It's a well-worn truism that teenagers take risks—whether its drugs, drinking, shoplifting, or drag racing down the L.A. River against their 30-year-old gang rivals. On the flip side of that truism, parents worry endlessly that those risks will result in life-altering consequences. And there's perhaps no risk more fraught with worry than when and how teenagers will become sexually active.
Boys and girls begin puberty early in their teens, an age established during our 200,000-year evolutionary history. Yet, this time frame is horribly mismatched with modern cultures and societies. Today's teenagers reach psychosocial maturity much later and build life plans centered on long-term education and career goals. Thankfully, in the 20th century we developed safe, effective contraceptives and prophylactics, granting us a chance to find harmony between our modern realities and evolutionary drives.
But do teenagers engage in safe sex, or are they taking unnecessary risks during their first sexual escapades? That's the question the CDC hopes to answer with its Youth Risk Behavior Surveillance System. This biennial, nationwide survey aims to monitor health-related risk behaviors among high school students. And when it comes to sex, the survey's findings are both promising and a tad terrifying.
Are the kids alright?
A graph showing the prevalence of condom and primary contraceptive use among high school students during their last sex act.
First some good news: About 90 percent of sexually active high school students report using either a condom or other primary contraceptive method. Condoms were the most used form of contraceptive, with about half of that cohort claiming to have used one during their previous act of intercourse. Sexually active students made up about a quarter of all respondents, meaning more adolescents are choosing to wait until at least their late teens to have sex.
Looking at long-term data, today's teenagers make better decisions than their '90s peers. When the survey began in 1991, more than 50 percent of respondents claimed to have engaged in sex at least once. Of those, 16 percent said they used no method of birth control while 10 percent said they had sex before the age of thirteen. In 2019, 38 percent of respondents claimed to have had sex at least once. Of those, only 12 said they used no birth control while 3 percent said they had sex before thirteen.
Overall, the CDC reports adolescence to be a healthy stage in people's lives.
Now for some bad news: Condom use among sexually active teens has decreased. While 2019's 54 percent represents an uptick from the 1990's, it is a headlong drop from 2003's high of 63 percent. Granted, condom use may be underestimated due to survey limitations. For example, respondents could only select one birth control method for their latest sexual act. This means they could have considered another method as their primary birth control while leaving condom use unaccounted for. Even so, 2019's tally still suggests too many teenagers take unnecessary risks with pregnancy and STD transmission.
Other troubling figures also emerged. About a fifth of sexually active teens report using either no contraception or using a highly ineffective method, such as withdrawal. Only 9 percent report pairing an effective birth control with a condom. That figure may also be underestimated as half of the respondents were teenage boys, who—let's face it—may not have the most reliable grasp on female contraception use.
Teenagers and people in their early 20s represent about half of the 20 million new cases of STDs each year in the U.S. So, while 90 percent of sexually active teenagers may be protecting themselves from unintended pregnancies, many still risk their health in other ways. This is why experts recommend teens pair a condom with an effective birth control. It provides extra protection from unintended pregnancy while adding a prophylactic element to hinder the spread of STDs.
Having the talk
What can be done to bolster positive trends and reverse negative ones? Continue advancing sex education and outreach programs. In the survey, the CDC notes the proven effectiveness of risk reduction education—that is, not fearmongering but comprehensive, evidence-based teaching.
Unfortunately for adults hoping to avoid awkward conversations with banana stand-ins, this means doing away with abstinence-only programs. A review of the scientific literature found that these programs contain "scientifically inaccurate information, distort[ed] data on topics such as condom efficacy, and [promotion] of gender stereotypes." It concluded that abstinence-only programs put teens at greater risk of unintended pregnancies and STDs. With the gap between sexual maturity and marriage ever-widening, such programs, no matter how well-intended, are simply unrealistic.
As Laura Grubb, author of the American Academy of Pediatrics guidelines on adolescent barrier protection, told CNN:
It does not have to be a controversial position. There is no evidence that providing contraception to adolescents makes them more sexually active or promotes risky behavior. […] In fact, comprehensive evidence-based sexuality education results in adolescents delaying sexual behavior, using contraception at first intercourse, and having less sexual partners at a young age."
The CDC also recommends strong partnerships between communities and clinics. Teens should have access to well-trained care providers to provide the information and services they need.
Sex comes with risks, and it is impossible to reduce a teen's risk factor to zero. That's not necessarily a bad thing. Risk-taking is how teenagers develop their independence and form the identities that will carry over into their adult lives. It helps them experience qualities of the world that were hidden to them as children. But without comprehensive education, the consequences of those risks may stay hidden until it's too late. And without access to proper outreach and resources, they may not have the means to mitigate those risks.
As for drugs, drinking, shoplifting, and drag racing down the L.A. river for pinks, those are topics for other surveys and articles.
The scientific community has been proceeding with caution as it explores the potential of gene editing. The high risk of unintended consequences, both immediate and long-term, has prompted reticence regarding experimentation with humans. And then there's He Jiankui, who announced in 2018 that he'd genetically modified two human embryos, twin sisters, "Lulu" and "Nana," born in October of that year. Last week, a Chinese court sentenced He to three years in jail and a fine of three million Chinese yuan, about $430,000, for engaging in "illegal medical practices." The court also confirmed rumors that He had modified the genome of a third child, likely born in June or July 2019.
He's experiments
He tells the world
Image source: Anthony Wallace/Getty
When He first announced his research in November 2018 at the Second International Summit on Human Genome Editing in Hong Kong, the scientific community was stunned at this deliberate flaunting of scientific consensus and Chinese law. A statement from 122 Chinese scientists referred to He's work as "crazy" and called it "a huge blow to the global reputation and development of Chinese science."
He, an associate professor at Southern University of Science and Technology in Shenzhen, China, claimed to have used CRISPR-cas9 in an attempt to provide embryos with immunity to HIV. The DNA in 16 embryos was altered, and 11 of these were used in six implant attempts that eventually led to the successful pregnancy of three infants.
After the announcement, Julian Savulescu of University of Oxford told The Guardian, "If true, this experiment is monstrous," adding that, "There are many effective ways to prevent HIV in healthy individuals: for example, protected sex. And there are effective treatments if one does contract it. This experiment exposes healthy normal children to risks of gene editing for no real necessary benefit." While there are HIV infections in China, there was no indication that the embryos had been infected.
In his announcement, He claimed to have inserted a mutated form of the CCR5 gene into the embryos' genome, a particular mutation that makes a small number of people immune to HIV. According to Kiran Musunuru of University of Pennsylvania, though, the mutation has a nasty downside: People who have it are at higher risk of contracting other, non-HIV viruses, and of dying of the flu. So, while potentially shielding his subjects from HIV, He was, in essence, consigning them to a lifetime of enhanced vulnerability to all sorts of more common infections.
It's likely, however, that He never actually produced or inserted the CCR5 mutation in any event. Excerpts of He's documentation published in MIT Technology Review suggest that what He created were some new kinds of CCR5 mutations, as well as unintended gene mutations elsewhere in the genome, and the effect of all of these edits are anyone's guess. After reviewing the excerpts, University of California, Berkeley's Fyodor Urnov concluded He's claim was "a deliberate falsehood."
What the court said
He Jiankui and his genetic research team
Image source: VCG/Getty
Two of He's colleagues involved in the research were also convicted by the Shenzhen court. According to Chinese news outlet Xinhua, the court found:
"The three accused did not have the proper certification to practice medicine, and in seeking fame and wealth, deliberately violated national regulations in scientific research and medical treatment. They've crossed the bottom line of ethics in scientific research and medical ethics."
The court also ruled that He had forged documents from an ethics review panel.
The other two researchers found guilty were Zhang Renli, who was sentenced to two years in prison and fined one million yuan (about $143,000), and Qin Jinzhou, whose 18-month sentence came with a two-year reprieve, and a 500,000 yuan ($71,000) fine.
Ever since Frankenstein, scientists have been keen to avoid the public perception that they are playing God. This is part of the reason why the scientific community reacted so strongly to the Chinese biophysicist He Jiankui's announcement in 2018 that he had genetically edited the embryos of two girls in order to make them more resilient to HIV. As a result of his work, He was fired from his position and may face criminal charges.
Now, new research published in Nature Medicine underscores the reason for this backlash. The study examined a database of the genetic profiles of over 400,000 individuals from the UK, narrowing in on those who had the delta-32 mutation to the CCR5 gene. When an individual inherits delta-32 from both parents, they have a markedly strong resistance to HIV — this is the same mutation that He introduced into two subjects known by their pseudonyms Lulu and Nana using the gene-editing technique CRISPR.
HIV resistance is an obvious benefit of this mutation, but the trouble with gene editing is that it can be wildly unpredictable. "This is far too premature," said Dr. Eric Topol, head of the Scripps Research Translational Institute in California. "We're dealing with the operating instructions of a human being. It's a big deal." The new research showed that this tampering did have some unintended consequences: Individuals with this genetic mutation live two years less than those without it.
Playing with fire
He Jiankui during a panel discussion after presenting his results at the Second International Summit on Human Genome Editing in Hong Kong.
ANTHONY WALLACE/AFP/Getty Images
He selected Lulu and Nana for gene editing because their father had HIV. It's far more common for HIV to pass from the mother to the offspring, but it is possible, albeit rare, for HIV to pass from the father to the offspring. Providing Lulu and Nana each with two copies of delta-32 mutation did likely protect them against this possibility as well as from catching HIV later in life.
However, some evidence exists that individuals with two copies of delta-32 catch influenza, West Nile, and certain other diseases more easily. While HIV is a grievous disease, these far more commonly encountered diseases can often be just as deadly, especially in one's older age. This is precisely the result that the researchers uncovered in their analysis. Individuals with two copies of delta-32 were 20% more likely to die before the age of 76, with the highest probability of death occurring at 74.
What's more, because Lulu and Nana had their genes edited while they were embryos, this mutation will be passed down to any offspring that they have later. Given this scope, its increasingly clear why scientists reacted with such horror at He's actions: Gene-editing an embryo could have long-lasting, unintended consequences that could seriously impair what would have been otherwise healthy individuals for generations.
Another potential unknown impact that delta-32 could have is related to the girls' ethnicities. The mutation is far more common in individuals from northern Europe, while its very rare for individuals from Asia and Africa. Some researchers argue that the presence of delta-32 in Europeans is due to the impact of plagues from the Middle Ages, such as the Black Death. The absence of this mutation in other parts of the world is likely because it simply isn't useful there—different environments have different diseases, against which delta-32 could be more deleterious than beneficial.
He's actions and studies such as this one underscore the importance of a smart, evidence-based regulatory framework for gene-editing technologies. One question we need to resolve is whether germline editing, such as that performed on Lulu and Nana, should be permitted since these changes can be passed down to subsequent offspring. We also need a way to gauge the impact of editing specific genes so that we're not surprised by unintended side effects, like the diminished lifespan caused by delta-32. All in all, this study and He's work show us that there are simply too many moving parts to just introduce genetic mutations and see how things go. We need to be more rigorous than that.
Recently, the New York Times reported that for the first time in over a decade, a person with HIV has been cured of the deadly virus. Now, it's come to light that another patient—the third in history—has been cured of HIV as well.
We first learned that curing HIV was possible in 2007, when a patient known initially as "the Berlin patient," was diagnosed with both leukemia and HIV. The patient, whose name is Timothy Ray Brown, received a bone marrow transplant to treat his leukemia; after this treatment, Brown's doctors discovered that his HIV had been cured as well.
Leukemia is a cancer of the bone marrow, which is why Brown needed a transplant. Bone marrow contains stem cells that eventually differentiate into the three basic types of blood cells: red blood cells, platelets, and—critical to the immune system—white blood cells. The fact that Brown had both leukemia and HIV isn't pure happenstance; HIV, which infects white blood cells and eventually causes AIDS, has been linked to the development of blood cancers such as leukemia and lymphoma.
Brown was treated with two bone marrow transplants, aggressive chemotherapy, and total body irradiation, a harsh treatment that landed him in a medically induced coma and nearly killed him. But after surviving his treatment, Brown found that both his leukemia and HIV were gone.
Dr. Steven Deeks, who treated Brown, told the New York Times, "He was really beaten up by the whole procedure. […] And so we've always wondered whether all that conditioning, a massive amount of destruction to his immune system, explained why Timothy was cured but no one else."
Despite repeated attempts at reproducing the treatment, Brown had been the sole person to be cured of HIV until recently. Twelve years later, "the London patient" was cured of HIV as a result of a similar procedure. And now there's news of a third, "the Düsseldorf patient," who also appears to have been cured of HIV.
Finding the right cure
A scanning electron microscope image of HIV. The virus, colored in green, can be seen budding from the surface of a lymphocyte. Image source: Centers for Disease Control and Prevention
Part of the challenge of recreating Brown's success was identifying which factor of his treatment cured his HIV. The successful treatment of the London and Düsseldorf patients seem to suggest that the key lies in a genetic mutation called CCR5delta32.
Brown, the London patient, and the Düsseldorf patient all had some form of blood cancer — which, as mentioned earlier, are particularly common in people with HIV. All of them had bone marrow transplants in order to treat their cancers, and all of their transplants came from donors with a mutated CCR5 gene.
This gene produces the CCR5 protein, which is dispersed on the surface of white blood cells. HIV latches onto this protein and uses it to infect white blood cells, and if the virus manages to do so enough times, it causes AIDS. But the CCR5delta32 mutation renders this protein nonfunctional, essentially deleting HIV's entry into white blood cells.
After receiving this rare bone marrow transplant, the London patient stayed on their HIV medication for nearly a year and a half before they were declared — for all intents and purposes — cured of HIV. The Düsseldorf patient stayed on their medication for only three-and-a-half months. In both patients, all that remains of the HIV viruses are broken bits of DNA that can no longer replicate.
Both patients were registered with IciStem, an international collaboration investigating how to cure HIV through stem cell transplants. IciStem has identified more than 22,000 donors with the rare CCR5delta32 mutation, which is most commonly found in caucasians (about 1 percent of them). It's possible that more good news on this treatment is on the way as well: 36 other patients registered with IciStem have received these transplants, though its too early to definitively say whether they've been cured or not.
Good news and bad
It's important to remember, however, that this treatment is still in its early stages. "To be clear, this is not an option yet for people with HIV, even in very rich countries, but it is a major step forward," says Professor Francois Venter of the Wits Reproductive Health and HIV Institute. "This is incredibly exciting, as it furthers our understanding of the complex immunology of HIV and should get us closer to a cure."
Part of the problem is that bone marrow transplants are extremely risky, which is why they're reserved for individuals with life-threatening blood cancers. Transplants like these are at high risk for causing graft-versus-host disease. Because the job of white blood cells is to attack foreign cells, like those from a virus, donated white blood cells from a bone marrow transplant can begin attacking the host's body. This is part of the reason why Brown came so close to death after his initial treatment.
Furthermore, another strain of HIV can enter cells without the CCR5 protein. This strain, called X4, uses the CXCR4 protein instead. Patients can harbor both strains of HIV, which occurred in at least one patient who received a CCR5delta32 transplant. While the normal strain of HIV subsided in this patient, the X4 strain moved to take its place.
In the admittedly small number of successful cases so far, the treatment has eradicated the normal strain of HIV. The X4 strain, if present, can be kept at bay with regular HIV medication, such as the daily pill Brown takes as a precaution against the alternative strain.
Moreover, rather than use a treatment as aggressive as a bone marrow transplant, it may soon be possible to use gene therapy techniques to add the rare mutation directly to HIV patients' genetic code. Along this vein, the Chinese scientist He Jiankui used CRISPR to modify the CCR5 protein in two children to make them resistant to HIV. It's extremely difficult to anticipate the ramifications of genetic modification like this, and Jiankui's lack of caution drew international criticism from the scientific community.
However, with more research, an approach like Jiankui's may be the way forward for curing HIV.
