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Ignacio Mena

Researcher at Icahn School of Medicine at Mount Sinai

Publications -  65
Citations -  3360

Ignacio Mena is an academic researcher from Icahn School of Medicine at Mount Sinai. The author has contributed to research in topics: Virus & Influenza A virus. The author has an hindex of 24, co-authored 55 publications receiving 2295 citations. Previous affiliations of Ignacio Mena include Spanish National Research Council & Carlos III Health Institute.

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SARS-CoV-2 Omicron virus causes attenuated disease in mice and hamsters

TL;DR: In this paper , the authors evaluated the ability of several B.1.529 isolates to cause infection and disease in immunocompetent and human ACE2 (hACE2)-expressing mice and hamsters.
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Origins of the 2009 H1N1 influenza pandemic in swine in Mexico

TL;DR: It is established that the swine virus responsible for the 2009 A/H1N1 influenza pandemic virus evolved in central Mexico, highlighting how the 2009 pandemic arose from a region not considered a pandemic risk, owing to an expansion of IAV diversity in swine resulting from long-distance live swine trade.
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A novel Zika virus mouse model reveals strain specific differences in virus pathogenesis and host inflammatory immune responses

TL;DR: It is demonstrated that Stat2-/- mice are highly susceptible to ZIKV infection, recapitulate virus spread to the central nervous system (CNS), gonads and other visceral organs, and display neurological symptoms, and this model is established a new murine model that supports ZikaV infection and demonstrates its utility in highlighting intrinsic differences in the inflammatory response induced by different ZikV strains leading to severity of disease.
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Cell Cycle Status Affects Coxsackievirus Replication, Persistence, and Reactivation In Vitro

TL;DR: The generation of a recombinant coxsackievirus B3 expressing the enhanced green fluorescent protein (eGFP) is described, which is used to mark and track infected cells in vitro and suggests that cell cycle status determines the distribution of CVB3 during acute infection and the persistence ofCVB3 in vivo may rely on infection of quiescent cells incapable of supporting viral replication.