Mechanisms of interaction between the influenza virus and the infected cell



Amelia Nieto

Group Leader



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.



Vasilijevic J, Zamarreño N, Oliveros JC, Rodriguez-Frandsen A, Gómez G, Rodriguez G, Pérez-Ruiz M, Rey S, Barba I, Pozo F, Casas I, Nieto A, Falcón A. Reduced accumulation of defective viral genomes contributes to severe outcome in influenza virus infected patients. PLoS Pathog. 2017 Oct 12;13(10):e1006650

Rodriguez P, Pérez-Morgado MI, Gonzalez VM, Martín ME, Nieto A. Inhibition of influenza virus replication bt DNA aptamers targeting a cellular component of translation initiation. Mol Ther Nucl Acids 2016; 5: e308

Marcos-Villar L, Pazo A, Nieto A. Influenza virus and the chromatin: Role of CHD1 chromatin remodeler on virus life cycle. J Virol 2016; 90: 3694-707

Rodríguez A, de Lucas S, Pérez-González A, Pérez-Cidoncha M, Roldan-Gomendio A, Pazo A, Landeras-Bueno S, Marcos-Villar, L Ortín J, Nieto A. hCLE/C14orf166, a cellular protein required for viral replication, is incorporated into influenza virus particles. Sci Rep 2016; 6: 20744

Ver LS, Marcos-Villar L, Landeras-Bueno S, Nieto A, Ortín J. The cellular factor NXP2/MORC3 is a positive regulator for influenza virus multiplication. J Virol 2015; 89:10023-30


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.







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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