Tsimané and Moseten Communities Had Widespread COVID-19 but Few Deaths

In June 2020, the first people in the Tsimané and Moseten territories of lowland Bolivia began reporting a familiar cluster of symptoms: fever, cough, weakness, headache and the sudden loss of taste or smell. By August, the outbreak was peaking at an estimated 250 to 300 new cases a day. The virus had reached communities that had tried voluntary collective isolation, then moved rapidly through them.

“COVID spread far and wide in the communities and it wasn’t just a minor thing,” Michael Gurven, an anthropologist at the University of California, Santa Barbara and a co-author of the study, said in a university press release. The Tsimané and Moseten live with limited access to hospitals and other medical services, and Indigenous communities around the world were widely considered at risk of disproportionate harm from COVID-19. A systematic review of 153 publications found that health-care access, poverty, communication and ecological conditions were among the systemic pressures shaping Indigenous communities’ pandemic experiences.

But when researchers reconstructed the first wave using interviews, blood samples and death surveillance, the expected catastrophe did not appear. SARS-CoV-2 had infected a majority of adults in both populations. Symptoms were common. Yet only three people died.

The Virus Reached Most Adults

The research team interviewed adults in 19 Tsimané and eight Moseten villages from July to December 2020, then followed up with some people through May 2021. They interviewed 85.4% of Tsimané adults in the study villages and 38.3% of Moseten adults. Blood samples were obtained from 42.0% and 38.6%, respectively, and tested for antibodies against SARS-CoV-2.

The antibody results put infection prevalence at 71.4% among 685 sampled Tsimané adults and 63.0% among 562 sampled Moseten adults. In the French comparison cohort tested with the same laboratory approach over a comparable period, the figure was 4.0%. Isolation had delayed neither the virus nor a high attack rate once it entered the communities.

Nor was this a largely silent outbreak. Among participants with SARS-CoV-2 antibodies, 79.5% reported one or more symptoms. Headache was reported by 73.5%, weakness or fatigue by 66.4%, fever by 61.2%, cough by 61.1% and loss of taste or smell by 54.5%. Half said they had been ill for more than a week, including one third who reported illness lasting more than two weeks.

Three Deaths Defied the Expected Pattern

One Tsimané man, aged 79, and two Moseten men, aged 67 and 71, died during the first wave. The resulting infection-fatality ratios were 0.009% for the Tsimané and 0.095% for the Moseten. Infection-fatality ratio means the proportion of infected people, not merely diagnosed cases, who die.

Age is normally the dominant driver of COVID-19 fatality. A global pre-vaccine analysis found that infection-fatality risk rises sharply after age 30, reaching an estimated 1.0% at age 60, 2.9% at age 70 and 8.0% at age 80. It also found that population age structure accounted for much of the cross-country variation in overall fatality rates. That analysis provides the backdrop for why the young demographic profile of the Tsimané and Moseten matters, but not enough to settle the Bolivian result.

The researchers modelled what mortality might have looked like if the populations had the same age structure and prevalence of hypertension, diabetes and obesity as France, the United States or the world at large. Their youthfulness did most of the explanatory work. Yet after retaining the populations’ actual age structures and low levels of metabolic disease, the model still projected 23 deaths among the Tsimané and 10 among the Moseten. The observed totals, one and two, remained far lower.

The Immune Response Looked Different

Blood collected after the outbreak carried a conspicuous signal. Among people who tested positive, anti-SARS-CoV-2 antibody levels were higher in the Moseten, then the Tsimané, than in the French comparison population. More than half of positive Tsimané and Moseten samples also contained neutralising antibodies, compared with 1.1% in the French sample over the same period.

These antibodies appeared after infection, so they cannot themselves explain why people avoided severe disease earlier in the illness. Instead, the team treats them as a possible marker of a more vigorous or effective response during the initial, flu-like phase, before infection reaches the lungs and triggers the dangerous inflammatory damage associated with severe COVID-19.

“The Tsimané still experienced that first stage of COVID, but they never quite got to that second stage where it enters your lungs,” Gurven said. He was describing the pattern researchers inferred from the outbreak, in which symptomatic infections were common but the overwhelming majority did not appear to progress to the severe pulmonary disease associated with respiratory support and death.

That idea fits older observations from the Tsimané, but it also introduces a complication. A 2016 study of 6,338 Tsimané people found elevated levels of several immune measures, including immunoglobulins, eosinophils, B cells and natural killer cells compared with US and European reference populations. The same study also found depleted naïve CD4 cells in older age groups. The immune profile is therefore different, not simply stronger.

Parasites May Regulate, Not Arm, Immunity

The Tsimané and Moseten are forager-horticulturalist populations with high lifetime exposure to pathogens and parasites. The new study proposes that this background may help maintain immune readiness while also improving regulation, allowing an early response to infection without the uncontrolled inflammation that can damage lungs and other organs.

There is some supporting evidence for the regulation part of that hypothesis. In a separate study of 179 Tsimané adults, helminth infection and higher eosinophil counts were associated with dampened cytokine responses when blood was exposed in the laboratory to H1N1 vaccine or bacterial material. That work did not test SARS-CoV-2 infection or COVID-19 outcomes, so it cannot show that parasites protected these communities. It does, however, show a biologically plausible route by which chronic parasite exposure could change inflammatory responses.

Physical activity may also have contributed. Both populations do demanding subsistence work, and their low prevalence of obesity, diabetes and hypertension removes established COVID-19 risk factors. In wider observational evidence, regular physical activity has been associated with lower risks of COVID-19 hospitalisation, severe illness and death, although those associations are much too modest to account by themselves for the mortality gap reported here. A meta-analysis of 1.85 million adults estimated a relative risk of COVID-19 death of 0.57 for regularly active people compared with inactive peers.

A Result That Should Not Become a Prescription

The study’s most important result is not that hardship, poor sanitation or parasite infection is good for health. The Tsimané and Moseten continue to experience substantial infectious-disease burdens and limited medical infrastructure. Many contributors could be operating at once: demographic structure, metabolic health, physical activity, prior microbial exposure, immune regulation, genetics and factors the study did not measure.

“There’s a confluence of factors that, in interaction, shape people’s risk,” Gurven said. “And so we shouldn’t be looking for a single magic bullet.” The researchers found no detectable pre-pandemic antibody cross-reactivity to SARS-CoV-2 in 43 stored samples, but those samples cannot rule out cross-reactive T-cell memory. They also did not directly measure immune responses during acute infection.

The small number of deaths means that even careful surveillance cannot resolve every uncertainty. The proposed mechanisms are leads for future work, not causal conclusions. What remains unusual is that the familiar steep rise in COVID-19 danger with age was muted in these communities.

“If there are lessons to learn that might generalize to conditions that are favorable toward being protected against infectious disease, well, that’s great,” Gurven said. “We need that.” Finding those lessons will require prospective studies that follow immune responses in real time, while respecting Indigenous governance over data and interpretation. The answer, if there is one, is likely to be a web of causes rather than a single protective ingredient.

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