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High fat diet increases neuroinflammation and alters behavior in mice latently‐infected with HSV ‐1
Author(s) -
Sheridan Patricia A,
Milner Justin,
Moy Sheryl S
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.222.6
Subject(s) - neuroinflammation , virus latency , priming (agriculture) , inflammation , herpes simplex virus , immunology , hippocampus , hsl and hsv , latency (audio) , biology , medicine , virus , psychology , endocrinology , viral replication , botany , germination , engineering , electrical engineering
Infectious agents and high fat (HF) diets have been implicated in causing neuroinflammation. We sought to determine if a diet high in saturated fat could prolong inflammation in the brains of latently herpes simplex virus (HSV)‐infected mice and effect behavior. Three months following the establishment of HSV latency in the low fat (LF) mice, there were no difference in the mRNA expression of markers of glial priming and activation compared to the LF uninfected controls. While HF diet alone increased expression of MHCII and IL‐10 it is only in the latent HSV/HF fed group that significant changes are seen in the majority of markers of glial priming and activation. At 7 months after infection, latent HSV‐1 results in changes in anxiety, motor learning and spatial learning acquisition and memory. Some of these behavioral changes are exacerbated by HF diet while some changes are a result of HF diet alone. We have developed a model for examining the biochemical and behavioral effects of latent infection with HSV and HF diets. This model mimics HSV latency in humans and that it reveals a unique role for a diet high in saturated fat in causing ongoing inflammation and prolonged microglial activation in the hippocampus.