Peter Palese

Effects of influenza A virus NS1 protein on protein expression: the NS1 protein enhances translation and is not required for shutoff of host protein synthesis.

Apical budding of a recombinant influenza A virus expressing a hemagglutinin protein with a basolateral localization signal.

New directions in vaccine research.

Influenza vaccines: present and future.

Cellular transcriptional profiling in influenza A virus-infected lung epithelial cells: the role of the nonstructural NS1 protein in the evasion of the host innate defense and its potential contribution to pandemic influenza.

The makings of a killer.

Existing antivirals are effective against influenza viruses with genes from the 1918 pandemic virus.

Functional replacement of the carboxy-terminal two-thirds of the influenza A virus NS1 protein with short heterologous dimerization domains.

Newcastle disease virus (NDV)-based assay demonstrates interferon-antagonist activity for the NDV V protein and the Nipah virus V, W, and C proteins.

Activation of tumor antigen-specific cytotoxic T lymphocytes (CTLs) by human dendritic cells infected with an attenuated influenza A virus expressing a CTL epitope derived from the HER-2/neu proto-oncogene.

The Ebola virus VP35 protein inhibits activation of interferon regulatory factor 3.

Chimeric influenza A viruses with a functional influenza B virus neuraminidase or hemagglutinin.

Newcastle disease virus V protein is a determinant of host range restriction.

Trafficking of viral genomic RNA into and out of the nucleus: influenza, Thogoto and Borna disease viruses.

Induction of protective immunity against malaria by priming-boosting immunization with recombinant cold-adapted influenza and modified vaccinia Ankara viruses expressing a CD8+-T-cell epitope derived from the circumsporozoite protein of Plasmodium yoelii.

Interferon antagonist proteins of influenza and vaccinia viruses are suppressors of RNA silencing.

Structure of the uncleaved human H1 hemagglutinin from the extinct 1918 influenza virus.

Pathogenicity and immunogenicity of influenza viruses with genes from the 1918 pandemic virus.

Nipah virus V and W proteins have a common STAT1-binding domain yet inhibit STAT1 activation from the cytoplasmic and nuclear compartments, respectively.

Induction of cellular immune responses to simian immunodeficiency virus gag by two recombinant negative-strand RNA virus vectors.

Influenza: old and new threats.

An unconventional NLS is critical for the nuclear import of the influenza A virus nucleoprotein and ribonucleoprotein.

A novel paramyxovirus?

Nuclear localization of the Nipah virus W protein allows for inhibition of both virus- and toll-like receptor 3-triggered signaling pathways.

Stimulation of human T cells by an influenza A vector expressing a CTL epitope from the HER-2/neu protooncogene results in higher numbers of antigen-specific TCRhi cells than stimulation with peptide. Divergent roles of IL-2 and IL-15.

Attenuation of equine influenza viruses through truncations of the NS1 protein.

A single amino acid substitution in 1918 influenza virus hemagglutinin changes receptor binding specificity.

Influenza virus PB1-F2 protein induces cell death through mitochondrial ANT3 and VDAC1.

Characterization of the reconstructed 1918 Spanish influenza pandemic virus.

Pathogenicity of influenza viruses with genes from the 1918 pandemic virus: functional roles of alveolar macrophages and neutrophils in limiting virus replication and mortality in mice.

Glycan microarray analysis of the hemagglutinins from modern and pandemic influenza viruses reveals different receptor specificities.

7a protein of severe acute respiratory syndrome coronavirus inhibits cellular protein synthesis and activates p38 mitogen-activated protein kinase.

What can we learn from reconstructing the extinct 1918 pandemic influenza virus?

Making better influenza virus vaccines?

Sequence analysis and receptor specificity of the hemagglutinin of a recent influenza H2N2 virus isolated from chicken in North America.

Engineered viral vaccine constructs with dual specificity: avian influenza and Newcastle disease.

The guinea pig as a transmission model for human influenza viruses.

Influenza A virus PB1-F2 protein contributes to viral pathogenesis in mice.

Genomic analysis of increased host immune and cell death responses induced by 1918 influenza virus.

Severe acute respiratory syndrome coronavirus open reading frame (ORF) 3b, ORF 6, and nucleocapsid proteins function as interferon antagonists.

A two-amino acid change in the hemagglutinin of the 1918 influenza virus abolishes transmission.

Effective replication of human influenza viruses in mice lacking a major alpha2,6 sialyltransferase.

Live-attenuated influenza viruses as delivery vectors for Chlamydia vaccines.

Severe acute respiratory syndrome coronavirus ORF6 antagonizes STAT1 function by sequestering nuclear import factors on the rough endoplasmic reticulum/Golgi membrane.

Specific residues of the influenza A virus hemagglutinin viral RNA are important for efficient packaging into budding virions.

A single mutation in the PB1-F2 of H5N1 (HK/97) and 1918 influenza A viruses contributes to increased virulence.

Protective immunity and susceptibility to infectious diseases: lessons from the 1918 influenza pandemic.

Influenza virus transmission is dependent on relative humidity and temperature.

Influenza A virus PB1-F2: a small protein with a big punch.

A combination in-ovo vaccine for avian influenza virus and Newcastle disease virus.

Highly conserved regions of influenza a virus polymerase gene segments are critical for efficient viral RNA packaging.

Human genes and influenza.

Expression of transgenes from newcastle disease virus with a segmented genome.

Influenza virus transmission: basic science and implications for the use of antiviral drugs during a pandemic.

Single gene reassortants identify a critical role for PB1, HA, and NA in the high virulence of the 1918 pandemic influenza virus.

High temperature (30 degrees C) blocks aerosol but not contact transmission of influenza virus.

Combinatorial antibody libraries from survivors of the Turkish H5N1 avian influenza outbreak reveal virus neutralization strategies.

A seven-segmented influenza A virus expressing the influenza C virus glycoprotein HEF.

Cellular proteins in influenza virus particles.

Modulation of influenza virus replication by alteration of sodium ion transport and protein kinase C activity.

Oseltamivir-resistant influenza A viruses are transmitted efficiently among guinea pigs by direct contact but not by aerosol.

Influenza B virus NS1-truncated mutants: live-attenuated vaccine approach.

Live attenuated influenza viruses containing NS1 truncations as vaccine candidates against H5N1 highly pathogenic avian influenza.

Transmission of influenza virus in a mammalian host is increased by PB2 amino acids 627K or 627E/701N.

Unsung hero Robert C. Gallo.

Blocking interhost transmission of influenza virus by vaccination in the guinea pig model.

Enhancement of oncolytic properties of recombinant newcastle disease virus through antagonism of cellular innate immune responses.

Nipah virus edits its P gene at high frequency to express the V and W proteins.

The biology of influenza viruses.

Universal epitopes of influenza virus hemagglutinins?

Transmission of influenza virus via aerosols and fomites in the guinea pig model.

Preparation of genetically engineered A/H5N1 and A/H7N1 pandemic vaccine viruses by reverse genetics in a mixture of Vero and chicken embryo cells.

Alpha-C-galactosylceramide as an adjuvant for a live attenuated influenza virus vaccine.

Unraveling the mystery of swine influenza virus.

Recombinant vectors as influenza vaccines.

Rewiring the RNAs of influenza virus to prevent reassortment.

Transmission of pandemic H1N1 influenza virus and impact of prior exposure to seasonal strains or interferon treatment.

Detection of free peritoneal cancer cells in gastric cancer using cancer-specific Newcastle disease virus.

Hemagglutinin-pseudotyped green fluorescent protein-expressing influenza viruses for the detection of influenza virus neutralizing antibodies.

Transmission of influenza virus in temperate zones is predominantly by aerosol, in the tropics by contact: a hypothesis.

Human host factors required for influenza virus replication.

Protection of mice against lethal challenge with 2009 H1N1 influenza A virus by 1918-like and classical swine H1N1 based vaccines.

PB1-F2 expression by the 2009 pandemic H1N1 influenza virus has minimal impact on virulence in animal models.

Broadly protective monoclonal antibodies against H3 influenza viruses following sequential immunization with different hemagglutinins.

A nine-segment influenza a virus carrying subtype H1 and H3 hemagglutinins.

Protection from the 2009 H1N1 pandemic influenza by an antibody from combinatorial survivor-based libraries.

Influenza virus vaccine based on the conserved hemagglutinin stalk domain.

Oseltamivir-resistant variants of the 2009 pandemic H1N1 influenza A virus are not attenuated in the guinea pig and ferret transmission models.

Vaccination with a synthetic peptide from the influenza virus hemagglutinin provides protection against distinct viral subtypes.

Pandemic 2009 H1N1 vaccine protects against 1918 Spanish influenza virus.

A single N66S mutation in the PB1-F2 protein of influenza A virus increases virulence by inhibiting the early interferon response in vivo.

Transmission of a 2009 pandemic influenza virus shows a sensitivity to temperature and humidity similar to that of an H3N2 seasonal strain.

Newcastle disease virus expressing a dendritic cell-targeted HIV gag protein induces a potent gag-specific immune response in mice.

Budding capability of the influenza virus neuraminidase can be modulated by tetherin.

Broad-spectrum antiviral that interferes with de novo pyrimidine biosynthesis.

Oncolytic specificity of Newcastle disease virus is mediated by selectivity for apoptosis-resistant cells.

A reassortment-incompetent live attenuated influenza virus vaccine for protection against pandemic virus strains.

The influenza virus protein PB1-F2 inhibits the induction of type I interferon at the level of the MAVS adaptor protein.

Biochemistry. Catching a moving target.

Why do influenza virus subtypes die out? A hypothesis.

The M segment of the 2009 new pandemic H1N1 influenza virus is critical for its high transmission efficiency in the guinea pig model.

The DBA.2 mouse is susceptible to disease following infection with a broad, but limited, range of influenza A and B viruses.

Therapeutic effects of a fusogenic newcastle disease virus in treating head and neck cancer.

The influenza A virus protein PB1-F2: killing two birds with one stone?

Don't censor life-saving science.

Pause on Avian Flu Transmission Research.

Pause on avian flu transmission research.

Transmission of influenza B viruses in the guinea pig.

H5N1 influenza viruses: facts, not fear.

Hemagglutinin stalk antibodies elicited by the 2009 pandemic influenza virus as a mechanism for the extinction of seasonal H1N1 viruses.

Efficient transmission of pandemic H1N1 influenza viruses with high-level oseltamivir resistance.

Seroevidence for H5N1 influenza infections in humans: meta-analysis.

Oncolytic Newcastle disease virus for cancer therapy: old challenges and new directions.

Influenza viruses expressing chimeric hemagglutinins: globular head and stalk domains derived from different subtypes.

Attenuated influenza virus construct with enhanced hemagglutinin protein expression.

A pan-H1 anti-hemagglutinin monoclonal antibody with potent broad-spectrum efficacy in vivo.

The influenza A virus PB2, PA, NP, and M segments play a pivotal role during genome packaging.

One influenza virus particle packages eight unique viral RNAs as shown by FISH analysis.

A novel small molecule inhibitor of influenza A viruses that targets polymerase function and indirectly induces interferon.

Influenza virus protein PB1-F2 inhibits the induction of type I interferon by binding to MAVS and decreasing mitochondrial membrane potential.

Influenza virus infection in guinea pigs raised as livestock, Ecuador.

NS1-truncated live attenuated virus vaccine provides robust protection to aged mice from viral challenge.

Hemagglutinin Stalk-Reactive Antibodies Are Boosted following Sequential Infection with Seasonal and Pandemic H1N1 Influenza Virus in Mice.

A majority of infectious Newcastle disease virus particles contain a single genome, while a minority contain multiple genomes.

A carboxy-terminal trimerization domain stabilizes conformational epitopes on the stalk domain of soluble recombinant hemagglutinin substrates.

Cross-neutralization of influenza A viruses mediated by a single antibody loop.

1976 and 2009 H1N1 influenza virus vaccines boost anti-hemagglutinin stalk antibodies in humans.

Identification of small molecules with type I interferon inducing properties by high-throughput screening.

Toward a universal influenza virus vaccine: prospects and challenges.

Transmission studies resume for avian flu.

H3N2 influenza virus infection induces broadly reactive hemagglutinin stalk antibodies in humans and mice.

Serum- and glucocorticoid-regulated kinase 1 is required for nuclear export of the ribonucleoprotein of influenza A virus.

Chimeric hemagglutinin influenza virus vaccine constructs elicit broadly protective stalk-specific antibodies.

Colocalization of Different Influenza Viral RNA Segments in the Cytoplasm before Viral Budding as Shown by Single-molecule Sensitivity FISH Analysis.

Recombinant IgA is sufficient to prevent influenza virus transmission in guinea pigs.

Induction of cross-reactive antibodies to novel H7N9 influenza virus by recombinant Newcastle disease virus expressing a North American lineage H7 subtype hemagglutinin.

In vivo bioluminescent imaging of influenza a virus infection and characterization of novel cross-protective monoclonal antibodies.

A small molecule multi-kinase inhibitor reduces influenza A virus replication by restricting viral RNA synthesis.

Neutralizing antibodies against previously encountered influenza virus strains increase over time: a longitudinal analysis.

Influenza virus hemagglutinin stalk-based antibodies and vaccines.

Guiding the immune response against influenza virus hemagglutinin toward the conserved stalk domain by hyper-glycosylation of the globular head domain.