Abstract
Previous research has linked perceived social isolation (loneliness) to reduced antiviral immunity, but the immunologic effects of the objective social isolation imposed by pandemic "shelter in place" (SIP) policies is unknown. We assessed the immunologic impact of SIP by relocating 21 adult male rhesus macaques from 2,000-m2 field cage communities of 70 to 132 other macaques to 2 wk of individual housing in indoor shelters. SIP was associated with 30% to 50% reductions in all circulating immune cell populations (lymphocytes, monocytes, and granulocytes), down-regulation of Type I interferon (IFN) antiviral gene expression, and a relative up-regulation of CD16- classical monocytes. These effects emerged within the first 48 h of SIP, persisted for at least 2 wk, and abated within 4 wk of return to social housing. A subsequent round of SIP in the presence of a novel juvenile macaque showed comparable reductions in circulating immune cell populations but reversal of Type I IFN reductions and classical monocyte increases observed during individual SIP. Analyses of lymph node tissues showed parallel up-regulation of Type I IFN genes and enhanced control of viral gene expression during juvenile-partnered SIP compared to isolated SIP. These results identify a significant adverse effect of SIP social isolation on antiviral immune regulation in both circulating immune cells and lymphoid tissues, and they suggest a potential behavioral strategy for ameliorating gene regulatory impacts (but not immune cell declines) by promoting prosocial engagement during SIP.
Highlights
Previous research has linked perceived social isolation to reduced antiviral immunity, but the immunologic effects of the objective social isolation imposed by pandemic “shelter in place” (SIP) policies is unknown
We examined the impact of 2-wk SIP on immune cell population dynamics and gene regulation in 21 adult rhesus macaques, finding 30 to 50% declines in circulating immune cells, decreases in antiviral gene expression, and increased inflammatory cells in blood and inflammatory gene expression in lymph nodes
Metagenomic sequencing confirmed the functional significance of changes in host antiviral gene transcription, documenting reduced viral gene expression during juvenile-partnered SIP relative to isolated SIP in both lymph nodes and circulating immune cells
Summary
Previous research has linked perceived social isolation (loneliness) to reduced antiviral immunity, but the immunologic effects of the objective social isolation imposed by pandemic “shelter in place” (SIP) policies is unknown. These results identify a significant adverse effect of SIP social isolation on antiviral immune regulation in both circulating immune cells and lymphoid tissues, and they suggest a potential behavioral strategy for ameliorating gene regulatory impacts (but not immune cell declines) by promoting prosocial engagement during SIP. Previous experimental studies of CTRA gene regulation have shown that prosocial engagement [36], caregiving [37], and generativity [38] can reduce expression of proinflammatory genes and increase expression of Type I IFN genes (i.e., reduce the CTRA profile) These prosocial modes of behavior are hypothesized to activate central nervous system (CNS) reward circuits that subsequently inhibit the CNS threat response systems that control peripheral SNS activity and CTRA gene expression [39,40,41,42]. Declines in antiviral gene expression (but not circulating immune cells) were blocked by the presence of a novel juvenile partner during SIP, suggesting a potential strategy for maintaining antiviral immunity during SIP by enhancing prosocial engagement
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