We recently held a patient feedback meeting at the Imperial College Medical School in London. Please see below slides from the meeting.
Archive for News
The child, whose identity is being protected, was born in 2007 and caught the virus from the mother, the BBC reported. The child was put on a clinical trial at 9 weeks old and received antiretroviral therapy for 40 weeks. The child was one of 143 children to receive the short course of drugs; another received 96 weeks’ worth of treatment. At the time, the use of ART for treating children with HIV was not standard practice.
“To our knowledge, this is the first reported case of sustained control of HIV in a child enrolled in a randomized trial of ART interruption following treatment early in infancy,” said Avy Violari of the Perinatal HIV Research Unit of the University of the Witwatersrand in Johannesburg, according to The Guardian. Violari presented the case study Monday to the International AIDS Society Conference in Paris.
“Technically, this baby is not totally cured of HIV, but it is certainly what is referred to as remission, in that there’s no virus circulating in the blood, and there is a normal immune system according to the range for children of their age,” says Sarah Fidler, speaking on behalf of the British HIV Association to Newsweek.
Fidler says it is important that HIV-positive people do not stop taking antiretroviral drugs as a result of the case. Usually, children remain on ART throughout their life and do not stop after a set period. Fidler says the only reason the South African 9-year-old did so is because the child was part of a randomized trial.
“It is certainly not to be taken from this one person that we would then recommend that lots of people who’ve been treated since birth should think about stopping therapy. That’s definitely not the message to be taken from one case,” says Fidler, a reader and honorary consultant physician in HIV at Imperial College London.
She says that eradicating HIV transmission from mothers to children must be a global priority. About 150,000 children became infected with HIV in 2015; transmission rates from mother to child can be as high as 45 percent if pregnant women are not provided with ART.
No adverse safety or virological changes 2 years following vorinostat in HIV-infected individuals on antiretroviral therapy
A study conducted by Sharon Lewin did not reveal any long-term toxicity or changes in markers of HIV persistence or transcription in participants on ART who had received 14 days of vorinostat.
Fake news is bang on trend in 2017, but misleading headlines are nothing new to the world of medical research. An almost inevitable outcome of new advances in HIV treatment is that someone somewhere will herald each new development as a cure. Since the epidemic was first recognised, a cure has eluded researchers, but as in other medical specialties, notably oncology, small advances or early-stage discoveries are frequently seized on by the media—especially the more click-hungry outlets—as major breakthroughs with imminent clinical impact. The consequences are raised hopes and vexed expectations that can damage relationships between people with HIV and their care providers and undermine trust between patients, the medical research community, and the media.
Two recent releases of preliminary trial results have both garnered widespread coverage—some of which has gone beyond reasonable interpretation of the facts. In October last year, a British man participating in a trial was widely reported to be cured of HIV after the early stages of a 5 year trial. While the word cure featured in numerous headlines, the specific details of the approach were barely reported, the highly preliminary nature of the results was glossed over, and the fact that the patient was also on combination antiretroviral therapy throughout was absent from many reports. The results of this study, combining vaccination and kick-and-kill, are eagerly anticipated—but the primary 42 week outcome will not be available until the end of this year at the earliest, and long-term follow-up will be essential before a cure can really be claimed with any degree of certainty. Similarly, early results of BCN01-Romi, a study designed to investigate the safety of a combined vaccination–kick-and-kill approach, were seized upon after presentation at the Conference on Retroviruses and Opportunistic Infections. Reports that patients were apparently virus free without drugs after pausing their antiretroviral treatment, touched lightly, if at all, on the fact that eight of 13 patients had viral rebound, and dwelt on the very early (in terms of weeks) results in five patients with virus loads below 2000 copies per mL—all of whom had started antiretroviral treatment very early and had suppressed virus for 3 years before entering the study.
In most cases, the worst these claims of a cure do is create unrealistic expectations for vulnerable patients and burden for care providers who have to explain the real meaning of the research behind the headlines. Patients’ groups often face the brunt of questions from people living with HIV—and their commitment to interaction with researchers and contributions to research are a cornerstone of progress in research into a cure for HIV. Indeed, the HIV cure research endeavour in general is an example to other medical specialties for how to engage with patients’ groups in research.
A cure will be found—maybe one of the approaches currently under investigation will deliver the goods, or perhaps some as yet unexplored avenue will finally provide a scalable method to enable people to permanently stop their medication safely. Perhaps in a few years, but potentially (although hopefully not) decades from now. Until we have a fully tested, proven cure, the HIV community must work harder with the lay media to ensure that advances are reported even-handedly, and should speak out when the headline does not reflect the story. We ask the media to think more carefully about the consequences of raising false hopes over cures with clickbait headlines, to disinter the caveats (which if presented at all are often buried at the end of their reports), and to give them the prominence they deserve. Most importantly, reporters should think twice before including the C word in a headline.
Editorial, Published April 2017
25 January 2017
A team led by UCL researchers has identified how HIV is able to infect macrophages, a type of white blood cell integral to the immune system, despite the presence of a protective protein. They discovered a treatment that can maintain macrophage defences which could be a key part of the puzzle of reaching a complete cure for HIV/AIDS.
Macrophages make an antiviral protein called SAMHD1, which prevents HIV from replicating in these cells – except for when the protein is switched off, as part of a natural process discovered by the UCL-led team.
“We knew that SAMHD1 is switched off when cells multiply, but macrophages do not multiply so it seemed unlikely that SAMHD1 would be switched off in these cells,” said Professor Ravindra Gupta (UCL Infection & Immunity), the senior author of the paper. “And yet we found there’s a window of opportunity when SAMHD1 is disabled as part of a regularly-occurring process in macrophages.”
Lead author of the EMBO Journal study, Dr Petra Mlcochova (UCL Infection & Immunity) said: “Other viruses can disable SAMHD1, but HIV cannot. Our work explains how HIV can still infect macrophages, which are disabling SAMHD1 by themselves.”
The reason why SAMHD1 gets switched off remains to be determined, but the authors suggest it might be done in order to repair damaged DNA, part of the normal functioning of the macrophage.
In a further part of the study, the researchers discovered how to close this window of opportunity by treating the cells with HDAC inhibitors, which are sometimes used in cancer treatments.
“Our findings could help explain why some people undergoing anti-retroviral therapy for HIV continue to have HIV replication in the brain, as the infected cells in the brain are typically macrophages. While this is a barrier to achieving control of HIV in just a minority of patients, it may more importantly be a barrier to a cure,” Gupta added.
The researchers say that macrophages can be an important reservoir of HIV infection that lingers away from the reach of existing treatments. Once a macrophage is infected, it will continually produce the HIV virus, so cutting off that point of infection within the body could be an important step towards safeguarding the entire immune system. HDAC inhibitors may be particularly helpful as they’re already known to reactivate latent HIV cells, thus making the virus vulnerable to the body’s defences, especially if supported by anti-retroviral therapy.
The series of tests involved cultures of macrophages derived from human cells in vitro, which responded well to HDAC inhibitor treatment, as well as macrophages residing in mouse brain tissues.
Study co-authors included researchers from the University of Oxford, King’s College London, and Emory University. The research was funded by Wellcome, the NIHR UCLH Biomedical Research Centre, the European Research Council, the Medical Research Council and the National Institutes of Health.