Deep spatial profiling of Venezuelan equine encephalitis virus reveals increased genetic diversity amidst neuroinflammation and cell death during brain infection
Open accessAbstract
Venezuelan equine encephalitis virus (VEEV) causes a febrile illness that can progress to neurological disease with the possibility of death in human cases. The evaluation and optimization of therapeutics that target brain infections demands knowledge of the host’s response to VEEV, the dynamics of infection, and the potential for within-host evolution of the virus. We hypothesized that selective pressures during infection of the brain may differ temporally and spatially and so we investigated the dynamics of the host response, viral transcript levels, and genetic variation of VEEV TC-83 in eight areas of the brain in mice over 7 days post-infection (dpi). Viral replication increased throughout the brain until 5–6 dpi and decreased thereafter with neurons as the main site of viral replication. Low levels of genetic diversity were noted on 1 dpi and were followed by an expansion in the genetic diversity of VEEV and nonsynonymous (Ns) mutations that peaked by 5 dpi. The pro-inflammatory response and the influx of immune cells mirrored the levels of virus and correlated with substantial damage to neurons by 5 dpi and increased activation of microglial cells and astrocytes. The prevalence and dynamics of Ns mutations suggest that the VEEV is under selection within the brain and that progressive neuroinflammation may play a role in acting as a selective pressure. IMPORTANCE: Treatment of encephalitis in humans caused by Venezuelan equine encephalitis virus (VEEV) from natural or aerosol exposure is not available, and hence, there is a great interest to address this gap. In contrast to natural infections, therapeutic treatment of infections from aerosol exposure will require fast-acting drugs that rapidly penetrate the blood-brain barrier, engage sites of infection in the brain and mitigate the emergence of drug resistance. Therefore, it is important to understand not only VEEV pathogenesis, but the trafficking of the viral population within the brain, the potential for within-host evolution of the virus, and how VEEV might evolve resistance.
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VEEV neuropathology shares similarities with Alzheimer's disease, including increased astrogliosis, glial nodules, and pathological indicators of neuroinflammation including perivascular cuffing.
“VEEV neuropathology shares similarities with AD, a widespread cognitive disorder of aging, including increased astrogliosis, glial nodules, and pathological indicators of neuroinflammation including perivascular cuffing (Nelson et al., 2012; Williams et al., 2023).”
From Arbovirus infection increases the risk for the development of neurodegenerative disease pathology in the murine model (2024) · cites this paper as Williams et al., 2023
The Results (page unavailable) report elevated GFAP and increased astrocyte numbers after VEEV infection, as well as perivascular cuffing and microglial clusters around damaged neurons. They do not explicitly identify those clusters as glial nodules or compare VEEV neuropathology with Alzheimer’s disease. (LLM, conf=0.84)
Experimental — accuracy not yet measuredVEEV triggers neurological sequelae in survivors that can be characterized by cognitive, motor, and sensory deficits likely through direct neuronal and glial cell infection.
“It is well documented that VEEV triggers neurological sequelae in survivors that can be characterized by cognitive, motor, and sensory deficits likely through direct neuronal and glial cell infection [7,8].”
From VEEV TC-83 Triggers Dysregulation of the Tryptophan–Kynurenine Pathway in the Central Nervous System That Correlates with Cognitive Impairment in Tg2576 Mice (2024) · cites this paper as [7]
The Introduction describes VEEV infection and damage of neurons, and the Discussion links infected brain regions to motor control and sensory pathways (page numbers unavailable). But the paper studies acute infection in mice, not cognitive, motor, and sensory deficits in survivors. Its Results describe microglia surrounding infected neurons and astrocytes responding to infection, not direct infection of glial cells. (LLM, conf=0.86)
Experimental — accuracy not yet measuredMultiple preclinical and clinical studies indicate that VEEV leads to increased neuroinflammatory profiles and potential demyelination.
“Multiple preclinical and clinical studies indicate that VEEV leads to increased neuroinflammatory profiles and potential demyelination [7].”
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Cited by
Sorted by citations
Neuropathogenesis of Encephalitic Alphaviruses in Non-Human Primate and Mouse Models of Infection
Lehman, C. W., Carney, S. K., & Kehn‐Hall, K. (2025) · Pathogens · doi:10.3390/pathogens14020193 · Cited by 20 · see citing works
“More recent studies have provided brain region-specific bulk RNAseq, spatial RNAseq, and single-cell RNAseq (scRNAseq) analyses of brain from VEEV-infected C3H/HeN mice [94].”
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“VEEV neuropathology shares similarities with AD, a widespread cognitive disorder of aging, including increased astrogliosis, glial nodules, and pathological indicators of neuroinflammation including peri-vascular cuffing (Nelson et al., 2012; Williams et al., 2023).”
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“Similarly, the C3H/HeN mice ( n = 8/group) were intranasally infected with VEEV TC-83 and treated twice per day with either PBS or with 6 mg kg −1 of BDGR-49.”
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Venezuelan Equine Encephalitis Virus Antagonizes the cGAS-STING Pathway
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- Authors
- Williams, E. P., Xue, Y., Lee, J., Fitzpatrick, E. A., Kong, Y., Reichard, W., Writt, H., & Jonsson, C. B.
- Affiliations
- University of Tennessee Health Science Center (US)
- Corresponding author
- Jonsson, Colleen B.
- Venue
- Journal of Virology
- Publisher
- American Society for Microbiology
- Published
- 2023-08-31
- Volume
- 97
- Issue
- 8
- Pages
- e0082723-e0082723
- ISSN
- 0022-538X (ISSN-L)
- 1098-5514
- PMC
- PMC10506382
- OpenAlex
- W4385716433
- Cited by
- 15
- References
- 44
- Citations by year
- 2026: 6 · 2025: 4 · 2024: 5
- FWCI
- 3.84
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Virology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- HHS | NIH | National Institute of Allergy and Infectious Diseases (U19AI142762)
- Topics
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Mosquito-borne diseases and control
- Health Sciences › Medicine › Infectious Diseases › Viral Infections and Vectors
- Health Sciences › Medicine › Infectious Diseases › Infectious Encephalopathies and Encephalitis
- Keywords
- Venezuelan equine encephalitis virus, within-host viral evolution, viral genetic diversity, neuroinflammation, neuronal cell death, microglial activation, astrocyte activation, non-synonymous mutations, host immune response, blood-brain barrier, drug resistance, aerosol exposure, mouse brain infection
- MeSH terms
- Animals, Brain, Encephalitis, Encephalitis Virus, Venezuelan Equine, Humans, Genetic Variation, Cell Death, Mice
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