Vox Meditantis

Flossie Wong-Staal (1946-2020) was the molecular biologist who first cloned HIV and decoded its genetic blueprint, providing the crucial evidence that this retrovirus caused AIDS. Her groundbreaking work in 1985 laid the foundation for every HIV test and treatment that followed. Born in China as Yee Ching Wong, she fled to Hong Kong as a child, became the first woman in her family to attend university, and rose to become the most-cited female scientist of the 1980s whilst working at the epicentre of the AIDS crisis.

Today we have the extraordinary privilege of speaking with Dr Flossie Wong-Staal, the pioneering virologist whose molecular detective work helped solve one of the most urgent medical mysteries of the 20th century. Dr Wong-Staal, it’s wonderful to have you with us.

Thank you for having me. It’s quite something, isn’t it, to be discussing work from forty years ago that still matters today. When I first cloned HIV in 1985, we had no idea it would become such a blueprint for tackling emerging diseases.

Let’s start with your journey. You were born Yee Ching Wong in Guangzhou in 1946, fled to Hong Kong during the Communist revolution, and eventually made your way to UCLA. What drove you from that young girl in Hong Kong to becoming a molecular biologist?

Well, you have to understand – in my family, I was absolutely the pioneer. No woman had ever worked outside the home, let alone studied science. But my parents, bless them, they saw something in me. At Maryknoll Convent School, the American nuns kept pushing me toward science because I was always asking “why?” Why did some people get sick and others didn’t? Why did diseases spread the way they did?

My teachers suggested I pick an English name for university applications. I wanted something distinctive – not the usual Mary or Susan the other girls chose. My father suggested “Flossie” after that massive typhoon that had just hit Southeast Asia. Rather fitting for someone who was about to storm into virology, wouldn’t you say?

Your decision to leave for UCLA at 18 must have been daunting.

Terrifying, more like. I spoke barely passable English, had never been away from family, and was heading to a country where I knew absolutely no one. But I was fascinated by this new field called molecular biology. The 1960s were electric with possibility – we were just beginning to understand how to manipulate DNA, how to peer into the very machinery of life.

I finished my bacteriology degree in three years, then dove straight into a Ph.D. in molecular biology. I was impatient, you see. There were so many questions I wanted to answer.

After your doctorate, you joined Robert Gallo’s laboratory at the National Cancer Institute in 1973. What was that environment like?

Bob’s lab was absolutely mad – in the best possible way. He had this medical intuition, this ability to see the big picture, and I brought the molecular tools to dissect it piece by piece. We were hunting for human retroviruses at a time when most scientists thought they didn’t exist in humans.

The early work on HTLV-1 was crucial. We proved that human retroviruses could cause cancer – specifically, certain leukaemias. This was heretical thinking then. But it prepared us perfectly for what was coming.

When AIDS emerged in 1981, you were positioned at the centre of the search for its cause.

Those years from 1981 to 1985 were absolutely dizzying. Patients were dying, the press was breathing down our necks, and we were racing against time and against other laboratories. The climate was electric with urgency and discovery, much like what you’ve seen with COVID-19.

We had this new retrovirus – what we initially called HTLV-III – but proving it caused AIDS required molecular evidence. That’s where my expertise became crucial.

Can you walk us through the technical process of cloning HIV? For our readers who understand molecular biology, what exactly did you do?

Right, let me explain this properly. In 1985, the tools we had were primitive compared to what you have now, but they were revolutionary for their time.

First, we had to isolate the viral DNA from infected cells – not the virus particles themselves, mind you, but the proviral DNA that HIV inserts into the host cell’s genome. We used restriction enzymes to cut the DNA into manageable fragments, then inserted these fragments into bacterial plasmids – essentially using bacteria as photocopying machines to produce identical copies of the viral genetic material.

The critical breakthrough was getting a complete, infectious molecular clone. This meant we had to piece together the entire HIV genome – roughly 9,000 base pairs – and show that when we transfected this cloned DNA into cells, it would produce infectious virus particles identical to the original.

We used Southern blotting techniques to map where each piece fit. Remember, we didn’t have automated sequencing then. Every step was manual, meticulous work. We’d run gels, transfer the DNA to nitrocellulose membranes, probe with radioactive tracers, and develop the results on X-ray film. Each experiment took days.

What advantages did molecular cloning provide over previous methods?

Enormous advantages. Before cloning, we were working with mixed populations of virus from patients – genetic soup, really. Each infected person carried multiple variants of HIV, all slightly different. It was like trying to understand a book when every page had different versions of the text.

Cloning gave us pure, defined genetic material. We could study exactly how HIV replicated, which genes controlled which functions, and why it was so bloody difficult to treat. More practically, it provided the basis for the second-generation HIV blood tests that detected viral DNA rather than just antibodies.

The efficiency gains were remarkable. Growing virus in culture was slow and often failed. With molecular clones, we could produce standardised virus in any laboratory, anywhere in the world.

You also discovered that HIV was highly variable within infected individuals. How did this change treatment approaches?

That discovery was absolutely crucial, though it brought sobering news. We found that HIV mutates constantly – not just between patients, but within a single infected person over time. This explained why the virus was so good at evading the immune system.

This variability had profound implications for treatment. It meant that single-drug approaches would inevitably fail as the virus mutated around them. Our data suggested that combination therapy – what became known as drug cocktails – would be necessary to stay ahead of viral evolution.

We measured error rates in HIV’s reverse transcriptase enzyme – it makes roughly one mistake per genome per replication cycle. For a virus that produces billions of copies daily, that’s extraordinary genetic flexibility.

Looking back, how do you view the controversy between your team and Luc Montagnier’s group in France over HIV discovery?

The politics of that period overshadowed the science, which was unfortunate. The French team deserves credit for the initial isolation of HIV – they published first, in May 1983. But isolation and proving causation are different scientific achievements.

Our laboratory provided the molecular proof that HIV caused AIDS. We grew the virus in continuous cell lines, cloned it completely, and demonstrated its infectious properties. Both contributions were essential.

The ugly truth is that laboratory contamination occurred. Some of our viral isolates accidentally contained French virus samples that had been sent to us for comparison. This wasn’t deliberate – it’s more common than people realise when laboratories exchange materials. But it created an absolute mess of accusations and investigations.

What frustrates me is that the scientific achievements got lost in the political noise. Patients needed answers, not arguments about priority.

You mentioned you never felt open discrimination as a woman scientist at NIH, but what challenges did you face?

Well, I was perhaps naïve, or maybe I was too focused on the work to notice subtle biases. The NIH in the 1970s and 1980s wasn’t exactly a bastion of diversity – I was often the only woman in meetings, certainly the only Asian woman.

But I had advantages. Bob Gallo supported my career completely. My work spoke for itself – by 1990, I was the most-cited female scientist of the decade. Numbers have a way of silencing critics.

The real challenge was the assumption that I was someone’s assistant rather than a principal investigator. I’d walk into meetings and people would assume I was there to take notes, not lead the discussion. That got old quickly.

You left NIH in 1990 to establish the Center for AIDS Research at UC San Diego. Why the change?

Frankly, I needed a fresh start. The HIV discovery controversy had created an atmosphere I found stifling. I wanted to build my own research program, mentor young scientists on my terms, and explore new approaches to HIV research.

At UCSD, I could pursue gene therapy approaches, investigate viral latency, and work on second-generation treatments. I was also drawn to the idea of translating our basic research more directly into clinical applications.

Plus, I’d always loved Southern California. After seventeen years of East Coast winters, the thought of year-round sunshine had definite appeal.

How do you reflect on mistakes or misjudgements during your career?

Oh, I made plenty. Early on, I was probably too trusting about laboratory security and sample tracking. The contamination issues that plagued our HIV work taught me hard lessons about documentation and quality control.

I also underestimated how vicious scientific politics could become. I thought if you did good work and published solid data, priority disputes would sort themselves out. I was wrong. Sometimes you have to fight for credit, even when it distracts from the science.

And I was perhaps too impatient with collaborators who couldn’t keep up with the pace we set. Science is a team effort, and I could have been a better team player at times.

Your work laid the foundation for rapid responses to emerging pathogens. How do you see its relevance to diseases like COVID-19?

The parallels are striking. The molecular techniques we pioneered for HIV – cloning, sequencing, genetic analysis – enabled the extraordinarily rapid response to SARS-CoV-2. Scientists had the COVID genome sequenced within weeks of the outbreak, not months or years.

The concept of combination therapy we developed for HIV influenced COVID treatment strategies. The idea that you need multiple approaches – antivirals, monoclonal antibodies, vaccines – to tackle a rapidly evolving pathogen came directly from our HIV experience.

What’s truly exciting is how the basic research infrastructure we built for HIV accelerated COVID vaccine development. The mRNA vaccine platforms had been tested for HIV vaccines first. Our failures taught lessons that enabled COVID successes.

What would you tell young women entering STEM today, particularly those from marginalised backgrounds?

First, don’t wait for permission. I didn’t ask whether molecular biology was appropriate for a Chinese woman from Hong Kong – I just did the work and let results speak for themselves.

Second, find mentors who believe in potential, not just current ability. Bob Gallo saw something in me before I’d proven anything significant. That support was transformational.

Third, embrace being different. My outsider perspective – being Chinese, being a woman, being an immigrant – gave me insights that insiders missed. Don’t try to fit in; bring your whole self to the science.

And finally, remember that science is ultimately about solving human problems. When I was cloning HIV, I wasn’t thinking about publications or citations. I was thinking about patients dying and doctors who couldn’t help them. That moral clarity will sustain you through any career challenge.

As we wrap up, what gives you the most satisfaction when you look back on your career?

You know, it’s not the awards or recognition, though those were gratifying. It’s knowing that somewhere in the world, someone is alive today because of work my laboratory did forty years ago. Every HIV test, every antiretroviral drug, every prevention strategy builds on that initial molecular foundation we laid.

Science is about extending human capability and compassion. When you’re hunched over a laboratory bench at midnight, trying to coax a stubborn virus to grow, you’re not just satisfying intellectual curiosity. You’re fighting for every person who might be helped by what you discover.

That’s what drove me then, and that’s what I hope drives the next generation of scientists. The problems may change, but the fundamental mission remains the same: use knowledge to reduce human suffering.

Dr Wong-Staal, thank you for sharing your remarkable story with us.

The pleasure was entirely mine. Keep asking those difficult questions – that’s how science advances.

Letters and emails

Following our conversation with Dr Wong-Staal, we’ve been inundated with correspondence from readers across the globe who were captivated by her insights into viral discovery, laboratory politics, and the intersection of science with human crisis. We’ve selected five particularly thoughtful letters and emails from our growing community who want to explore more about her pioneering methods, her personal journey through scientific controversy, and what wisdom she might offer to those walking in her footsteps today.

Luciana Herrera, 34, Epidemiologist, São Paulo, Brazil:
Dr Wong-Staal, you mentioned that HIV’s high mutation rate meant single-drug approaches would inevitably fail. In Latin America, we’re seeing similar challenges with dengue virus evolution and vaccine effectiveness. Could you walk us through how you actually measured those mutation rates in the 1980s without automated sequencing? And do you think the principles you discovered about viral evolution could inform our approach to other rapidly mutating pathogens like influenza or dengue?

Ah, Luciana, that’s a splendid question – and one that takes me right back to those frantic days in the laboratory when we were racing to understand this new plague.

You have to remember, we didn’t have the luxury of modern sequencing machines. No automated DNA sequencers, no real-time PCR, certainly nothing like what you use for dengue surveillance today. We were working with radioactive tracers, X-ray film, and an enormous amount of patience.

To measure HIV’s mutation rate, we used what I’d call molecular detective work. We’d take viral isolates from patients at different time points – sometimes months apart – and compare their genetic sequences manually. This meant growing virus in culture, extracting the DNA, cutting it with restriction enzymes, running endless electrophoretic gels, and doing Southern blot hybridizations. Each experiment took weeks, not hours.

The breakthrough came when we realized we could track specific regions of the viral genome – particularly the envelope gene, which codes for the surface proteins the virus uses to enter cells. We’d clone these regions into bacterial vectors, sequence perhaps fifty to a hundred clones from each time point, and literally count the differences by hand. Tedious work, but it revealed something extraordinary: HIV was mutating roughly a thousand times faster than any DNA virus we’d studied.

We calculated that HIV’s reverse transcriptase enzyme – the one that converts viral RNA into DNA – made approximately one error per 10,000 nucleotides copied. That might sound accurate, but consider that HIV replicates billions of times daily in an infected person. The mathematics were staggering – every possible single mutation was likely occurring somewhere in the patient every day.

What made this particularly relevant to your dengue work is that we discovered HIV existed as what Manfred Eigen had called “quasi-species” – not a single virus, but a swarm of related variants. This concept has proven crucial for understanding all RNA viruses, including dengue. The principles we established – that high mutation rates allow rapid adaptation but also create vulnerability if you can push the virus beyond its error threshold – are directly applicable to flaviviruses like dengue.

The methods we pioneered – molecular cloning, sequence comparison over time, mathematical modelling of viral evolution – became the foundation for modern viral surveillance. Your dengue monitoring systems use the same basic principles, just with infinitely better tools. What took us months in the 1980s, you can accomplish in days with deep sequencing and computational analysis.

The sobering lesson we learned was that any single-drug approach would inevitably fail against such a rapidly evolving target. This insight drove the development of combination therapy – hitting the virus with multiple drugs simultaneously so it couldn’t easily mutate around all of them. I suspect similar principles will prove essential for dengue vaccine development, given the virus’s own impressive capacity for antigenic variation.

Arun Chatterjee, 28, Biotechnology PhD Student, Mumbai, India:
What fascinates me is how you managed to create infectious molecular clones using such basic tools compared to what we have today. When you were piecing together those 9,000 base pairs of the HIV genome, what was your strategy for ensuring you hadn’t introduced artifacts or mutations during the cloning process? Did you have any quality control methods, and how confident could you be that your clones truly represented the original virus?

Ah, Arun, you’ve hit upon one of the most critical aspects of our work – and frankly, one of the most nerve-wracking parts of those early days. Remember, we were working without a safety net. No automated sequencers to catch our mistakes, no computer programs to verify our constructs. Everything depended on meticulous technique and, honestly, a fair bit of luck.

Our approach to quality control was essentially forensic work. When we assembled those 9,000 base pairs of HIV, we had to piece together multiple restriction fragments – sometimes twenty or thirty pieces from different cloning vectors. Each junction was a potential failure point where we could introduce artifacts.

First, we used what we called “restriction mapping” – cutting our clones with multiple enzymes and running the fragments on agarose gels next to known standards. If the banding patterns matched our predictions, we knew the gross structure was correct. But that only caught major rearrangements or deletions.

For finer detail, we relied on Southern blot hybridization using radiolabelled probes specific to different regions of the HIV genome. We’d probe our clones against known viral sequences to confirm we had the right pieces in the right orientation. Time-consuming work – each blot took three or four days to develop.

The real test, though, was biological activity. We’d transfect our molecular clones into human T-cell lines – particularly H9 cells, which were permissive for HIV infection – and look for viral protein production. We used immunofluorescence assays to detect viral antigens, and we’d monitor for reverse transcriptase activity in the culture supernatants. If we saw both, we knew we had infectious virus.

But here’s the thing – we had no way to sequence the entire clone routinely. DNA sequencing in 1985 meant Maxam-Gilbert chemical sequencing or Sanger’s dideoxy method, both done manually. Sequencing 9,000 base pairs would have taken months and cost a fortune. So we spot-checked critical regions – the long terminal repeats, key regulatory sequences, parts of the envelope gene – using short sequencing runs.

Our confidence levels were probably lower than what you’d accept today. We were working on faith that our techniques were sound and that the biological assays would catch major problems. Looking back, it was rather terrifying how much we trusted to careful pipetting and prayer.

The breakthrough that gave us real confidence was when we compared our clonal virus to the original clinical isolates in head-to-head experiments. Same growth kinetics, same cytopathic effects, same antigenic properties. When multiple independent assays told the same story, we knew we had something genuine.

Of course, we later discovered that some of our early clones carried passengers – additional DNA sequences that had no business being there. But the core HIV sequences were intact, which was what mattered for proving viral causation of AIDS.

The irony is that today’s automated systems, for all their sophistication, sometimes miss things we would have caught with our crude methods. There’s something to be said for understanding every step of your process intimately, even if it takes six months longer.

Adeola Akinyemi, 41, Science Policy Researcher, Lagos, Nigeria:
You’ve spoken about being an outsider bringing fresh perspective to virology. As someone who studies how scientific knowledge travels across borders, I’m curious about something more personal: How did your experience as a refugee from China, then an immigrant student in America, actually shape your scientific thinking? Did that displacement give you insights into viral behaviour – perhaps seeing patterns that researchers who’d never left their home countries might miss?

Adeola, what a profound question – and one that gets to the heart of how scientific insight develops. You know, I never really thought about my refugee experience as shaping my virology work until much later in my career, but looking back, the connections are absolutely striking.

When you’re six years old and your family suddenly packs everything into suitcases and flees across a border, you develop a very acute sense of how quickly familiar worlds can collapse. In Hong Kong, we were always temporary – refugees waiting to see what would happen next. That uncertainty taught me to look for patterns others might miss, to pay attention to early warning signs.

In the laboratory, this translated into what I’d call “outsider alertness.” When we first started seeing these strange immunodeficiency cases in 1981, many established researchers dismissed them as anomalies – perhaps drug reactions or rare genetic disorders. But having lived through upheaval, I recognised the hallmarks of something spreading silently through a population. Displacement teaches you that what looks stable on the surface can be utterly transformed underneath.

More practically, being an immigrant meant I never took scientific dogma for granted. American-born scientists had learned certain “rules” about how viruses behaved, what was possible, what wasn’t worth investigating. I hadn’t internalised those limitations. When we proposed that a retrovirus might cause AIDS, senior colleagues said it was unlikely – retroviruses were associated with cancer, not immunodeficiency. But I hadn’t been raised on those assumptions.

My language experience also proved crucial. In Hong Kong, I grew up switching between Cantonese, Mandarin, and English depending on context – different languages for different worlds. This mental flexibility turned out to be essential for molecular biology, where you’re constantly translating between different representational systems – genetic code, protein structure, cellular behaviour, clinical symptoms. Each tells part of the story, but you need all of them to understand what’s really happening.

Perhaps most importantly, being displaced taught me that identity is fluid, not fixed. I’d been Yee Ching in China, become something different in Hong Kong, then reinvented myself again as Flossie in America. This prepared me to think about HIV in similarly fluid terms – not as a static entity, but as something constantly changing, adapting, evolving.

The refugee experience also gave me a particular urgency about time. When you’ve seen how quickly everything can change, you don’t have the luxury of leisurely academic contemplation. Those early AIDS years, when patients were dying and we had no answers – that felt familiar in a way that perhaps wasn’t true for colleagues who’d never experienced crisis.

Culturally, being Chinese meant I approached problems more collectively than individually. Western science often celebrates the lone genius, but my upbringing emphasised group harmony and shared responsibility. This made me a natural collaborator, which was essential for tackling something as complex as HIV. No single laboratory could solve it alone.

I also think growing up between cultures gave me a different relationship with authority. In Chinese culture, you respect your elders and teachers, but in American culture, you’re encouraged to challenge established ideas. I learned to do both – to be respectful but not deferential, to question assumptions while maintaining collegial relationships.

The irony is that HIV itself is a kind of immigrant virus – it crossed species barriers, adapted to new host environments, evolved rapidly to survive in unfamiliar territory. Understanding its behaviour required someone who instinctively grasped what it meant to navigate between worlds, to constantly adapt while maintaining core identity.

Matteo Bianchi, 45, Philosophy of Science Professor, Rome, Italy:
Here’s a thought experiment that keeps me awake at night: What if HIV had emerged not in the early 1980s, but in 1995, when molecular biology tools were more advanced, or alternatively, in 1970, when they were even more primitive? How do you think the different technological landscapes would have changed not just the timeline of discovery, but the actual scientific questions you could ask and the public health responses that would have been possible?

Matteo, what a fascinating thought experiment! You know, timing in science is everything – not just when discoveries happen, but what tools are available to understand them. I’ve thought about this quite a bit, actually, because our HIV work sat right at this crucial inflection point in molecular biology.

If HIV had emerged in 1970, frankly, we’d have been stuffed. We barely had restriction enzymes then – Werner Arber and Hamilton Smith had just discovered them. No cloning vectors, no DNA sequencing, certainly no way to culture T-cells reliably. We would have been looking at this immunodeficiency syndrome with 1950s tools – essentially just clinical observation and crude serology.

The tragedy is that patients would have died for decades while we fumbled around with electron microscopy and tissue culture, trying to prove viral causation. Without molecular cloning, we couldn’t have demonstrated Koch’s postulates definitively. The whole Gallo versus Montagnier controversy would have been moot because neither laboratory could have provided definitive molecular proof.

But here’s what’s interesting – the epidemic might have evolved differently. In 1970, global travel was more limited, sexual liberation was just beginning, and the blood supply wasn’t yet commercialised on today’s scale. The virus might have remained more geographically contained, giving us more time even with primitive tools.

Now, if HIV had emerged in 1995 – completely different ballgame. By then we had automated DNA sequencers, PCR was routine, cell culture was standardised. The Human Genome Project was well underway, so we understood genetic databases and bioinformatics. Most crucially, we had experience with other retroviruses and established protocols for viral isolation.

I suspect we would have had the viral sequence within months, not years. Phylogenetic analysis would have immediately revealed its relationship to simian immunodeficiency viruses, solving the origin question that took us decades. Drug screening could have begun immediately using established high-throughput methods.

But here’s the paradox – the urgency that drove our discoveries might not have existed. In 1995, we had effective treatments for many viral diseases. The scientific community might have approached HIV more methodically, perhaps missing the window for rapid intervention.

What really strikes me is how the technological landscape shaped not just our methods, but our questions. In 1985, we were asking “What is this virus?” and “How do we prove it causes AIDS?” With 1995 tools, we’d immediately be asking “How do we target its replication cycle?” and “Can we prevent integration into the host genome?”

The social response would have been completely different too. In 1970, the stigma around homosexuality was even more entrenched, and public health responses more paternalistic. But by 1995, we had activist movements, patient advocacy groups, and established frameworks for drug approval. The activism that transformed AIDS research simply wouldn’t have been necessary.

Most intriguingly, if HIV had waited until 1995, we might never have developed the collaborative research model that emerged from the AIDS crisis. The urgency forced unprecedented cooperation between basic scientists, clinicians, epidemiologists, and patient advocates. That model now guides our response to every emerging pathogen, from SARS to COVID-19.

So while better tools would have accelerated discovery, they might have slowed innovation in research methodology and public health response. Sometimes scientific progress requires the right problem at the right time with just adequate tools – enough to make breakthroughs possible, but not so much that you lose the urgency that drives real innovation.

Kayla Patterson, 29, Biotech Startup Founder, Toronto, Canada:
If you could go back and change one decision you made during the HIV discovery years – not the science itself, but maybe how you handled the politics, the media attention, or the credit disputes – what would it be? I ask because as women in science today, we still struggle with visibility and recognition. Looking back with four decades of hindsight, is there anything you’d do differently to protect your contributions or your team’s morale during those intense years?

Kayla, that’s a question that cuts right to the bone – and one I’ve thought about plenty over the years. You know, looking back with four decades of hindsight, there’s definitely one decision I’d change completely.

I should have been much more assertive about ensuring my name appeared on the key publications as first author, not just a co-author buried in the middle of a long list. When we published our HIV cloning work, I did the majority of the molecular biology – the restriction mapping, the cloning, the sequence analysis. But academic protocol at the time dictated that the senior scientist, Bob Gallo, would be the corresponding author, and his name carried more weight in the field.

Here’s what I didn’t grasp then: in science, authorship order determines historical credit. Decades later, when people reference “the HIV discovery,” they mention Gallo or Montagnier, rarely the women who actually did much of the bench work. I was so focused on getting the science right and published quickly – patients were dying, remember – that I didn’t fight hard enough for proper attribution.

My mother always taught me not to make waves, to be gracious and let my work speak for itself. Classic Asian upbringing, right? But that’s terrible advice in competitive science. Work doesn’t speak for itself – you have to make it heard. I should have pushed back when colleagues suggested that having too many Asian names on a paper might “confuse” readers. Can you imagine? Yet I accepted it because I wanted to fit in.

I’d also handle the media attention completely differently. During the height of the HIV controversy, journalists would call looking for quotes, but I’d defer to Bob or other senior colleagues. I thought it was inappropriate for a junior scientist to speak publicly. What nonsense! I was the one who understood the molecular details better than anyone. I should have been front and centre explaining our findings.

You know what really galls me? There were several science documentaries made about HIV discovery in the 1990s. They interviewed Bob extensively, showed footage of him in the laboratory, but I was barely mentioned. When I finally complained to one producer, he said they thought viewers would find it “more compelling” to focus on the senior male scientists. As if molecular biology was less interesting when done by women!

The political battles were another place I could have been smarter. When the accusations about sample contamination started flying, I tried to stay above the fray. I thought if I just kept my head down and continued doing good science, the controversy would blow over. Wrong again. Science is politics, especially when it involves public health crises and massive research funding.

I should have cultivated relationships with science journalists, written popular articles explaining our work, spoken at more public conferences. Visibility isn’t vanity – it’s professional survival. The women who succeeded in getting proper recognition for their discoveries were the ones who learned to play that game effectively.

But here’s what I got right: I mentored every young scientist in my laboratory, especially the women and minorities. I made sure their names appeared on papers, that they presented their work at conferences, that they understood the importance of professional networking. Several of them now run their own laboratories and they’ve remembered those lessons.

My advice to women in science today? Be generous with collaboration but fierce about credit. Document everything. Keep meticulous records of who contributed what to every project. Don’t let anyone diminish your role in discoveries, even if they’re senior to you. And never, ever assume that good work automatically leads to recognition. You have to fight for your place in the scientific record.

The field has improved, but not nearly enough. I still see brilliant young women scientists being overshadowed by male colleagues who are better at self-promotion. Don’t let that happen to you.

Reflection

Dr Flossie Wong-Staal died on 8th July 2020 at the age of 73, from complications of pneumonia. Her passing marked the end of a remarkable journey that began as a six-year-old refugee fleeing China and culminated in becoming the most-cited female scientist of the 1980s.

Through our conversation, several themes emerged that illuminate both the brilliance and frustration of her career. Her ingenuity in developing molecular cloning techniques with primitive tools laid the foundation for today’s rapid pandemic responses. Yet her story also exposes the persistent erasure of women’s contributions to STEM – how authorship protocols, media narratives, and institutional hierarchies conspired to diminish recognition of her pivotal role in HIV discovery.

What strikes me most is how Wong-Staal’s perspective differed from official accounts. While historical records focus on the Gallo-Montagnier priority disputes, she revealed the profound impact of her refugee experience on scientific thinking – how displacement taught pattern recognition that proved crucial for identifying viral behaviour. Her account also highlighted the collaborative molecular detective work that official narratives often reduce to individual genius.

Gaps remain in understanding her full contributions. Laboratory contamination controversies obscured the technical precision of her cloning work, whilst the focus on senior male colleagues overshadowed her molecular insights that enabled every subsequent HIV test and treatment.

Today, as scientists tackle COVID-19 variants and prepare for future pandemics, they rely on the very techniques Wong-Staal pioneered – viral cloning, genetic sequencing, combination therapy principles. Her methods now inform responses to emerging pathogens from SARS to monkeypox.

Perhaps her greatest legacy lies not just in the science, but in her final advice: be generous with collaboration but fierce about credit. In an era when women still struggle for visibility in STEM, Wong-Staal’s story reminds us that brilliance alone isn’t enough – we must also fight to ensure our voices are heard in the scientific record.

Who have we missed?

This series is all about recovering the voices history left behind – and I’d love your help finding the next one. If there’s a woman in STEM you think deserves to be interviewed in this way – whether a forgotten inventor, unsung technician, or overlooked researcher – please share her story.

Email me at voxmeditantis@gmail.com or leave a comment below with your suggestion – even just a name is a great start. Let’s keep uncovering the women who shaped science and innovation, one conversation at a time.

Editorial Note: This interview is a dramatised reconstruction based on extensive historical research, published papers, archived interviews, and biographical sources about Dr Flossie Wong-Staal‘s life and scientific contributions. Whilst grounded in documented facts about her work, personal background, and the scientific context of her era, the specific dialogue and responses represent an informed interpretation of her likely perspectives and voice. This reconstruction aims to honour her legacy whilst acknowledging the inherent limitations of posthumous interviews in capturing the full complexity of any individual’s lived experience.

Bob Lynn | © 2025 Vox Meditantis. All rights reserved. | 🌐 Translate