Background South Africa's national lockdown introduced serious threats to public mental health in a society where one in three individuals develops a psychiatric disorder during their life. We aimed to evaluate the mental health impacts of the COVID-19 pandemic using a mixed-methods design. Methods This longitudinal study drew from a preexisting sample of 957 adults living in Soweto, a major township near Johannesburg. Psychological assessments were administered across two waves between August 2019 and March 2020 and during the first 6 weeks of the lockdown (late March–early May 2020). Interviews on COVID-19 experiences were administered in the second wave. Multiple regression models examined relationships between perceived COVID-19 risk and depression. Results Full data on perceived COVID-19 risk, depression, and covariates were available in 221 adults. In total, 14.5% of adults were at risk for depression. Higher perceived COVID-19 risk predicted greater depressive symptoms (p < 0.001), particularly among adults with histories of childhood trauma, though this effect was marginally significant (p = 0.063). Adults were about two times more likely to experience significant depressive symptoms for every one unit increase in perceived COVID-19 risk (p = 0.021; 95% CI 1.10–3.39). Qualitative data identified potent experiences of anxiety, financial insecurity, fear of infection, and rumination. Conclusions Higher perceived risk of COVID-19 infection is associated with greater depressive symptoms during the first 6 weeks of quarantine. High rates of severe mental illness and low availability of mental healthcare amidst COVID-19 emphasize the need for immediate and accessible psychological resources.

Prenatal exposure to maternal stress is commonly associated with variation in Hypothalamic Pituitary Adrenal (HPA)-axis functioning in offspring. However, the strength or consistency of this response has never been empirically evaluated across vertebrate species. Here we meta-analyzed 114 results from 39 studies across 14 vertebrate species using Bayesian phylogenetic mixed-effects models. We found a positive overall effect of prenatal stress on offspring glucocorticoids (d’ = 0.43) though the 95% Highest Posterior Density Interval overlapped with 0 (−0.16–0.95). Meta-regressions of potential moderators highlighted that phylogeny and life history variables predicted relatively little variation in effect size. Experimental studies (d’ = 0.64) produced stronger effects than observational ones (d’ = −0.01), while prenatal stress affected glucocorticoid recovery following offspring stress exposure more strongly (d’ = 0.75) than baseline levels (d’ = 0.48) or glucocorticoid peak response (d’ = 0.36). These findings are consistent with the argument that HPA-axis sensitivity to prenatal stress is evolutionarily ancient and occurs regardless of a species’ overall life history strategy. These effects may therefore be especially important for mediating intra-specific life-history variation. In addition, these findings suggest that animal models of prenatal HPA-axis programming may be appropriate for studying similar effects in humans.