On July 10, the National Institutes of Health announced the child "cured" of HIV was found to have detectible levels of the virus after two years of no antiretroviral treatment. Kent Sepkowitz wrote this past spring that other HIV "cures" didn't last long and this one was likely to be a letdown.
Another year, another national meeting on AIDS with reports of a baby (maybe) cured of the disease.
Last year, we had the Mississippi Baby (now re-branded as the “Mississippi Child”) who seemed to be free of fully-formed virus (called “replication-competent” virus) many months after stopping potent anti-viral medications.
Subsequent publication of that case in the prestigious New England Journal of Medicine laid out a compelling argument that (maybe) the child, one of the 250,000 children infected with HIV that year, had indeed cleared infection from the bloodstream.
But that was 2013. For 2014, a new child, this one a girl from Long Beach, California, was presented at the annual meeting. (Click here for a video of the scientific presentation, complete with Powerpoint slides.) Her story is completely different in every way from her Mississippi counterpart. The California child was born from a mother with advanced AIDS; the mother’s HIV viral load was 138,000 copies and she had a CD4 cell count of 70 cells, both values indicate advanced disease. In contrast, the mother of the Mississippi Child had mild, probably early infection; with an HIV viral load of about 2400 copies and a CD4 cell count of 644 cells— suggesting she had a normal or nearly normal immune system.
This difference in the HIV stage of the mother has possible implications regarding contagiousness and the amount and type of virus each may have transmitted; yet this distinction pales against the enormous other difference between the two cases. Unlike the Mississippi Child, who stopped therapy and remained without any detectable or mature virus for many months, the infant from California remains on treatment. She, like millions of other infected people, has undetectable viral load in the setting of ongoing administration of potent anti-HIV medications.
So what sets her apart from anyone else on treatment? She, unlike the other millions, has no detectable antibody to HIV. A quick primer: with any infection, there are two different ways to make a diagnosis: one can measure antibody – body’s response to infection – or one can look for the actual infection. Older techniques were mostly antibody-based whereas in the last 10-15 years, there have been many breakthroughs in detection of the infection itself.
In general, a person who has had an infection maintains detectable antibody against that infection for life. For example, though I had chicken pox decades ago, I still have antibody to chicken pox. In contrast, the actual chicken pox virus long ago exited my bloodstream and is not detectable.
Similarly, with HIV, infected patients maintain detectable antibody against the virus. Sometimes, in the very advanced stages of infection, usually when death is weeks or months away, antibody may fade out as the immune system shuts down. But in health, people with HIV always maintain readily detectable antibody.
Except the California case—ergo the news buzz. Yet it is very difficult to get excited about a patient on treatment with undetectable virus—again there are millions who fit the bill. In that regard, no one knows whether cessation of potent anti-HIV medications will result in newly detectable virus. I certainly worry that this is exactly what will happen. (And I hope that no one is cruel enough to experiment on the child.)
So we are left with a strong “maybe” for the Mississippi case and a California case that should barely raise an eyebrow. But here we are with screeching headlines about the cure, all because of a weird arithmetic that says that one apple blossom plus a photo of an orange peel equals two pieces of newsworthy edible fruit. Or some such mixed up metaphor.
So consider this: 14 years ago, there was an amazing (to me) case of a patient who received a transfused unit of blood from a donor with undetected HIV infection. About fifty hours after receipt of the tainted blood, the patient was given potent anti-HIV medications to prevent establishment of infection. It worked: she took anti-HIV meds for 9 months, stopped them, and remained HIV negative for more than six months after stopping the treatment— despite the certain introduction of virus into her bloodstream.
But you never read about the case, perhaps because it was not presented at a fancy national meeting. See, national meetings of professional medical societies now come equipped with a powerful PR machine that selects a handful of scientific papers in advance and then carpet bombs every media outlet in the country. In my 25-year academic career, I have been selected for the “big push” once or twice. A big brouhaha was made, before which I was prepped by experts as if about to give testimony in a murder trial. I wore a smart tie and a clean shirt; I spoke slowly and I rehearsed. Oh how I rehearsed. A crowd came, listened, and asked some hard-edged questions. But alas in the morning I was not in papers; nor did Your NewsGuys at 10 show interest. Drat.
So maybe it’s sour grapes on my part. But having witnessed the vast apparatus built by professional societies to draw public attention (and eventually funding, one hopes) to their field, I am certain of one thing: the mix of science and PR is toxic in every way. It distorts the doctor’s sense of himself beyond recognition and it distorts the journalist’s perspective of a problem. But most destructively, it distorts that most precious of all commodities for a patient with a disease: hope.
