The COVID-19 pandemic has precipitated a global crisis, with more than 1,430,000 confirmed cases and more than 85,000 confirmed deaths globally as of 9 April 2020 1-4 . Mitigation and suppression of new infections have emerged as the two predominant public health control strategies 5 . Both strategies focus on reducing new infections by limiting human-to-human interactions, which could be both socially and economically unsustainable in the long term. We have developed and analyzed an epidemiological intervention model that leverages serological tests 6,7 to identify and deploy recovered individuals 8 as focal points for sustaining safer interactions via interaction substitution, developing what we term 'shield immunity' at the population scale. The objective of a shield immunity strategy is to help to sustain the interactions necessary for the functioning of essential goods and services 9 while reducing the probability of transmission. Our shield immunity approach could substantively reduce the length and reduce the overall burden of the current outbreak, and can work synergistically with social distancing. The present model highlights the value of serological testing as part of intervention strategies, in addition to its well-recognized roles in estimating prevalence 10,11 and in the potential development of plasma-based therapies 12-15 .In the absence of reliable pharmaceutical interventions against SARS-CoV-2, multiple public health strategies are being deployed to slow the coronavirus pandemic 1,5,16 . These strategies can be broadly grouped into two approaches: mitigation and suppression. Mitigation includes a combination of social distancing (including school and university closures), case testing and symptomatic case isolation to reduce epidemic spread and burden on hospitals. Mitigation is intended to lessen an outbreak. However, the number of cases might still overwhelm health services 5 . Some jurisdictions have either preemptively or reactively adopted a combination of travel restrictions (shown to be effective in curtailing dispersion if implemented early enough 17,18 ) and suppression, which involves imposing complete shutdowns of the bulk of non-essential services for extended periods. Suppression strategies have led to marked decreases in new case rates in the short term by combining case isolation, quarantine, use of separate facilities for treating COVID-19 patients and large-scale

The genus Micromonas comprises phytoplankton that show among the widest latitudinal distributions on Earth, and members of this genus are recurrently infected by prasinoviruses in contrasted thermal ecosystems. In this study, we assessed how temperature influences the interplay between the main genetic clades of this prominent microalga and their viruses. The growth of three Micromonas strains (Mic-A, Mic-B, Mic-C) and the stability of their respective lytic viruses (MicV-A, MicV-B, MicV-C) were measured over a thermal range of 4-32.5°C. Similar growth temperature optima (T opt ) were predicted for all three hosts but Mic-B exhibited a broader thermal tolerance than Mic-A and Mic-C, suggesting distinct thermoacclimation strategies. Similarly, the MicV-C virus displayed a remarkable thermal stability compared with MicV-A and MicV-B. Despite these divergences, infection dynamics showed that temperatures below T opt lengthened lytic cycle kinetics and reduced viral yield and, notably, that infection at temperatures above T opt did not usually result in cell lysis. Two mechanisms operated depending on the temperature and the biological system. Hosts either prevented the production of viral progeny or maintained their ability to produce virions with no apparent cell lysis, pointing to a possible switch in the viral life strategy. Hence, temperature changes critically affect the outcome of Micromonas infection and have implications for ocean biogeochemistry and evolution.