Publications by authors named "M T Sanchez-Aparicio"

The result of the multidisciplinary collaboration of researchers from different areas of knowledge to validate a solar radiation model is presented. The MAPsol is a 3D local-scale adaptive solar radiation model that allows us to estimate direct, diffuse, and reflected irradiance for clear sky conditions. The model includes the adaptation of the mesh to complex orography and albedo, and considers the shadows cast by the terrain and buildings.

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Infectious Bursal Disease Virus (IBDV) is the causative agent of an immunosuppressive disease that affects domestic chickens () severely affecting poultry industry worldwide. IBDV infection is characterized by a rapid depletion of the bursal B cell population by apoptosis and the atrophy of this chief lymphoid organ. Previous results from our laboratory have shown that exposure of infected cells to type I IFN leads to an exacerbated apoptosis, indicating an important role of IFN in IBDV pathogenesis.

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We have previously described polyglutamine-binding protein 1 (PQBP1) as an adapter required for the cyclic GMP-AMP synthase (cGAS)-mediated innate response to the human immunodeficiency virus 1 (HIV-1) and other lentiviruses. Cytoplasmic HIV-1 DNA is a transient and low-abundance pathogen-associated molecular pattern (PAMP), and the mechanism for its detection and verification is not fully understood. Here, we show a two-factor authentication strategy by the innate surveillance machinery to selectively respond to the low concentration of HIV-1 DNA, while distinguishing these species from extranuclear DNA molecules.

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In this issue of Cell Host & Microbe, Talbot-Cooper et al. highlight how viruses develop strategies that can target universal activators of the innate immune response. The authors unravel a common mechanism between poxviruses and paramyxoviruses to limit the expression of antiviral genes and promote virulence.

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Article Synopsis
  • The fate of influenza A virus (IAV) in host cells is determined by the interplay between the cell's defense systems and the virus's strategies to evade those defenses.
  • A comprehensive analysis combining genetic screens, transcriptomics, and proteomics identified key cell mechanisms, particularly the role of autophagy regulator TBC1D5, in inhibiting IAV replication.
  • The IAV M2 protein impedes TBC1D5's function by disrupting its interaction with Rab7, allowing the virus to avoid degradation and continue its replication and spread.
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