Vaccines just aren't as easy to discover as they used to be

Edward Jenner had it easy. Swab some cowpox in 1796, scratch the nastiness into the arm of a little kid (see below), and, PRESTO, instant immortality. 

Vaccine success after vaccine success followed. Measles, mumps, rubella, polio... one after another global scourge quaked before the mighty pipettes of vaccine researchers.

I admit, the stalwarts who discovered those vaccines did more than transfer cow-pus to an un-consented minor research subject prior to doing a victory lap around the farm. Rather, they earned their laurels by working hard, and by being brilliant.

But ease wrought hubris, and as deadly viral menaces fell in succession, you could forgive one noted twentieth century sage, US Surgeon General William Stewart (pictured below), for saying, "It’s time to close the books on infectious diseases, declare the war against pestilence won, and shift national resources to such chronic problems as cancer and heart disease."

Whoops!

These early triumphs gave way to a long, hard slog. Vaccines against HIV, tuberculosis, herpes, staphylococci, and hepatitis C, among others, have proven far more elusive. Amid small successes, and spectacular failures, we have discovered an uncomfortable fact: we don't really know what makes a good vaccine tick. 

This week I was glad to contribute both heat and noise to the mix. In an op-ed in the Health Affairs blog, I write about the dangers of dogmatism and the lessons learned on the road to a new HIV vaccine. And, we also published preclinical data this week on a new scalable version of our tuberculosis vaccine. Data from our Phase 1 trial of the same vaccine should come out soon!

Who knows if all this will lead to glory. Probably not! Either way, it's been a pleasure to try. 

The missing microbial link

It turns out the oily wind that a subway train brings into a subway station carries its own passengers with it: bacteria DNA.

As passengers step into the car and compete for seats, they do so thickly coated with the DNA of millions of microscopic parasites. 

But do not be alarmed. Recent news stories have reassured us that while DNA for bubonic plague can be found in the nooks and crannies of New York City subways, we should not worry a cross-town ride risks the plague any more than asymptomatic patient Craig Spencer spread Ebola.

We should extend the same logic to hospital infection control.

Every few months there is a new article confirming that doctors, nurses and the things they wear and use are not sterile. NOOO! Stethoscopes, ties and our beloved white coats in particular have drawn ample attention for their unsurprising propensity to - gasp! - have bacteria on them. 

This is useful research, and hypothesis forming. Might doctors and nurses contribute to the epidemic of healthcare-associated infection (HAI) via fomites like these?

Absolutely, they could.

But our reactions to this interesting hypothesis have been far from scientific. We have gone from hypothesis to heartfelt belief in five seconds flat.

One second we know stethoscopes and ties and white coats have bacteria on them and the next we conclude that we should do away with the lot of them. Britain's NHS, for instance, famously adopted a "bare below the elbows" stance in 2008, and US infection control mavens have recommended a similar policy recently.

Where's the science? 

We all want to prevent HAI's, and lord knows the physician fashion index would rise by fully 2.5 points if we left our silly white coats at home (excellent logistical points made by an esteemed surgical blogger aside). But before we invest in nationwide changes to attire and clinical practice, we should convert these reasonable hypotheses into real evidence. 

If going bare below the elbows, or skipping neckties, or burning our white coats, really will protect patients, then we should be able to prove it.

Before we draw conclusions, let's do the damn experiment: compare infection rates in comparable patients cared for by providers who do or do not wear neckties, or who do or do not subscribe to a BBE policy, whatever. Bring on the data!

It's not that easy, you say?

I understand. Science is hard. 

If we can't show the intervention works, why invest in it? It is no great challenge to leave our ties at home, but until we base our recommendations in science the hard work of culture change may not be worth it. Why not just make the change? Well - how well is that argument working so far?

Let's be scientists people, lest we get schooled one day that these stories of stethoscope contamination are as alarming as bubonic plague DNA found in the New York City subway.

Why we shouldn't say we have a "cure" for HIV until it's really true

The Berlin patient, Timothy Ray Brown, is historically unique - he is the only person ever truly cured of HIV. 

But in recent years scientific journals and the popular press alike have published multiple claims of HIV cures. From the French "functional cure" to the Mississippi baby, we have seen the word "cure" used a lot -- as well as vague synonyms for it like "cleared" and "HIV-free" -- and yet each time we've had to walk the hype back. 

Check out my new post over at The Conversation on why we shouldn't overhype HIV "cures."

How to Read Education Data without Jumping to Conclusions

Education has entered the era of Big Data. The Internet is teeming with stories touting the latest groundbreaking studies on the science of learning and pedagogy. Education journalists are in a race to report these findings as they search for the magic formula that will save America's schools. But while most of this research is methodologically solid, not all of it is ready for immediate deployment in the classroom.

To read the rest of my new article, written with the lovely and talented education writer Jessica Lahey, visit The Atlantic.

This just in: how HIV kills

New findings by researchers at the Gladstone Institute of Virology at the University of California at San Francisco (UCSF) have upended how we understand the pathogenesis of the acquired immunodeficiency syndrome (AIDS). 

Enter Warner Greene, a dapper white-haired professor of medicine at UCSF and its Gladstone Institute of Virology. In a feat of scientific hutzpah sure to trigger fits of envy among other scientific heavy-hitters, Greene shattered the existing model of AIDS pathogenesis in two simultaneous groundbreaking articles in the prestigious journals Science and Nature in late December 2013.

Greene’s team made multiple seminal observations. Their key findings were ...

Read my new post at Scientific American guest blogs to learn more

Earlier Is Better

For years now there has been controversy about whether early HIV infection should be treated. Could the immune system be spared the ravages of the HIV virus through early therapy? Or does early therapy just make treatment last longer? The jury has been out, and might still be deliberating, but a new piece of evidence has emerged. 

 Deeks et al have shown that, compared to people treated later in HIV disease, those treated within 6 months of initial infection show less immune system damage over time. This might be a sign that early treatment is good.  

We still lack clear evidence that such benefits of early treatment outweigh the downsides of HIV treatment. The side effects, costs and other risks are real. So, we still await a clear sign. 

When face-to-face with a patient with early HIV infection, I tell them what we know, and what we don't, and we share the decision-making. Does the possibility of ongoing immune damage scare them enough to make taking an HIV pill or two daily worth it? Or  does the prospect of starting decades of therapy freak them out more? We talk through it, and most (but not all) start therapy. 

Someday, let's hope we know more.

HIV Cures: Where We Are, Realistically

Newswires remain abuzz around two reports of "functional" HIV cures.  What does "functional cure" mean? Should the Nobel Committee be dusting off medals?

Click here to read my full article at The Atlantic

New paper about HIV-related tuberculosis

We found that HIV-infected adults who had tuberculosis before had double the risk of getting tuberculosis again. We should target preventive interventions here.

Click here to read my article in Clinical Infectious Diseases