Unveiling HERV‐K113‐ENV as SARS‐CoV‐2 severity admissible biomarker by mining transcriptome data

Desingu, Perumal Arumugam; Nagarajan, K.

doi:10.1002/jmv.28149

Cited by 5 publications

(2 citation statements)

References 7 publications

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“…This vaccine induces M1 polarization of macrophages [213] and thus would induce HERV-K102 particle production [99]; and may promote the V9V2 T cells which help protect against SARS-CoV-2 [213] as well as cancers [3]. Indeed, in addition to identifying M1-like foamy macrophages in recovery from COVID-19 [61], several papers have directly confirmed the role of HERV-K102 proviral expression or Env antibodies in recovery from COVID-19 [137,147,214,215]. In addition, HERV-K HML-2 elements played a role in recovery from COVID-19 in children [216] and others have provided indirect evidence for HERV-K102 activation in recovery [217,218].…”

Section: Future Directionsmentioning

confidence: 97%

Antibody Dependent Enhancement (ADE) of Infection into Macrophages Validates the Importance of HERV-K102 Particle Production for Pandemic Preparedness

Laderoute

2023

Preprint

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Historically, macrophages have been long implicated in the control of the severity of infectious diseases. This has been based on the observations of a higher risk of severe disease and death upon rechallenge with viral variants due to antibody dependent enhance-ment (ADE) of infection into macrophages. The question remains as to what can account for this potent heterologous protection in macrophages? Here it is argued that the elusive defense mechanism of M1-like pro-inflammatory macrophages may pertain to a novel virus anti-virus response. This system initiates with high replication of human endogenous retrovirus K102 (HERV-K102), a non-pathogenic, protector foamy retrovirus of humans which generates M1-like pro-inflammatory foamy macrophages, glycolysis, and epigenetic changes, all characteristic of trained immunity. This virus-anti-virus system kills virally infected cells by several mechanisms, amplifies the innate interferon response via ‘viral mimicry’, has many unique components that interfere with exoge-nous virus replication, and may be especially adept at neutralizing enveloped exogenous pandemic viruses, such as SARS-CoV-2 and HIV-1. The goal of this treatise is to introduce the multifaceted HERV-K102 protector system, to illustrate how SARS-CoV-2 may target the HERV-K102 protector system by ADE, and to explore how this innate defense system may be exploited for pandemic preparedness.

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Section: Future Directionsmentioning

confidence: 97%

Antibody Dependent Enhancement (ADE) of Infection into Macrophages Validates the Importance of HERV-K102 Particle Production for Pandemic Preparedness

Laderoute

2023

Preprint

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“…Here, we leverage publicly available transcriptome and chromatin datasets of infected cell lines and patient-derived samples to decipher the impact of SARS-CoV-2 on the TE expression profiles of virus-infected or -exposed cells. Several studies have reported an induction of HERV-K [7][8][9], HERV-W [10,11] or HERV-L [12][13][14][15][16] upon SARS-CoV-2 infection. In line with this, we found that SARS-CoV-2 infection induces the activation of a particular subset of endogenous retroviruses (ERVs), so-called LTR69 repeats.…”

Section: Introductionmentioning

confidence: 99%

SARS-CoV-2 infection activates endogenous retroviruses of the LTR69 subfamily

Arora

Kolberg

Badarinarayan

et al. 2023

Preprint

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Accumulating evidence suggests that endogenous retroviruses (ERVs) play an important role in the host response to infection and the development of disease. By combining RNA- and ChIP-sequencing analyses with RT-qPCR, we show that SARS-CoV-2 infection induces the LTR69 subfamily of ERVs, both in vitro and in vivo. Using functional assays, we identified one SARS-CoV-2-activated LTR69 locus, termed Dup69, which exhibits enhancer activity and is responsive to the transcription factors IRF3 and p65/RelA. LTR69-Dup69 is located about 500 bp upstream of a long non-coding RNA gene (ENSG00000289418) and within the PTPRN2 gene encoding a diabetes-associated autoantigen. Both ENSG00000289418 and PTPRN2 showed a significant increase in expression upon SARS-CoV-2 infection. Thus, our study sheds light on the interplay of exogenous with endogenous viruses and helps to understand how ERVs regulate gene expression during infection.

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SARS-CoV-2 infection induces epigenetic changes in the LTR69 subfamily of endogenous retroviruses

Arora,

Kolberg,

Srinivasachar Badarinarayan

et al. 2023

Mobile DNA

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Accumulating evidence suggests that endogenous retroviruses (ERVs) play an important role in the host response to infection and the development of disease. By analyzing ChIP-sequencing data sets, we show that SARS-CoV-2 infection induces H3K27 acetylation of several loci within the LTR69 subfamily of ERVs. Using functional assays, we identified one SARS-CoV-2-activated LTR69 locus, termed Dup69, which exhibits regulatory activity and is responsive to the transcription factors IRF3 and p65/RELA. LTR69_Dup69 is located about 500 bp upstream of a long non-coding RNA gene (ENSG00000289418) and within the PTPRN2 gene encoding a diabetes-associated autoantigen. Both ENSG00000289418 and PTPRN2 showed a significant increase in expression upon SARS-CoV-2 infection. Thus, our study sheds light on the interplay of exogenous with endogenous viruses and helps to understand how ERVs regulate gene expression during infection.

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Unveiling HERV‐K113‐ENV as SARS‐CoV‐2 severity admissible biomarker by mining transcriptome data

Cited by 5 publications

References 7 publications

Antibody Dependent Enhancement (ADE) of Infection into Macrophages Validates the Importance of HERV-K102 Particle Production for Pandemic Preparedness

Antibody Dependent Enhancement (ADE) of Infection into Macrophages Validates the Importance of HERV-K102 Particle Production for Pandemic Preparedness

SARS-CoV-2 infection activates endogenous retroviruses of the LTR69 subfamily

SARS-CoV-2 infection induces epigenetic changes in the LTR69 subfamily of endogenous retroviruses

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