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      Effect of Single Housing on Innate Immune Activation in Immunodeficiency Virus–Infected Pigtail Macaques ( Macaca nemestrina) as a Model of Psychosocial Stress in Acute HIV Infection

      , DVM, , BS, , MA, MPH, PhD, , MS, , VMD, , DVM, , MS, , MS, , BS, , DVM, , DVM, PhD, , PhD, , MS, PhD, , DVM, PhD, , DVM, PhD, , PhD, , DVM, PhD
      Psychosomatic Medicine
      Lippincott Williams & Wilkins
      simian immunodeficiency virus, psychosocial stress, innate immunity, infectious disease, animal models, human immunodeficiency virus, ART = antiretroviral therapy, B = unstandardized β coefficient, CBC = complete blood count, CSF = cerebrospinal fluid, CNS = central nervous system, HIV = human immunodeficiency virus, PWH = people with HIV, SE = standard error, SIV = simian immunodeficiency virus

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          Simian immunodeficiency virus (SIV) infection of macaques recapitulates many aspects of HIV pathogenesis and is similarly affected by both genetic and environmental factors. Psychosocial stress is associated with immune system dysregulation and worse clinical outcomes in people with HIV. This study assessed the impact of single housing, as a model of psychosocial stress, on innate immune responses of pigtailed macaques ( Macaca nemestrina) during acute SIV infection.


          A retrospective analysis of acute SIV infection of 2- to si6-year-old male pigtailed macaques was performed to compare the innate immune responses of socially ( n = 41) and singly ( n = 35) housed animals. Measures included absolute monocyte count and subsets, and in a subset ( n ≤ 18) platelet counts and activation data.


          SIV infection resulted in the expected innate immune parameter changes with a modulating effect from housing condition. Monocyte number increased after infection for both groups, driven by classical monocytes (CD14 +CD16 ), with a greater increase in socially housed animals (227%, p < .001, by day 14 compared with preinoculation time points). Platelet numbers recovered more quickly in the socially housed animals. Platelet activation (P-selectin) increased by 65% ( p = .004) and major histocompatibility complex class I surface expression by 40% ( p = .009) from preinoculation only in socially housed animals, whereas no change in these measures occurred in singly housed animals.


          Chronic psychosocial stress produced by single housing may play an immunomodulatory role in the innate immune response to acute retroviral infection. Dysregulated innate immunity could be one of the pathways by which psychosocial stress contributes to immune suppression and increased disease severity in people with HIV.

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          Social isolation has been recognized as a major risk factor for morbidity and mortality in humans for more than a quarter of a century. Although the focus of research has been on objective social roles and health behavior, the brain is the key organ for forming, monitoring, maintaining, repairing, and replacing salutary connections with others. Accordingly, population-based longitudinal research indicates that perceived social isolation (loneliness) is a risk factor for morbidity and mortality independent of objective social isolation and health behavior. Human and animal investigations of neuroendocrine stress mechanisms that may be involved suggest that (a) chronic social isolation increases the activation of the hypothalamic pituitary adrenocortical axis, and (b) these effects are more dependent on the disruption of a social bond between a significant pair than objective isolation per se. The relational factors and neuroendocrine, neurobiological, and genetic mechanisms that may contribute to the association between perceived isolation and mortality are reviewed.
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            The characterization of primary HIV infection by the analysis of serial plasma samples from newly infected persons using multiple standard viral assays. A retrospective study involving two sets of archived samples from HIV-infected plasma donors. (A) 435 samples from 51 donors detected by anti-HIV enzyme immunoassays donated during 1984-1994; (B) 145 specimens from 44 donors detected by p24 antigen screening donated during 1996-1998. Two US plasma products companies. The timepoints of appearance of HIV-1 markers and viral load concentrations during primary HIV infection. The pattern of sequential emergence of viral markers in the 'A' panels was highly consistent, allowing the definition and estimation of the duration of six sequential stages. From the 'B' panels, the viral load at p24 antigen seroconversion was estimated by regression analysis at 10 000 copies/ml (95% CI 2000-93 000) and the HIV replication rate at 0.35 log copies/ml/day, corresponding to a doubling time in the preseroconversion phase of 20.5 h (95% CI 18.2-23.4 h). Consequently, an RNA test with 50 copies/ml sensitivity would detect HIV infection approximately 7 days before a p24 antigen test, and 12 days before a sensitive anti-HIV test. The sequential emergence of assay reactivity allows the classification of primary HIV-1 infection into distinct laboratory stages, which may facilitate the diagnosis of recent infection and stratification of patients enrolled in clinical trials. Quantitative analysis of preseroconversion replication rates of HIV is useful for projecting the yield and predictive value of assays targeting primary HIV infection.
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              Research over the past several decades has documented psychosocial influences on the development and progression of several major medical illnesses. The field is now increasingly focused on identifying the biological and behavioral mechanisms underlying these effects. This review takes stock of the knowledge accumulated in the biological arena to date and highlights conceptual and methodological approaches that have proven especially productive. It emphasizes the value of a disease-centered approach that "reverse engineers" adverse health outcomes into their specific biological determinants and then identifies psychologically modulated neuroendocrine and immunologic dynamics that modulate those pathological processes at the cellular and molecular levels.

                Author and article information

                Psychosom Med
                Psychosom Med
                Psychosomatic Medicine
                Lippincott Williams & Wilkins
                October 2022
                7 September 2022
                : 84
                : 8
                : 966-975
                From the Department of Molecular and Comparative Pathobiology (Castell, Guerrero-Martin, Shirk, Brockhurst, Lyons, Najarro, Queen, Li, Bullock, Carlson, Adams, Morrell, Gama, Graham, Zink, Mankowski, Clements, Metcalf Pate), Johns Hopkins University School of Medicine, Baltimore, Maryland; Division of Comparative Medicine and Department of Biological Engineering (Guerrero-Martin, Lyons, Metcalf Pate), Massachusetts Institute of Technology, Boston, Massachusetts; Departments of Neurology (Rubin, Mankowski, Clements, Metcalf Pate) and Psychiatry and Behavioral Sciences (Rubin), Johns Hopkins University School of Medicine; Departments of Epidemiology (Rubin) and Molecular Microbiology and Immunology (Zink), Johns Hopkins University Bloomberg School of Public Health; Department of Pathology (Mankowski, Clements), Johns Hopkins University School of Medicine; and Department of Molecular Biology and Genetics (Clements), Johns Hopkins University School of Medicine, Baltimore, Maryland.
                Author notes
                [*]Address correspondence to Kelly A. Metcalf Pate, DVM, PhD, 77 Massachusetts Ave, 16-825c, Cambridge, MA 02139. E-mail: kpate@ 123456mit.edu
                PSYMED_220246 00013
                Copyright © 2022 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Psychosomatic Society.

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal.

                : 22 August 2021
                : 27 July 2022
                Original Articles
                Custom metadata

                simian immunodeficiency virus,psychosocial stress,innate immunity,infectious disease,animal models,human immunodeficiency virus,art = antiretroviral therapy,b = unstandardized β coefficient,cbc = complete blood count,csf = cerebrospinal fluid,cns = central nervous system,hiv = human immunodeficiency virus,pwh = people with hiv,se = standard error,siv = simian immunodeficiency virus


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