Social distancing and isolation have been widely introduced to counter the COVID-19 pandemic. Adverse social, psychological and economic consequences of a complete or near-complete lockdown demand the development of more moderate contact-reduction policies. Adopting a social network approach, we evaluate the effectiveness of three distancing strategies designed to keep the curve flat and aid compliance in a post-lockdown world. These are: limiting interaction to a few repeated contacts akin to forming social bubbles; seeking similarity across contacts; and strengthening communities via triadic strategies. We simulate stochastic infection curves incorporating core elements from infection models, ideal-type social network models and statistical relational event models. We demonstrate that a strategic social network-based reduction of contact strongly enhances the effectiveness of social distancing measures while keeping risks lower. We provide scientific evidence for effective social distancing that can be applied in public health messaging and that can mitigate negative consequences of social isolation.

BackgroundStudies have suggested that CMV infection may influence cardiovascular disease (CVD) risk and mortality. However, there have been no large-scale examinations of these relationships among demographically diverse populations. The inflammatory marker C-reactive protein (CRP) is also linked with CVD outcomes and mortality and may play an important role in the pathway between CMV and mortality. We utilized a U.S. nationally representative study to examine whether CMV infection is associated with all-cause and CVD-related mortality. We also assessed whether CRP level mediated or modified these relationships.Methodology/Principal FindingsData come from subjects ≥25 years of age who were tested for CMV and CRP level and were eligible for mortality follow-up on December 31st, 2006 (N = 14153) in the National Health and Nutrition Examination Survey (NHANES) III (1988–1994). Cox proportional hazard models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI) for all-cause and CVD-related mortality by CMV serostatus. After adjusting for multiple confounders, CMV seropositivity remained statistically significantly associated with all-cause mortality (HR 1.19, 95% CI: 1.01, 1.41). The association between CMV and CVD-related mortality did not achieve statistical significance after confounder adjustment. CRP did not mediate these associations. However, CMV seropositive individuals with high CRP levels showed a 30.1% higher risk for all-cause mortality and 29.5% higher risk for CVD-related mortality compared to CMV seropositive individuals with low CRP levels.Conclusions/SignificanceCMV was associated with a significant increased risk for all-cause mortality and CMV seropositive subjects who also had high CRP levels were at substantially higher risk for both for all-cause and CVD-related mortality than subjects with low CRP levels. Future work should target the mechanisms by which CMV infection and low-level inflammation interact to yield significant impact on mortality.

Current empirical evidence linking SES to cortisol and AL is weak. Future work should standardize approaches to measuring SES, chronic stress and cortisol to better understand these relationships.