字幕表 動画を再生する 英語字幕をプリント With its uncanny ability to disguise itself from the body's immune system, HIV is a mysterious and powerful virus. HIV is the most dynamic disease that we've ever seen. So, how does HIV re-write your body's DNA? And how can a disease that was once a death sentence now be managed with just one pill per day, with some patients living well into their 90's? Life expectancy has improved over years, and I'm very happy to be part of this journey. My name is Sabin Nsanzimana. I work for Rwanda Medical Centre. I'm a medical doctor and an epidemiologist. So I've been working for the Rwanda health sector for the past 14 years. My role was head of HIV Care and Treatment Department. HIV is a virus. It belongs to the broader category of a retrovirus. My name is Dr. Anthony Fauci and I'm the director of the National Institute of Allergy and Infectious Diseases at the National Institutes of Health. I'm also an AIDS physician and scientist who runs a laboratory studying HIV/AIDS pathogenesis Like Ebola and the coronavirus SARS-COV-2, HIV is a zoonosis, meaning it jumped to humans from another species. In this case, it originated as Simian Immunodeficiency Virus in chimpanzees and other non-human primates. So some decades and decades ago, the virus jumped species from an animal—we don't know how—possibly because individuals in central and southern Africa took non-human primates, butchered them, and ate them and it is likely that during that process the virus got into the immune system of a human and then continued to spread from human to human, predominantly by sexual contact. But it's not just the infamous sexual transmission that spreads HIV. The virus can also be spread via injection drug use, contaminated blood transfusions, or from mother to baby in utero, or during childbirth or breastfeeding. Once it enters the body, HIV heads straight for specific white blood cells within the immune system: T-lymphocytes, derived from the thymus, which is an organ just beneath the chest. One type of T-lymphocyte has on its surface a receptor, which is actually the CD4 molecule. When the virus comes in, the virus binds to that receptor, fuses with and enters the CD4-positive T-cells that are the predominant conductor of the orchestra of the immune system. It's through those CD4 T-lymphocyte cells that HIV integrates itself into the body's DNA. This is what retroviruses do best, but doctors are still stumped as to how exactly HIV manages to sneak past the body's defenses. We don't know how the virus, the HIV, actually convinces the cell to open up the window. It's like you open up the window for your enemy. The virus, after it's changed itself, will penetrate the nucleus of our cell. It will start to provide messages through our RNA messenger to create new viruses. Like a factory, it starts reproducing itself, spitting out virus, infecting other CD4-positive lymphocytes, killing them, diminishing their function. You become very susceptible to a variety of infections that you otherwise would not have to worry about. They're called opportunistic infections. When CD-4 cells drop below a certain level, HIV progresses to its most dangerous phase, AIDS. AIDS not only weakens the body's defenses against standard pathogens, like bacteria and viruses, but also certain types of cancers like Kaposi's Sarcoma, which can cause tumors in the lungs, liver, or digestive tract, or patchy, visible lesions on the legs and face. In the 1980s, the AIDS epidemic shocked the world, and societal stigmatization, particularly against at-risk groups like gay and bisexual men, ethnic minorities, sex workers, and the homeless didn't speed the search for a cure. In fact, the first ray of hope came in the form of a drug initially intended for a different purpose. AZT, our first molecule, was meant for cancer treatment. And it worked, it stopped the virus' progression. But the virus has many entry points: to the cell outer protection, to inside the integration the virus, and after that also the virus will produce new viruses. All these stages need treatment. The first treatments, unfortunately, were too many drugs. So patients would tell you that they could take up to 20 pills a day. Today, thankfully, it's a different story. When HIV is caught soon enough, more options are available to patients. It takes up to 72 hours to go deeper into the lymphocytes, so cells that would keep it forever. At that stage we can stop the virus by providing treatment we call post-exposure prophylaxis. Pre- and post-exposure prophylaxis are known as PrEP and PEP, respectively. When administered on a daily basis or within 72 hours of exposure, these methods can be up to 99% effective for preventing HIV from taking hold. Once diagnosed, however, taking just one pill per day can slow the virus' multiplication and allow the body's CD4 cell-count to catch up. While it isn't a cure, this treatment, known as antiretroviral therapy, can bring patients' viral loads down to below detectable levels, meaning they can't pass the virus on sexually. Long-Acting treatment, injectables are coming very soon. The same way we see for family planning, you take an implant for several months or years. This is the near future. While the current cohort of HIV patients grows older, new infections are down by 40% from the peak of the epidemic in the late 1990s. But certain areas of the world, like Southern Africa, are still reeling from its effects. Currently, throughout the world, there are 37 and a half million people living with HIV. There are a little bit less than a million deaths per year. Those fatalities are largely in places where the stigma of a diagnosis and the cost of treatment present huge barriers to patients. And this makes developing an HIV vaccine a sort of 'holy grail' for this global epidemic. Turns out that's proving to be as complex and nuanced as HIV itself, as the virus can mutate over time. The way that it tricks the immune system means that there really aren't any natural human antibodies to it that we can use as a starting point, as we do with other vaccines. Unlike almost any other infection that the body deals with, the body does not make a very adequate immune response against natural infection with HIV. In a clinical trial known as RV144, an investigational vaccine regimen showed a modest level of efficacy, protecting 30% of patients from the virus' invasion. Since it ended in 2009, scientists have worked to build on those results, testing candidates all over the world. As we speak now, the candidates are being tried in the United States, in Asia, in Africa. Here in Rwanda we have a vaccine trial site. But still efforts are going on and we hope that one day we may have a vaccine that can stop or can help people to get protected against HIV. Now all that's left is to better implement the tools we do have—like improving the cost and convenience of antiretroviral therapy—and continue the search for the vaccine that will put HIV to rest for good. It might not be in the next 525,600 minutes, but we'll keep you posted.