By stymieing three
genes in cells infected with HIV, researchers stop the virus from spreading to other cells
Not exact matches
The overlap
in gene expression changes when neural progenitor
cells are
infected by African or Asian strains of Zika virus.
«We hypothesized that individual mutations
in viral
genes could be expected to have a range of effects on the virus's ability to replicate, to
infect new
cells and escape the immune system,» Carlson says.
The virus, redesigned using sophisticated protein engineering techniques, works: With its shield and its adapter, these viral
gene shuttles efficiently
infected tumor
cells in laboratory animals.
By studying
infected cells grown
in a laboratory, the team found that a large number of CMV's
genes help it hide from the immune system by allowing it to destroy many of the proteins produced by the body during virus infection and preventing them from activating immune
cells to destroy the virus.
Epigenetic therapies are thought to work
in two ways to fix these errors
in cancer
cells — by correcting the «position» of the
gene switches and by making the
cell appear as though it's
infected by a virus, triggering the immune system.
Even if this did happen
in the body, the resulting virus would resemble HIV, as the hybrid contains no Ebola
genes — and HIV can not
infect lung
cells.
The virus can not
infect noncancerous
cells, Kirn explained, because researchers deleted its thymidine kinase
gene, which it needs to replicate
in the body.
With chronically
infected mice as their model, the researchers used a new technology called ATAC - seq to map the regulatory regions of the genome — the sections of DNA involved
in switching
genes on and off —
in the animals» exhausted and functional CD8 + T
cells.
Single -
cell mouse embryos were
infected in vitro with recombinant lentiviral vectors to generate transgenic mice carrying the green fluorescent protein (GFP)
gene driven by a ubiquitously expressing promoter.
The team is the first to demonstrate that HIV - 1 replication can be completely shut down and the virus eliminated from
infected cells in animals with a powerful
gene editing technology known as CRISPR / Cas9.
In clinical trials already underway, for example, researchers have used an older gene - editing technique, enzymes call zinc finger nucleases, in immune cells to deactivate the gene for CCR5, a surface protein that HIV latches onto in order to infect cell
In clinical trials already underway, for example, researchers have used an older
gene - editing technique, enzymes call zinc finger nucleases,
in immune cells to deactivate the gene for CCR5, a surface protein that HIV latches onto in order to infect cell
in immune
cells to deactivate the
gene for CCR5, a surface protein that HIV latches onto
in order to infect cell
in order to
infect cells.
The research showed the beta - lactamase
genes in Klebsiella pneumoniae were on all the time, whether or not the bacteria were
infecting human
cell cultures.
Of course, it makes sense that viruses would choose to turn off
genes that the immune system needs to fight the virus, «like interferon - b, which is a highly anti-viral
gene expressed
in virtually all
cell types; or
genes that T
cells need to recognize virus -
infected cells,» Kuss - Duerkop says.
Niles» team was able to disrupt this
gene in 100 percent of parasites treated with the CRISPR system; red blood
cells infected by those parasites remained smooth.
Moving their studies from
cells to whole animals, the researchers tested the effects of knocking out the Zbp1
gene in mice
infected with influenza.
A quantitative assay of the suppressor tRNA activity
in these mammalian
cells is described; it is based on the amount of tRNA - mediated readthrough of a terminating codon
in the influenza virus NS1
gene after the
cells are
infected with virus.
In 2009, for example, Sangamo Therapeutics in Richmond, California, began using zinc finger nucleases to modify genes in immune cells from HIV - infected people, hoping to make the cells resistant to the viru
In 2009, for example, Sangamo Therapeutics
in Richmond, California, began using zinc finger nucleases to modify genes in immune cells from HIV - infected people, hoping to make the cells resistant to the viru
in Richmond, California, began using zinc finger nucleases to modify
genes in immune cells from HIV - infected people, hoping to make the cells resistant to the viru
in immune
cells from HIV -
infected people, hoping to make the
cells resistant to the virus.
They did so using a technique called RNA interference, or RNAi, to clamp down on three
genes found
in infected cells, blocking the wily virus from moving to other
cells.
Because they carry mutations
in a key immune system
gene, many of these
cells are
infected with flu viruses (green).
The researchers used RNAi to block three
genes: two found
in the virus itself and one found
in mouse T
cells — the primary immune system
cells infected by the virus.
She found a
gene for what's known as the major histocompatibility complex (MHC)--
cell surface molecules that help the immune system recognize foreigners — that was remarkably similar to one
in humans that allows
infected people to keep the virus
in check for decades.
In tests using human neural progenitor
cells (NPCs)-- self - renewing, multipotent
cells that generate neurons and other brain
cell types — the scientists found that exposure to sofosbuvir not only rescued dying NPCs
infected with the Zika virus, but restored
gene expression linked to their antiviral response.
Another, previously unknown
gene — when the investigators worked out its protein's structure and studied it
in tissue culture — proved to do just the opposite: The protein helped the schizont leave the
infected blood
cell.
That
gene, HLA - B * 5701, codes for a protein on immune
cells that plays a central role
in clearing the body of HIV -
infected cells.
(B, C) Flow cytometric analysis of HIV - 1
gene expression
in (B) mock
infected or (C) latently
infected CD4 + T
cells under non-polarizing conditions, either at the basal state or after reactivation with antibodies against CD3 and CD28.
Previously we engineered zinc - finger nucleases (ZFNs) to specifically disrupt the CCR5
gene in primary human T
cells, the predominant
cell type
infected and killed by HIV.
Second, the AAV preps generally used for
gene editing are low titre, and are therefore able to
infect only a small subset of the
cells used
in a given experiment.
The use of viral vectors
in research is beneficial for a number of reasons, including but not limited to: helping to get difficult - to - deliver DNA into mammalian
cells, increasing the efficiency of
gene transduction, allowing for control over which
cells are
infected through viral pseudotyping, and ease of vector cloning and modification.
The researchers used the new technique to mutate the
genes CXCR4 and CCR5, which encode receptor molecules that different strains of the HIV virus use to sneak
in and
infect immune
cells and which have been targeted
in previous
cell therapy trials.
The first reports that
gene - editing of bone marrow stem
cells in monkeys
infected with a variant of simian immunodeficiency virus (SIV) significantly reduces the number of dormant «viral reservoirs» that pose a risk of reactivation.
Characterization of varicella - zoster virus
gene 21 and 29 proteins
in infected cells.
The first reports that
gene - editing of bone marrow stem cells in monkeys infected with a variant of simian immunodeficiency virus (SIV) significantly reduces the number Read more about Gene - editing and vaccines could improve HIV treatment - Sc
gene - editing of bone marrow stem
cells in monkeys
infected with a variant of simian immunodeficiency virus (SIV) significantly reduces the number Read more about
Gene - editing and vaccines could improve HIV treatment - Sc
Gene - editing and vaccines could improve HIV treatment - Scimex
The third Objective (IRF3) brings together promising scientists and clinicians from the University of Pennsylvania and the Rockefeller University to combine
gene therapy strategies, independently tested
in humans, with the goal of engineering, growing, and administering killer
cells that are uniquely empowered to find and kill HIV -
infected cells.
This type of «killer» T
cell responds to previously encountered
cell - surface molecules — including the fragments of SIV proteins encoded by the
genes in the CMV / SIV vaccine — and destroys SIV -
infected cells.
Now, a novel computational method shows that a viral protein found
in EBV -
infected human
cells may activate
genes associated with increased risk for autoimmunity.
In 2007, a research group at Children's Hospital of Philadelphia (CHOP) led by Jean Bennett began inserting a working version of the RPE65
gene into the eye by means of a harmless virus that carries the
gene and «
infects» the DNA of the RPE
cells.
JJ Miranda, PhD, reported that certain drugs affect
genes in tumor
cells infected with the Epstein - Barr Virus.
But by placing the
gene under the control of a «promoter» — an on - off switch for
gene expression — from a
gene (SM22a) that is expressed only
in smooth muscle
cells, Dr. Parmacek's team found that no matter which types of
cells were
infected, the
gene was only «turned on»
in smooth muscle
cells.
In a study published in the journal Biochemical and Biophysical Research Communications, a team led by Miranda examined how certain drugs affect genes in EBV - infected tumor cell
In a study published
in the journal Biochemical and Biophysical Research Communications, a team led by Miranda examined how certain drugs affect genes in EBV - infected tumor cell
in the journal Biochemical and Biophysical Research Communications, a team led by Miranda examined how certain drugs affect
genes in EBV - infected tumor cell
in EBV -
infected tumor
cells.
Developed by Kotin et al. (37), the BEVS uses Spodoptera frugiperda (Sf9)
cells infected with recombinant baculoviruses containing the vector genome, helper
genes, and capsids to generate yields of 1014 — 1016 viral genomes per liter
in 100 - L to 200 - L bioreactors (4, 38).
These reporters will give us the ability to sort
infected cultures to analyze changes
in gene expression
in directly
infected cells and bystander
cells and compare to uninfected
cells.
Partial block to transcription of human adenovirus type 2 late
genes in abortively
infected monkey
cells
First cloning of the
gene for prion protein (PrP), demonstration that PrP knockout mice are resistant to prion disease and that PrP antibodies abrogate prions
in infected cells.
We combine biochemical, structural, cellular and functional information using purified proteins, mutant and transgenic plants, yeast and chemical genomic screening systems, transient
gene expression assays, confocal microscopy and
in silico data analysis to compare ROP - centered kinase signaling during
cell polarity (
in vitro pollen tubes), morphogenesis (whole plant) and pathogenesis (fungi -
infected cells).