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.

This study examined the relation between immune response to cytomegalovirus (CMV) and all-cause and cardiovascular disease (CVD) mortality, and possible mediating mechanisms. Data were derived from the Sacramento Area Latino Study on Aging, a population-based study of older Latinos (aged 60-101 years) in California followed in 1998-2008. CMV immunoglobulin G (IgG), tumor necrosis factor, and interleukin-6 were assayed from baseline blood draws. Data on all-cause and CVD mortality were abstracted from death certificates. Analyses included 1,468 of 1,789 participants. For individuals with CMV IgG antibody titers in the highest quartile compared with lower quartiles, fully adjusted models showed that all-cause mortality was 1.43 times (95% confidence interval: 1.14, 1.79) higher over 9 years. In fully adjusted models, the hazard of CVD mortality was also elevated (hazard ratio = 1.35, 95% confidence interval: 1.01, 1.80). A composite measure of tumor necrosis factor and interleukin-6 mediated a substantial proportion of the association between CMV and all-cause (18.9%, P < 0.001) and CVD (29.0%, P = 0.02) mortality. This study is the first known to show that high CMV IgG antibody levels are significantly related to mortality and that the relation is largely mediated by interleukin-6 and tumor necrosis factor. Further studies investigating methods for reducing IgG antibody response to CMV are warranted.

General self-rated health (SRH) is widely used to study trends and inequalities in population health. Recently, there has been an increased interest in understanding the measurement properties of SRH. This study evaluated for the first time the test-retest reliability of SRH among US adults. Analyses were based on a nationally representative sample of 9,235 adults interviewed in the 2005-2008 National Health and Nutrition Examination Survey (NHANES). Respondents reported SRH on 2 occasions (about 1 month apart). Kappa statistics, polyserial correlations, and agreement tabulations were used to assess reliability across population subgroups; regression models tested the association of sociodemographic factors and the stability of the rating. Nearly 40% of respondents changed their health rating between interviews, indicating moderate test-retest reliability of SRH. Reliability differed significantly by sociodemographic characteristics: Racial/ethnic minorities and adults with less education had lower reliability of SRH judgments. Health events between interviews did not influence consistency, but conditional on a rating change, they increased the odds of downgrading one's health. The results suggest that 1) there is a substantial amount of error in individuals' self-assessment of health and 2) reliability is worse for disadvantaged sociodemographic groups, potentially biasing estimates of health inequalities among US adults.

Background The purpose of this study is to test whether the predictive power of an individual's self-rated health (SRH) on subsequent mortality risk differs by socioeconomic status (SES) in the United States. MethodsWe use the National Health Interview Survey 1986-94 linked to Multiple Cause of Death Files 1986-97 (NHIS-MCD). Analyses are based on non-Hispanic Black and White adults 25 and older (n ¼ 358 388). Cox proportional hazard models are used to estimate the effect of SRH on mortality risk during follow-up.Interactions of SRH and level of education and SRH and level of income are used to assess differences in the predictive power of SRH for subsequent mortality risk. ResultsThe effect of SRH on subsequent mortality risk differs by level of education and level of income. Lower health ratings are more strongly associated with mortality for adults with higher education and/or higher income relative to their lower SES counterparts.Conclusions Our findings suggest that individuals with different education or income levels may evaluate their health differently with respect to the traditional five-point SRH scale, and hence their subjective health ratings may not be directly comparable. These results have important implications for research that tries to quantify and explain socioeconomic inequalities in health based on self-rated health.

BackgroundEpstein-Barr virus (EBV) is a common herpesvirus linked to infectious mononucleosis and multiple cancers. There are no national estimates of EBV seroprevalence in the United States. Our objective was to estimate the overall prevalence and sociodemographic predictors of EBV among U.S. children and adolescents aged 6–19.MethodsWe calculated prevalence estimates and prevalence ratios for EBV seroprevalence using data from the 2003–2010 U.S. National Health and Nutrition Examination Survey (NHANES) for children aged 6–19 (n = 8417). Poisson regression was used to calculate multivariable-adjusted prevalence ratios across subgroup categories (sex, race/ethnicity, parental education, household income, household size, foreign-born, BMI, and household smoking).FindingsOverall EBV seroprevalence was 66.5% (95% CI 64.3%–68.7%.). Seroprevalence increased with age, ranging from 54.1% (95% CI 50.2%–57.9%) for 6–8 year olds to 82.9% (95% CI 80.0%–85.9%) for 18–19 year olds. Females had slightly higher seroprevalence (68.9%, 95% CI 66.3%–71.6%) compared to males (64.2%, 95% CI 61.7%–66.8%). Seroprevalence was substantially higher for Mexican-Americans (85.4%, 95% CI 83.1%–87.8%) and Non-Hispanic Blacks (83.1%, 95% CI 81.1%–85.1%) than Non-Hispanic Whites (56.9%, 95% CI 54.1%–59.8%). Large differences were also seen by family income, with children in the lowest income quartile having 81.0% (95% CI 77.6%–84.5%) seroprevalence compared to 53.9% (95% CI 50.5%–57.3%) in the highest income quartile, with similar results for parental education level. These results were not explained by household size, BMI, or parental smoking. Among those who were seropositive, EBV antibody titers were significantly higher for females, Non-Hispanic Blacks and Mexican-Americans, with no association found for socioeconomic factors.ConclusionsIn the first nationally representative U.S. estimates, we found substantial socioeconomic and race/ethnic differences in the seroprevalence of EBV across all ages for U.S. children and adolescents. These estimates can help researchers and clinicians identify groups most at risk, inform research on EBV-cancer etiology, and motivate potential vaccine development.

SummaryThere is a strong relationship between socioeconomic status (SES) and health outcomes in the U.S, though the mechanisms are poorly understood. Increasing evidence points to links between lifelong exposure to infectious disease and subsequent chronic disease. Exposure and susceptibility to infections may be one way SES affects long-term health, though little populationbased research to date has examined social patterning of infections in the U.S. This paper tests the relationship between income, education, race/ethnicity and seroprevalence of cytomegalovirus (CMV) infection at different ages in a representative sample of the U.S. population, and tests potential mediators for these relationships. The study finds significant racial and socioeconomic disparities in CMV seroprevalence beginning at early ages and persisting into middle age. Potential exposures do not explain the relationship between socioeconomic status and CMV positivity. Because reactivation of latent CMV infections may contribute to chronic disease and immune decline later in life, future research should determine the exposure or susceptibility pathways responsible for these disparities in the prevalence of CMV infection.