

Source: Gilead GÉNESE Program 2016 edition
Title: Role of the ectosomes in the dissemination of HIV infection in CNS and their contribution to HIV-associated dementia.
PI: José M. Azevedo-Pereira
Period: 2017-2018

Source: Gilead GÉNESE Program 2016 edition
Title: HIV-TRANFERSOME: fusion inhibitor incorporated in transfersomes for transdermal delivery”Source.
PI: Quirina Santos-Costa
Period: 2017-2018

Source: Janssen prize for innovation 2016 edition
Title: Role of cathepsins in Mycobacterium survival within macrophages.
PI: Elsa Anes
Period: 2017-2018

Recent Most Relevant Publications

Pires D, Bernard E, Pombo JP, Carmo N, Fialho C, Gutierrez MG, Bettencourt P and Anes E. Mycobacterium tuberculosis Modulates miR-106b-5p to Control Cathepsin S Expression Resulting in Higher Pathogen Survival and Poor T-Cell Activation. Front Immunol 2017; 8:1819.

Vale FF, Nunes A, Oleastro M, Gomes JP, Sampaio DA, Rocha R, Vítor JM, Engstrand L, Pascoe B, Berthenet E, Sheppard SK, Hitchings MD, Mégraud F, Vadivelu J, Lehours P. Genomic structure and insertion sites of Helicobacter pylori prophages from various geographical origins. Sci Rep 2017; 7:42471.

Pires D, Marques J, Pombo JP, Carmo N, Bettencourt P, Neyrolles O, Lugo-Villarino G and Anes E. Role of Cathepsins in Mycobacterium tuberculosis Survival in Human Macrophages. Sci Rep 2016; 6:32247.

Gíria M, Santos L , Louro J, Rebelo-de-Andrade H. Reverse genetics vaccine seeds for influenza: Proof of concept in the source of PB1 as a determinant factor in virus growth and antigen yield. Virology 2016; 96:21 –27.

Santos-Costa Q, Lopes M, Calado M, Azevedo-Pereira J. HIV-2 interaction with cell coreceptors: aminoacids within the V1/V2 region of viral envelope are determinant for CCR8, CCR5 and CCR4 usage. Retrovirology 2014; 11:99.

Group Members

PhD Students

  • João Louro
  • Marta Calado

Master Students

  • Catarina Fialho
  • Vanessa Monteiro


  • Francisco Olivença
  • Ricardo Calderón
  • Tomás Serra Velez