Patients with psychosis spectrum disorders hospitalized during the COVID-19 pandemic unravel overlooked SARS-CoV-2 past infection clustering with HERV-W ENV expression and chronic inflammation

Tamouza, Ryad; Meyer, Urs; Lucas, Alexandre; Richard, Jean Romain; Nkam, Irène; Pinot, Armand; Djonouma, Ndilyam; Boukouaci, Wahid; Charvet, Benjamin; Pierquin, Justine; Brunel, Joanna; Fourati, Slim; Rodriguez, Christophe; Barau, Caroline; Le Corvoisier, Philippe; El Abdellati, Kawtar; De Picker, Livia; Perron, Hervé; Leboyer, Marion

doi:10.1038/s41398-023-02575-3

Cited by 9 publications

(5 citation statements)

References 46 publications

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“…In this context, HERVK overexpression may well be restricted to a subgroup of patients, as already mentioned in the initial study reporting increased expression [25]. Such stratification of cases was recently reported for HERVW expression in psychotic spectrum patients [36] and the induction of HERVW ENV expression by SARS-CoV-2 [37]. The disease-associated expression of HERV may, therefore, be more common than previously reported.…”

Section: Discussionmentioning

confidence: 63%

New Insights into Endogenous Retrovirus-K Transcripts in Amyotrophic Lateral Sclerosis

Moreno-Martinez,

Macías-Redondo,

Strunk

et al. 2024

IJMS

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Retroviral reverse transcriptase activity and the increased expression of human endogenous retroviruses (HERVs) are associated with amyotrophic lateral sclerosis (ALS). We were interested in confirming HERVK overexpression in the ALS brain, its use as an accessory diagnostic marker for ALS, and its potential interplay with neuroinflammation. Using qPCR to analyze HERVK expression in peripheral blood mononuclear cells (PBMCs) and in postmortem brain samples from ALS patients, no significant differences were observed between patients and control subjects. By contrast, we report alterations in the expression patterns of specific HERVK copies, especially in the brainstem. Out of 27 HERVK copies sampled, the relative expression of 17 loci was >1.2-fold changed in samples from ALS patients. In particular, the relative expression of two HERVK copies (Chr3-3 and Chr3-5) was significantly different in brainstem samples from ALS patients compared with controls. Further qPCR analysis of inflammation markers in brain samples revealed a significant increase in NLRP3 levels, while TNFA, IL6, and GZMB showed slight decreases. We cannot confirm global HERVK overexpression in ALS, but we can report the ALS-specific overexpression of selected HERVK copies in the ALS brain. Our data are compatible with the requirement for better patient stratification and support the potential importance of particular HERVK copies in ALS.

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Section: Discussionmentioning

confidence: 63%

New Insights into Endogenous Retrovirus-K Transcripts in Amyotrophic Lateral Sclerosis

Moreno-Martinez,

Macías-Redondo,

Strunk

et al. 2024

IJMS

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show abstract

“…HERVs have been demonstrated to be activated during certain infections associated with a risk of developing psychiatric diseases. The W family envelope protein (HERV-W env) has been linked with several neurological and psychiatric disorders; in SARS-CoV-2 seropositive cases with psychosis spectrum disorders, HERV W ENV and cytokine expression were significantly influenced by the SARS-CoV-2 virus [67].…”

Section: Hervs As Transposable Elementsmentioning

confidence: 99%

A Unifying Hypothesis for the Genome Dynamics Proposed to Underlie Neuropsychiatric Phenotypes

Gericke

2024

Genes

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The sheer number of gene variants and the extent of the observed clinical and molecular heterogeneity recorded in neuropsychiatric disorders (NPDs) could be due to the magnified downstream effects initiated by a smaller group of genomic higher-order alterations in response to endogenous or environmental stress. Chromosomal common fragile sites (CFS) are functionally linked with microRNAs, gene copy number variants (CNVs), sub-microscopic deletions and duplications of DNA, rare single-nucleotide variants (SNVs/SNPs), and small insertions/deletions (indels), as well as chromosomal translocations, gene duplications, altered methylation, microRNA and L1 transposon activity, and 3-D chromosomal topology characteristics. These genomic structural features have been linked with various NPDs in mostly isolated reports and have usually only been viewed as areas harboring potential candidate genes of interest. The suggestion to use a higher level entry point (the ‘fragilome’ and associated features) activated by a central mechanism (‘stress’) for studying NPD genetics has the potential to unify the existing vast number of different observations in this field. This approach may explain the continuum of gene findings distributed between affected and unaffected individuals, the clustering of NPD phenotypes and overlapping comorbidities, the extensive clinical and molecular heterogeneity, and the association with certain other medical disorders.

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“…HERVs have been demonstrated to be activated durIng certain infections associated with a risk of developing psychiatric diseases. The W family envelope protein (HERV-W env) has been linked with several neurological and psychiatric disorders; in SARS-CoV-2 seropositive cases with psychosis spectrum disorders, HERV W ENV and cytokine expression were significantly influenced by the SARS-CoV-2 virus [68].…”

Section: Hervs As Transposable Elementsmentioning

confidence: 99%

A Unifying Hypothesis for the Genome Dynamics Proposed to Underly Neuropsychiatric Phenotypes

Gericke

2024

Preprint

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The sheer number of gene variants and the extent of the observed clinical and molecular heterogeneity recorded in neuropsychiatric disorders (NPDs), could be due to the magnified downstream effects initiated by a smaller group of genomic higher order alterations in response to endogenous or environmental stress. Chromosomal common fragile sites (CFS) are functionally linked with microRNA’s, gene copy number variants (CNVs), sub-microscopic deletions and duplications of DNA, rare single-nucleotide variants (SNVs/SNPs) and small insertions/deletions (indels), as well as chromosomal translocations, gene duplications, altered methylation, microRNA and L1 transposon activity and 3-D chromosomal topology characteristics. These genomic structural features have been linked with various NPDs in mostly isolated reports, and have usually only been viewed as areas harboring potential candidate genes of interest. The suggestion to use a higher level entry point, (the ‘fragilome’ and associated features), activated by a central mechanism (‘stress’) for studying NPD genetics, has the potential to unify the existing vast number of different observations in this field. This approach may explain the continuum of gene findings distributed between affected and unaffected individuals, the clustering of NPD phenotypes and overlapping comorbidities, the extensive clinical and molecular heterogeneity and the association with certain other medical disorders.

show abstract

Patients with psychosis spectrum disorders hospitalized during the COVID-19 pandemic unravel overlooked SARS-CoV-2 past infection clustering with HERV-W ENV expression and chronic inflammation

Cited by 9 publications

References 46 publications

New Insights into Endogenous Retrovirus-K Transcripts in Amyotrophic Lateral Sclerosis

New Insights into Endogenous Retrovirus-K Transcripts in Amyotrophic Lateral Sclerosis

A Unifying Hypothesis for the Genome Dynamics Proposed to Underlie Neuropsychiatric Phenotypes

A Unifying Hypothesis for the Genome Dynamics Proposed to Underly Neuropsychiatric Phenotypes

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