Scientists Use the Tweaked Genes of a Virus to Halt Vision Loss

iStock
iStock

What if you could tweak the genes of a virus to turn its ability to invade cells into a delivery system for eyesight therapy? That’s what researchers at Johns Hopkins School of Medicine say they’ve done by modifying an adenovirus, a type of virus that can infect tissue linings. The cutting edge gene therapy was developed to help those who suffer vision loss from a particular eye disorder—wet age-related macular degeneration (AMD).

Approximately 1.6 million Americans have AMD, the number one cause of vision loss. The disease is characterized by the growth of abnormal blood vessels that leak retinal fluid into the eye and destroy the macula, an area near the retina important for high acuity vision. This gene therapy both reduces fluid buildup and improves vision loss in humans, according to study results published in The Lancet.

The best current treatment for the disease requires injections of antibodies into the retina to suppress vascular endothelial growth factor (VEGF), a protein that is responsible for the growth of blood vessels—which in turn cause leaking fluid. But the problem is that patients must obtain these injections at four- to six-week intervals, or else the disease symptoms return and worsen over time. Peter Campochiaro, a professor of ophthalmology and neuroscience at Johns Hopkins Medicine's Wilmer Eye Institute and one of the authors of the study, explains that during this treatment, if a patient takes too long to get their next injection, the abnormal blood vessel net grows larger and recruits other cells. “That scarring causes permanent decrease in vision,” he tells Mental Floss. So over time, it’s common even for patients in treatment to “end up with less vision.”

His team has been working to make a form of injections that last longer, so patients don’t have to come in as frequently. For phase one of this trial, Campochiaro’s team recruited 19 participants to participate in a 52-week study. He was looking for people “who don’t have great visual potential, but have evidence of the disease process that you can measure in effect,” he says.

Since viruses are naturally good at getting into cells and depositing their genetic material, the researchers decided to modify a virus to deposit a gene that codes for a protein called sFLT01. sFLT01 blocks the factor that causes the abnormal vessels and fluid production. When the modified virus is injected into the eye, “the viral vector enters cells and deposits the gene, and the gene begins to produce the [sFLT01] protein,” he says. The protein binds to VEGF, preventing it from causing vessel growth and subsequent fluid leakage.

The 19 participants were divided into five different groups and given increasing doses of the viral vector. After determining there was no toxicity at the dose-limit of the first three groups, they proceeded to increase the dosage to its highest level.

Of the 11 participants with symptoms judged to be reversible, six showed “a substantial reduction in the fluid,” and four of those six saw “a pretty dramatic effect.” Those patients had big pockets of fluid in their retinas decrease, Campochiaro says. Better yet, the treatment lasted throughout the yearlong study, though the protein numbers peaked at 26 weeks, and then declined slightly (although not enough to reactivate disease symptoms).

In assessing why five patients saw no reduction in fluid, the scientists discovered those patients had pre-existing antibodies to the virus. They theorize that in these patients, the immune system may have killed the viral vector before it could deposit the genes, though they will have to do more research to prove this. This could be a problem in using this particular virus—a carrier virus called AAV2—since some 60 percent of patients tend to have these antibodies.

A possible solution might be to give resistant patients a surgical injection instead. During this procedure, scientists could take out the vitreous—a gel-like substance that gives your eye its round shape—and inject the vector surgically under the retina instead. While patients might prefer not to have surgery, “our data suggests that it doesn’t matter if there’s pre-existing antibodies [with this method],” he says.

Alternately, other viral vectors have proven to be more effective than AAV2, including a variation on the virus, AAV8, which provides better infections of the virus into the cell. Even more promising, the researchers recently finished a four-year study on a lentiviral vector (a totally different group of viruses) “that take [the genes] into the nucleus of the cell and inserts the gene right into the chromosomes,” Campochiaro explains.

His next steps will be to retest the treatment with a longer study period to identify just how long-lasting the effects are, as well as to test higher doses of the viral vector.

But right now, he is just excited that the gene therapy works. “We injected this gene, the gene is producing a protein, and you can measure that protein in the eye over time,” he says.

Celebrate the Holidays With the 2020 Harry Potter Funko Pop Advent Calendar

Funko
Funko

Though the main book series and movie franchise are long over, the Wizarding World of Harry Potter remains in the spotlight as one of the most popular properties in pop-culture. The folks at Funko definitely know this, and every year the company releases a new Advent calendar based on the popular series so fans can count down to the holidays with their favorite characters.

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Right now, you can pre-order the 2020 edition of Funko's popular Harry Potter Advent calendar, and if you do it through Amazon, you'll even get it on sale for 33 percent off, bringing the price down from $60 to just $40.

Funko Pop!/Amazon

Over the course of the holiday season, the Advent calendar allows you to count down the days until Christmas, starting on December 1, by opening one of the tiny, numbered doors on the appropriate day. Each door is filled with a surprise Pocket Pop! figurine—but outside of the trio of Harry, Hermione, and Ron, the company isn't revealing who you'll be getting just yet.

Calendars will start shipping on October 15, but if you want a head start, go to Amazon to pre-order yours at a discount.

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Your Tattoos Could Be Messing With Your Sweat Glands

Tattoos might inhibit a person's ability to sweat.
Tattoos might inhibit a person's ability to sweat.
vgajic/iStock via Getty Images

For centuries, tattoos have reflected cultural traditions, personal beliefs, self-expression, and one’s preferred motorcycle club affiliation. But those who have used their bodies as a giant canvas for permanent ink with meaning might have a little trouble cooling off. That’s because tattoos might actually be interfering with sweating, according to a new study.

A paper published in the Journal of Applied Physiology recruited 10 subjects with tattoos and had them wear tube-lined suits containing warm water. When fitted against the skin, the warmth induced sweating. Skin covered by a tattoo produced roughly 15 percent less sweat than unmarked skin in the same subject.

While the sample size was small, the study follows other research into the effects of tattooing on sweat glands. In 2017, Alma College’s Maurie Luetkemeier used an electric current to produce sweat and found inked skin produced 50 percent less sweat, though the method to promote the sweat was considerably different than how the body cools itself naturally. Another study used exercise to observe sweating and found no difference in tattooed and non-tattooed skin.

This latest research seems to indicate that thermal-induced sweating can indeed be interrupted by tattoo ink and that a person’s sweat glands suffer an undetermined amount of damage as a result of being tattooed, which involves a needle being inserted into the skin’s dermal layer. While further research will be needed to make more solid conclusions, it’s something to consider the next time you ponder getting that full-back dragon rendering.

[h/t New Atlas]