If we just take the average number of partners, we are ignoring the fact that not everyone’s sex lives are the same. This variability is important: if someone has a lot of partners, we’d expect them to be both more likely to get infected and more likely to pass the infection on. We therefore need to account for the fact that they can contribute to transmission in these two different ways. Yorke and his colleagues argued that this might explain why there could be a gonorrhea epidemic, despite people having few partnerships on average: people with lots of contacts might be contributing disproportionality to the spread, pushing the reproduction number above one. Anderson and May would later show that the more variation there was in the number of partners people had, the higher we’d expect the reproduction number to be.
Identifying people who are at higher risk – and finding ways to reduce this risk – can help stop an outbreak in its early stages. In the late 1980s, Anderson and May suggested that STIs would initially spread quickly through such high-risk groups, even though the overall outbreak would be smaller than we’d expect if everyone mixed at random.[61]
By breaking contagion down into its basic DOTS components – duration, opportunities, transmission probability, susceptibility – and thinking about how network structure affects contagion, we can also estimate the risk posed by a new STI. In 2008, an American scientist returned home to Colorado after a month working in Senegal. A week later, he’d fallen ill with a headache, extreme tiredness, and a rash on his torso. Soon after, his wife – who hadn’t travelled – developed the same symptoms. Subsequent lab tests indicated both had been exposed to the Zika virus. Prior Zika research had focused on transmission from mosquitoes, but the Colorado incident suggested the virus had access to another route: it could infect people during sexual encounters.[62] As Zika spread around the globe in 2015–16, more reports of sexual transmission would follow, fueling speculation about a new type of outbreak. ‘Zika: The Millennials’ S.T.D.?’ asked one opinion piece in the New York Times during 2016.[63]
Based on the DOTS for Zika, our research group estimated that the reproduction number for sexual transmission was below one; the virus would probably not cause an STI epidemic. Zika could potentially cause small outbreaks in groups with a lot of sexual contacts, but it was unlikely to pose a major risk in areas without mosquitoes.[64] Unfortunately, the same has not been true for other STIs.
Gaëtan dugas was blond, charming, and had a lot of sex. A Canadian flight attendant, he’d slept with over two hundred men a year prior to March 1984, when he died of aids a few weeks after his 31st birthday. Three years later, journalist Randy Shilts featured Dugas in his bestselling book And the Band Played On. Shilts suggested that Dugas had played a central part in the early spread of the disease. He dubbed Dugas ‘patient zero’, a term still used today to refer to the first case in an outbreak. Shilts’ book fuelled speculation that Dugas was the person who introduced the epidemic to North America. The New York Post called him ‘The Man Who Gave Us aids’; the National Review said he was ‘the Columbus of aids’.
The idea of Dugas as patient zero was certainly attention-grabbing, and has been repeated often in the decades since. But it turned out to be fiction. In 2016, a team of researchers published an analysis of hiv viruses from a range of patients, including men diagnosed with aids in the 1970s and Dugas himself. Based on the genetic diversity of these viruses and the rate of hiv evolution, the team estimated that hiv had arrived into North America in 1970 or 1971. However, they found no evidence that Dugas had introduced hiv to the US. He was just another case in a much wider epidemic.[65]
So how did the patient zero designation come about? In the original outbreak investigation, Dugas hadn’t actually been listed as ‘Patient 0’, but rather as ‘Patient O’, the ‘O’ short for ‘Outside California’. In 1984, William Darrow, a researcher with the Centers for Disease Control and Prevention (CDC), had been assigned to investigate a cluster of deaths among gay men in Los Angeles.[66] The CDC generally gave each case a number based on the order in which they had been reported, but the cases had been relabelled for the LA analysis. Before Dugas had been linked to the Los Angeles cluster, he was simply ‘Patient 057’.
When investigators traced how the cases were linked, it suggested that the deaths might be the result of an as-yet-unknown STI. Dugas appeared prominently in the network, with links to multiple cases in New York and LA. This was in part because he’d tried to help the investigators, naming 72 of his partners in the preceding three years. Darrow pointed out that this had always been the aim of the investigation: to understand how cases were linked, rather than find out who had started the outbreak. ‘I never said that he was the first case in the United States,’ he later commented.
When investigating outbreaks, we face a gap between what we want to know and what we can measure. Ideally, we’d have data on all the ways in which people are connected, and how infection has spread through these links. What we can actually measure is very different. A typical outbreak investigation will reconstruct some of the links between people who were infected. Depending on which
