SARS-CoV-2 brings out an endogenous retrovirus protein to cause severe COVID-19 and Long COVID syndrome

Do you know that there are viral genes in all humans? They are called Human Endogenous Retroviruses (HERV). HERVs are nucleotide sequences from viral infections that infected our ancestors millions of years ago.

HERVs comprise ∼5-8% of the human genome, with over 22 HERV families.[1] Nucleotides are instructions to make amino acids which are the building block of proteins.

If retrovirus sounds familiar, that’s because the Human Immunodeficiency Virus (HIV) and human T cell leukemia virus (HTLV) are both retroviruses. HERVs possess a similar genomic organization to HIV and HTLV.

HERVs have lost their ability to replicate and therefore don’t cause infections. But since they are made of nucleotide sequences, they can produce or express proteins if the right conditions exist, and the proteins they express influence the immune system in two ways.

The HERV-W envelope (Syncytin-1)

Some viruses have envelopes that serve as an outer cover. Those viruses will have nucleotide sequences in their genes for those envelopes. One particular HERV, the HERV-W, has a sequence for its envelope called the HERV-W envelope or Syncytin-1. [3]

Like anything, syncytin-1 has a duality. It can be good, or it can have bad effects. The first is immune tolerance. In pregnancy, syncytin-1 allows the placenta to adhere to the uterus.

That is important because the fetus has 50% of its genes or proteins coming from the father and therefore is foreign to the mother. In the absence of syncytin-1, the fetuses will be rejected by the mother’s immune system.

On the other hand, immune dysregulation can happen with HERVs, and some can cause cancers.[2] Syncytin-1 has been implicated in autoimmune diseases like Type-1 diabetes, multiple sclerosis, Amyotrophic lateral sclerosis (Lou Gehrig’s disease), and rheumatoid arthritis. [3][4][6][7]

Immune dysregulation can also happen in a hyperactive immune response like cytokine storms in COVID-19.

Syncytin-1/HERV-W envelopes and COVID-19

A study of patients with severe COVID-19 showed syncytin-1 circulating in their blood. Syncytin-1 is superantigenic and can elicit an immune response, resulting in more T cells and cytokines to aggravate inflammation. [7]

With that observation, a study was made to investigate whether the effect of syncytin-1 can persist among COVID-19 patients who survive.[1]. The study showed that 21% of SARS-CoV-2 positive cases have syncytin-1 in white blood cells. In contrast, syncytin-1 was not detected among people who tested negative for SARS-COV-2.

The study also found that the more severe the COVID-19, the greater the syncytin-1 expression in the T cells and plasma of the patients.

Upon examining the cadavers of patients who died of COVID-19, syncytin-1 was detected in the inner lining of the nose, the olfactory bulb, the lungs, the heart muscles, and the brain. These same tissues also showed evidence of SARS-CoV-2 infection.

The autopsy findings suggest that the presence of HERV-W envelope protein elicits a greater autoimmune response that contributed to worse COVID-19 and deaths. In the middle or late COVID-19 course, the virus is gone, but the immune response against the virus is causing damage to the patient’s body.

Another interesting finding is that when they tested only the spike protein against the cells, some cells produced the HERV-W envelope protein. This suggests the spike protein is enough to make the body produce syncytin-1.

That means injection with the mRNA COVID shots that lead to SARS-CoV-2 spike protein production can also elicit an autoimmune response thru syncytin-1.

Long COVID syndrome and HERV-W envelope

Long COVID syndrome or Post Acute Sequelae of COVID-19 describes a group of symptoms among survivors of COVID-19 that last longer than four weeks. Lethargy, depression, chronic pain, headache, muscle pains, seizures, and sleep disorders are often described.

Yale Medicine says, “Long COVID can affect anyone, including children, and it can develop in people who had asymptomatic, mild, or severe COVID-19.”

My previous article, Persistent inflammation explains Long COVID syndrome, featured a study showing continued inflammation in the olfactory bulb. The olfactory bulb receives smell signals from the nose where COVID-19 starts. The olfactory bulb is connected to other brain structures like the thalamus and striatum.

The thalamus receives sensory input from all senses and relays that information to the rest of the brain. The major role of the thalamus is the support of motor and language systems and is involved in consciousness, sleep and wake cycle, cognition, and memory.

The dorsal part of the striatum mediates motor function and certain executive functions like inhibitory control and impulsivity. A stroke in the striatum can cause Bell’s palsy. [8] Bell’s palsy is a paralysis of one side of the face. OpenVAERS reports 13,137 Bell’s palsy complications after COVID-19 shots.

Chronic inflammation in the olfactory bulb affects its functions with downstream effects on the thalamus and striatum. It may cause symptoms consistent with the Long COVID syndrome and post-vaccine inflammatory syndrome, where people get the COVID-shots may experience symptoms similar to Long COVID syndrome.

The findings of this study open up the possibility that neurological diseases like multiple sclerosis and psychiatric conditions like some inflammatory types of schizophrenia and bipolar disorders [10] may manifest in the future among genetically susceptible people who got COVID-19 or its vaccines.

In summary, the study SARS-CoV-2 induces human endogenous retrovirus type W envelope protein expression in blood lymphocytes and in tissues of COVID-19 patients suggests that a percentage of individuals with an underlying susceptibility to Long COVID syndrome may be linked to the activation of HERV-W ENV (syncytin-1) expression.

Take away message

Not all who get COVID-19 or its shots will have syncytin-1-related complications. The immunological experience and genetic makeup differed for each person. Only 21% of SARS-CoV-2-positive individuals tested positive for the HERV-W envelope protein in the research.[1]

A high SARS-CoV-2 viral load leads to more inflammation and worse COVID-19. I think giving early treatment to all who test positive for SARS-CoV-2 will lower the risk of severe COVID-19 and the development of Long COVID.

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References:

Charvet, et al. SARS-CoV-2 induces human endogenous retrovirus type W envelope protein expression in blood lymphocytes and in tissues of COVID-19 patients

medRxiv 2022.01.18.21266111; doi: https://doi.org/10.1101/2022.01.18.21266111
Matteucci C. et al., Human endogenous retroviruses role in cancer cell stemness. Semin Cancer Biol. 2018; 53: 17-30
Levet S. Medina J. Joanou J. et al. An ancestral retroviral protein identified as a therapeutic target in type-1 diabetes. JCI Insight. 2017; 2: e94387
Garcia-Montojo M, et al. Syncytin-1/HERV-W envelope is an early activation marker of leukocytes and is upregulated in multiple sclerosis patients. Eur J Immunol. 2020 May;50(5):685-694. doi: 10.1002/eji.201948423. Epub 2020 Feb 11. PMID: 32012247.
Küry P. et al. Human endogenous retroviruses in neurological diseases. Trends Mol Med. 2018; 24: 379-394
Balestrieri et al. Evidence of the pathogenic HERV-W envelope expression in T lymphocytes in association with the respiratory outcome of COVID-19 patients. Published: April 15, 2021, DOI:https://doi.org/10.1016/j.ebiom.2021.103341
Posso-Osorio I et al. Human endogenous retroviruses (HERV) and non-HERV viruses incorporated into the human genome and their role in the development of autoimmune diseases. J Transl Autoimmun. 2021;4:100137. Published 2021 Dec 9. doi:10.1016/j.jtauto.2021.100137
Song W et al. Disrupted functional connectivity of striatal sub-regions in Bell’s palsy patients. Neuroimage Clin. 2017 Jan 15;14:122-129. doi: 10.1016/j.nicl.2017.01.008. PMID: 28180070; PMCID: PMC5279691.
Grandi, N. and E. Tramontano, Human Endogenous Retroviruses Are Ancient Acquired Elements Still Shaping Innate Immune Responses. Front Immunol, 2018. 9: p. 2039.DOI: 10.3389/fimmu.2018.02039.
Tamouza R, et al. Identification of inflammatory subgroups of schizophrenia and bipolar disorder patients with HERV-W ENV antigenemia by unsupervised cluster analysis. Transl Psychiatry. 2021 Jul 6;11(1):377. doi: 10.1038/s41398-021-01499-0.

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