Platelet activation (P-selectin) increased by 65% ( p =. Platelet numbers recovered more quickly in the socially housed animals. 001, by day 14 compared with preinoculation time points).
Monocyte number increased after infection for both groups, driven by classical monocytes (CD14 +CD16 −), with a greater increase in socially housed animals (227%, p <. SIV infection resulted in the expected innate immune parameter changes with a modulating effect from housing condition. Measures included absolute monocyte count and subsets, and in a subset ( n ≤ 18) platelet counts and activation data. MethodsĪ 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. 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. Psychosocial stress is associated with immune system dysregulation and worse clinical outcomes in people with HIV. Simian immunodeficiency virus (SIV) infection of macaques recapitulates many aspects of HIV pathogenesis and is similarly affected by both genetic and environmental factors.
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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. Received for publication Augrevision received July 27, 2022. E-mail: Īlternate corresponding author: Natalie Castell (e-mail: ). Metcalf Pate, DVM, PhD, 77 Massachusetts Ave, 16-825c, Cambridge, MA 02139. 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.Īddress correspondence to Kelly A.
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