Adolfo Garcı́a-Sastre

ORCID: 0000-0002-6551-1827
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About
Contact & Profiles
Research Areas
  • Influenza Virus Research Studies
  • interferon and immune responses
  • Respiratory viral infections research
  • SARS-CoV-2 and COVID-19 Research
  • Immune Response and Inflammation
  • Viral Infections and Vectors
  • Immune Cell Function and Interaction
  • Animal Virus Infections Studies
  • COVID-19 Clinical Research Studies
  • Virology and Viral Diseases
  • Animal Disease Management and Epidemiology
  • Viral gastroenteritis research and epidemiology
  • Virus-based gene therapy research
  • Immunotherapy and Immune Responses
  • vaccines and immunoinformatics approaches
  • Mosquito-borne diseases and control
  • Viral Infections and Immunology Research
  • RNA and protein synthesis mechanisms
  • Cytokine Signaling Pathways and Interactions
  • Viral Infections and Outbreaks Research
  • HIV Research and Treatment
  • RNA Research and Splicing
  • SARS-CoV-2 detection and testing
  • RNA modifications and cancer
  • Monoclonal and Polyclonal Antibodies Research

Icahn School of Medicine at Mount Sinai
2016-2025

Tisch Cancer Institute
2019-2024

Tisch Hospital
2019-2024

Johnson & Johnson (Israel)
2024

Mount Sinai Hospital
2021-2024

Rensselaer Polytechnic Institute
2024

Synairgen (United Kingdom)
2024

Cancer Institute (WIA)
2019-2023

Mount Sinai Health System
2020-2023

Quantitative BioSciences
2021-2023

The pandemic influenza virus of 1918-1919 killed an estimated 20 to 50 million people worldwide. With the recent availability complete 1918 coding sequence, we used reverse genetics generate bearing all eight gene segments study properties associated with its extraordinary virulence. In stark contrast contemporary human H1N1 viruses, had ability replicate in absence trypsin, caused death mice and embryonated chicken eggs, displayed a high-growth phenotype bronchial epithelial cells....

10.1126/science.1119392 article EN Science 2005-10-06

ABSTRACT Alpha/beta interferon immune defenses are essential for resistance to viruses and can be triggered through the actions of cytoplasmic helicases retinoic acid-inducible gene I (RIG-I) melanoma differentiation-associated 5 (MDA5). Signaling by each is initiated recognition viral products such as RNA occurs downstream interaction with IPS-1 adaptor protein. We directly compared innate signaling requirements representative Flaviviridae , Orthomyxoviridae Paramyxoviridae Reoviridae...

10.1128/jvi.01080-07 article EN Journal of Virology 2007-10-18

The NS1 protein is the only nonstructural encoded by influenza A virus. It has been proposed that performs several regulatory functions during viral replication cycle, including regulation of synthesis, transport, splicing, and translation mRNAs. Through use reverse genetics, a viable transfectant virus (delNS1) which lacks gene generated. Our results indicate an auxiliary (virulence) factor plays crucial role in inhibiting interferon-mediated antiviral responses host.

10.1006/viro.1998.9508 article EN cc-by-nc-nd Virology 1998-12-01

ABSTRACT We have rescued influenza A virus by transfection of 12 plasmids into Vero cells. The eight individual negative-sense genomic viral RNAs were transcribed from containing human RNA polymerase I promoter and hepatitis delta ribozyme sequences. three proteins the nucleoprotein expressed protein expression plasmids. This plasmid-based reverse genetics technique facilitates generation recombinant viruses specific mutations in their genes.

10.1128/jvi.73.11.9679-9682.1999 article EN Journal of Virology 1999-11-01

Dengue virus is a worldwide-distributed mosquito-borne flavivirus with positive strand RNA genome. Its transcribed polyprotein cleaved by host- and virus-encoded peptidases into 10 proteins, some of which are unknown function. Although dengue virus-infected cells seem to be resistant the antiviral action IFN, viral products that mediate this resistance unknown. Therefore, we have analyzed ability proteins antagonize IFN response. We found expression in human A549 nonstructural NS2A, NS4A, or...

10.1073/pnas.2335168100 article EN Proceedings of the National Academy of Sciences 2003-11-11

Fatal human respiratory disease associated with the 1918 pandemic influenza virus and potentially H5N1 viruses is characterized by severe lung pathology, including pulmonary edema extensive inflammatory infiltrate. Here, we quantified cellular immune response to infection in mouse flow cytometry demonstrate that mice infected highly pathogenic (HP) H1N1 exhibit significantly high numbers of macrophages neutrophils lungs compared low (LP) viruses. Mice a recent isolate show considerable...

10.1371/journal.ppat.1000115 article EN cc-by PLoS Pathogens 2008-07-31

The recent emergence of B.1.1.529, the Omicron variant

10.1038/s41586-022-04441-6 article EN cc-by Nature 2022-01-21

ABSTRACT We present a novel mechanism by which viruses may inhibit the alpha/beta interferon (IFN-α/β) cascade. The double-stranded RNA (dsRNA) binding protein NS1 of influenza virus is shown to prevent potent antiviral response inhibiting activation regulatory factor 3 (IRF-3), key regulator IFN-α/β gene expression. IRF-3 and, as consequence, IFN-β mRNA induction are inhibited in wild-type (PR8) virus-infected cells but not infected with an isogenic lacking (delNS1 virus). Furthermore, be...

10.1128/jvi.74.17.7989-7996.2000 article EN Journal of Virology 2000-09-01

The retinoic acid-inducible gene I product (RIG-I) has been identified as a cellular sensor of RNA virus infection resulting in beta interferon (IFN-beta) induction. However, many viruses are known to encode viral products that inhibit IFN-beta production. In the case influenza A virus, nonstructural protein 1 (NS1) prevents induction promoter by inhibiting activation transcription factors, including IRF-3, involved transcriptional activation. inhibitory properties NS1 appear be due at least...

10.1128/jvi.01265-06 article EN Journal of Virology 2006-12-27

The 1918 influenza pandemic was a catastrophic series of virus outbreaks that spread across the globe. Here, we show only modest change in hemagglutinin receptor binding site alters transmissibility this virus. Two amino acid mutations cause switch preference from human α-2,6 to avian α-2,3 sialic resulted incapable respiratory droplet transmission between ferrets but maintained its lethality and replication efficiency upper tract. Furthermore, poor with dual specificity suggests predominant...

10.1126/science.1136212 article EN Science 2007-02-02
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