Mechanisms of interaction between the influenza virus and the infected cell

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Amelia Nieto

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Research summary

Influenza virus employs an unusual RNA transcription mechanism that uses as primers short-capped oligonucleotides scavenged from newly synthesised RNA polymerase II (RNAP II) transcripts; this fact entirely decides its life cycle. It first requires functional coupling between viral and cellular transcription machineries. Second, viral and cell mRNAs contain a 5' cap structure and a 3' polyA tail and are thus structurally equivalent; influenza virus must therefore have developed sophisticated strategies to discriminate and favour translation of its own mRNA.

 

Publications

Falcon A, Rodriguez A, Cuevas MT, Pozo F, Guerra S, García-Barreno B, Martinez-Orellana P, Pérez-Breña P, Montoya M, Melero JM, Pizarro M, Ortín J, Casas I, Nieto A. Characterization in vitro and in vivo of a pandemic H1N1 influenza virus from a fatal case. PLoS One 2013; 8:e53515

Alfonso R, Rodriguez A, Lutz TH, Nieto A. CHD6, a cellular repressor of influenza virus replication is degraded in human alveolar epithelial cells and mice lungs during infection. J Virol 2013; 87:4534-4544

Yángüez E, García-Culebras A, Frau A, Llompart C, Knobeloch KP, Gutierrez-Erlandsson S, García-Sastre S, Esteban M, Nieto A, Guerra S. ISG15 regulates peritoneal macrophages functionality against viral infection. PloS Pathogen 2013; 9:e1003632

Llompart C, Nieto C, Rodríguez-Frandsen A. Specific residues of PB2 and PA influenza virus polymerase subunits confer the ability for RNA polymerase II degradation and virus pathogenicity in mice. J Virol 2014; 88:3455-3463

Pérez-González A, Pazo A, Navajas R, Ciordia S, Rodríguez-Frandsen A Nieto A. hCLE/C14orf166 associates with DDX1-HSPC117-FAM98B in a novel transcription-dependent shuttling RNA-transporting complex. PLoS One 2014; 9:e90957

 

Influenza virus polymerase establishes productive interactions with host-cell factors, including components of the cellular transcription and translation apparatus. We study the role of host factors that modulate both positive and negatively influenza virus replication and characterize the endogenous functions of these factors. hCLE and CHD6 are some of these viral polymerase-interacting proteins. hCLE, a shuttling protein that associates with common interacting proteins in the nucleus and the cytosol, is a positive modulator of influenza virus replication. Its nuclear import requires active transcription, which suggests a prominent role in nuclear and cytoplasmic RNA function. The chromatin remodeller CHD6 is a negative modulator of influenza virus replication that controls cell proliferation by promoting DNA synthesis.

Viral pathogenicity mediated by influenza virus polymerase has also been studied. We associated individual changes in PA and PB2 polymerase subunits with increased pathogenicity in a mouse model. In addition, a human influenza virus isolated from a fatal case showed individual changes in PA and PB2 polymerase subunits, which supports the role of viral polymerase as a pathogenicity factor. We also studied the role of human host factors, which might increase the fatality rate in influenza infection and could constitute high risk factors. The CCR5 chemokine receptor has a crucial role in this process; its loss of function increases the fatality rate several-fold. CCR5 deletion or loss of function is thus a high risk factor in man.

 

Figure1ANieto

Figure2ANieto

 

grupoAmeliaNieto

 

Name
Position
Contact
Amelia Nieto Principal investigator
Ana Falcón Postdoctoral scientists
Laura Marcos-Villar Postdoctoral scientists
Paloma Rodríguez Predoctoral scientist
Alejandra Pazo Predoctoral scientist
Noelia Zamarreño Technician

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