So people with H.I.V. now must take drugs every day for life, which some researchers say is not a sustainable solution for tens of millions of infected people.
CCR5,
This is what was done with the Trenton patient. Some of the man's white blood cells were removed from his body and treated with a gene therapy developed by Sangamo BioSciences. The therapy induced the cells to produce proteins called zinc-finger nucleases that can disrupt the CCR5 gene.
Millions of people worldwide are currently affected by HIV and many have died from AIDS. Scientists have been trying for many years to find a cure for the epidemic, but now many are trying to find a way to prevent the passing on of the virus for future generations. Although no definite treatment has been discovered yet, recent findings have shown promising results for the future.
With the fast developing biological technologies we are seeing today, scientists hope's are growing stronger.
Maybe one of us one day will be a part of the phenomenon, in search of a way to help the millions affected by the epidemic
Many forms of HIV, initially use CCR5 to enter and infect host cells. A few individuals carry a mutation known as CCR5 delta 32 in the CCR5 gene, protecting them against these strains of HIV.
Incase some of us forgot, AIDs stands for Acquired immune deficiency syndrome, a disease in which there is a severe loss of the body's cellular immunity. And HIV stands for Human immunodeficiency virus, a virus that causes AIDs
For all but four diseases, the genetic data would fail to determine who is likely to contract the condition in most cases,
genetics are only part of the story when it comes to determining health. Lifestyle, environment and random chance play a bigger role than genes, or work with genes, to cause or protect against disease.
microbes in bee colonies that have previously been associated with fermentation in humans and other animals
communities of active bacteria harbored by honey bee colonies
research suggests honey bees may take advantage of these beneficial symbiotic bacteria to convert indigestible material into nutritious food and to enhance protection from pathogens
Genes represent only a tiny fraction -- 1 percent -- of our overall genetic material. Then there's the other 99 percent of our DNA -- the stuff that doesn't make protein
Researchers have found that some of this noncoding DNA is in fact essential to how our genes function and plays a role in how we look, how we act and the diseases that afflict us.
Embedded in this 99 percent is DNA responsible for the mechanics of gene behavior: regulatory DNA. Greg Wray of Duke University's Institute for Genome Sciences and Policy describes the regulatory DNA as the software for our genes, a set of instructions that tells the genome how to use the traditional coding genes.
"It's like a recipe book," Wray said. "It tells you how to make the meal. You need to know the amounts. You need to know the order. The noncoding DNA tells you how much to make, when to make it and under what circumstances."
common diseases are probably more influenced by regulatory differences, Harismendy said. These include Type 2 diabetes, Crohn's disease, Alzheimer's Disease and a variety of cancers, including breast, colon, ovarian, prostate and lung.
According to Wray, research has shown that diseases like bipolar syndrome and clinical depression may be associated with noncoding mutations that determine whether the brain is producing too much or not enough of a particular neurotransmitter. One noncoding mutation gives a person almost complete protection against the nasty malaria parasite, plasmodium vivax.
Another piece of noncoding DNA regulates the enzyme responsible for lactose tolerance, the ability to digest milk. Research by Wray and other scientists has shown that in four populations where dairy consumption is a vital part of the diet, new mutations have appeared that essentially keep the gene that produces the lactase enzyme from switching off.
And recent research done by evolutionary biologists suggests that differences in regulatory DNA may represent a major part of what separates us from chimpanzees.
DNA methylation is a chemical process where a methyl group is added on either the cytosine ring or the adenine ring, used in "higher leveled" organisms. Important in cell differentiation since methylation will cause cells to "remember" and remain differenciated instead of expressing other genes.
Epigenetics is defined as modifications of the genome, heritable during
cell division, that do not involve a change in the DNA sequence.
Epigenetic alterations in cancer include global hypomethylation
the promoters of housekeeping genes
that are generally protected from methylation.
may lead to aberrant silencing of tumor suppressor genes
discovered loss of imprinting (LOI) in
cancer
Genomic imprinting, the subject of the report by
Nakagawa et al. (2), is an epigenetic modification of a
specific parental allele of a gene, or the chromosome on which it
resides, in the gamete or zygote, leading to differential expression of
the two alleles of the gene in somatic cells of the offspring.
we found that LOI can occur in the normal
colonic mucosa of colorectal cancer patients with LOI in their tumors
This LOI was linked to cases showing
microsatellite instability (MSI) in the tumors
However, these patients
do not have mutations in mismatch repair genes
One potential
cause of MSI in these sporadic cancers is hypermethylation and
epigenetic silencing of the hMLH1 mismatch repair gene
Nakagawa et al. (2) now confirm the original study of Cui
et al. that LOI occurs in both tumor and normal tissue of
patients
The present study (2) also offers an intriguing mechanistic
hypothesis to explain the relationship between H19 DMR
methylation and LOI in these patients
Nevertheless, the study calls attention
to this remarkable highly conserved multifunctional protein,
The potential link to CTCF suggested by this study also calls our
attention to the link among DNA methylation, epigenetics, and
chromatin.
A clue to the link between MSI and epigenetics may be provided by
another sometimes overlooked common thread in epigenetics, namely DNA
replication
repeat-induced gene silencing is thought to
be propagated through hemimethylated intermediates during DNA
replication
The studies of Cui et al. (11), Nishihara et
al. (20), and Nakagawa et al. (2) suggest a new and
provocative view of the timing of epigenetic changes in cancer.
Studies of transgenic mice with
constitutive biallelic expression of IGF2, comparable to
LOI, show reduced apoptosis and increased tumor formation
I conclude by noting that the distinction between cancer genetics
and epigenetics has blurred considerably in recent years
Many
conventional “genetic” mechanisms directly affect proteins that
regulate chromatin,