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AbstractFinancial incentives to encourage healthy and prosocial behaviours often trigger initial behavioural change1–11, but a large academic literature warns against using them12–16. Critics warn that financial incentives can crowd out prosocial motivations and reduce perceived safety and trust, thereby reducing healthy behaviours when no payments are offered and eroding morals more generally17–24. Here we report findings from a large-scale, pre-registered study in Sweden that causally measures the unintended consequences of offering financial incentives for taking the first dose of a COVID-19 vaccine. We use a unique combination of random exposure to financial incentives, population-wide administrative vaccination records and rich survey data. We find no negative consequences of financial incentives; we can reject even small negative impacts of offering financial incentives on future vaccination uptake, morals, trust and perceived safety. In a complementary study, we find that informing US residents about the existence of state incentive programmes also has no negative consequences. Our findings inform not only the academic debate on financial incentives for behaviour change but also policy-makers who consider using financial incentives to change behaviour.

Acute viral infections can have durable functional impacts on the immune system long after recovery, but how they affect homeostatic immune states and responses to future perturbations remain poorly understood

During the COVID-19 pandemic, sizeable groups of unvaccinated people persist even in countries with high vaccine access1. As a consequence, vaccination became a controversial subject of debate and even protest2. Here we assess whether people express discriminatory attitudes in the form of negative affectivity, stereotypes and exclusionary attitudes in family and political settings across groups defined by COVID-19 vaccination status. We quantify discriminatory attitudes between vaccinated and unvaccinated citizens in 21 countries, covering a diverse set of cultures across the world. Across three conjoined experimental studies (n = 15,233), we demonstrate that vaccinated people express discriminatory attitudes towards unvaccinated individuals at a level as high as discriminatory attitudes that are commonly aimed at immigrant and minority populations3-5. By contrast, there is an absence of evidence that unvaccinated individuals display discriminatory attitudes towards vaccinated people, except for the presence of negative affectivity in Germany and the USA. We find evidence in support of discriminatory attitudes against unvaccinated individuals in all countries except for Hungary and Romania, and find that discriminatory attitudes are more strongly expressed in cultures with stronger cooperative norms. Previous research on the psychology of cooperation has shown that individuals react negatively against perceived 'free-riders'6,7, including in the domain of vaccinations8,9. Consistent with this, we find that contributors to the public good of epidemic control (that is, vaccinated individuals) react with discriminatory attitudes towards perceived free-riders (that is, unvaccinated individuals). National leaders and vaccinated members of the public appealed to moral obligations to increase COVID-19 vaccine uptake10,11, but our findings suggest that discriminatory attitudes-including support for the removal of fundamental rights-simultaneously emerged.

AbstractMiddle East respiratory syndrome coronavirus (MERS-CoV) and several bat coronaviruses use dipeptidyl peptidase-4 (DPP4) as an entry receptor1–4. However, the receptor for NeoCoV—the closest known MERS-CoV relative found in bats—remains unclear5. Here, using a pseudotype virus entry assay, we found that NeoCoV and its close relative, PDF-2180, can efficiently bind to and use specific bat angiotensin-converting enzyme 2 (ACE2) orthologues and, less favourably, human ACE2 as entry receptors through their receptor-binding domains (RBDs) on the spike (S) proteins. Cryo-electron microscopy analysis revealed an RBD–ACE2 binding interface involving protein–glycan interactions, distinct from those of other known ACE2-using coronaviruses. We identified residues 337–342 of human ACE2 as a molecular determinant restricting NeoCoV entry, whereas a NeoCoV S pseudotyped virus containing a T510F RBD mutation efficiently entered cells expressing human ACE2. Although polyclonal SARS-CoV-2 antibodies or MERS-CoV RBD-specific nanobodies did not cross-neutralize NeoCoV or PDF-2180, an ACE2-specific antibody and two broadly neutralizing betacoronavirus antibodies efficiently inhibited these two pseudotyped viruses. We describe MERS-CoV-related viruses that use ACE2 as an entry receptor, underscoring a promiscuity of receptor use and a potential zoonotic threat.

AbstractFeedback inhibition of humoral immunity by antibodies was first documented in 19091. Subsequent studies showed that, depending on the context, antibodies can enhance or inhibit immune responses2,3. However, little is known about how pre-existing antibodies influence the development of memory B cells. Here we examined the memory B cell response in individuals who received two high-affinity anti-SARS-CoV-2 monoclonal antibodies and subsequently two doses of an mRNA vaccine4–8. We found that the recipients of the monoclonal antibodies produced antigen-binding and neutralizing titres that were only fractionally lower compared than in control individuals. However, the memory B cells of the individuals who received the monoclonal antibodies differed from those of control individuals in that they predominantly expressed low-affinity IgM antibodies that carried small numbers of somatic mutations and showed altered receptor binding domain (RBD) target specificity, consistent with epitope masking. Moreover, only 1 out of 77 anti-RBD memory antibodies tested neutralized the virus. The mechanism underlying these findings was examined in experiments in mice that showed that germinal centres formed in the presence of the same antibodies were dominated by low-affinity B cells. Our results indicate that pre-existing high-affinity antibodies bias germinal centre and memory B cell selection through two distinct mechanisms: (1) by lowering the activation threshold for B cells, thereby permitting abundant lower-affinity clones to participate in the immune response; and (2) through direct masking of their cognate epitopes. This may in part explain the shifting target profile of memory antibodies elicited by booster vaccinations9.