Underlying Piezo2 Channelopathy-Induced Neural Switch of COVID-19 Infection
The focal “hot spot” neuropathologies in COVID-19 infection are revealing footprints of a hidden underlying collapse of a novel ultrafast ultradian Piezo2 signaling system within the nervous system. Paradoxically, the same initiating pathophysiology may underpin the systemic findings in COVID-19 inf...
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2025-07-01
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| author | Balázs Sonkodi |
| author_facet | Balázs Sonkodi |
| author_sort | Balázs Sonkodi |
| collection | DOAJ |
| description | The focal “hot spot” neuropathologies in COVID-19 infection are revealing footprints of a hidden underlying collapse of a novel ultrafast ultradian Piezo2 signaling system within the nervous system. Paradoxically, the same initiating pathophysiology may underpin the systemic findings in COVID-19 infection, namely the multiorgan SARS-CoV-2 infection-induced vascular pathologies and brain–body-wide systemic pro-inflammatory signaling, depending on the concentration and exposure to infecting SARS-CoV-2 viruses. This common initiating microdamage is suggested to be the primary damage or the acquired channelopathy of the Piezo2 ion channel, leading to a principal gateway to pathophysiology. This Piezo2 channelopathy-induced neural switch could not only explain the initiation of disrupted cell–cell interactions, metabolic failure, microglial dysfunction, mitochondrial injury, glutamatergic synapse loss, inflammation and neurological states with the central involvement of the hippocampus and the medulla, but also the initiating pathophysiology without SARS-CoV-2 viral intracellular entry into neurons as well. Therefore, the impairment of the proposed Piezo2-induced quantum mechanical free-energy-stimulated ultrafast proton-coupled tunneling seems to be the principal and critical underlying COVID-19 infection-induced primary damage along the brain axes, depending on the loci of SARS-CoV-2 viral infection and intracellular entry. Moreover, this initiating Piezo2 channelopathy may also explain resultant autonomic dysregulation involving the medulla, hippocampus and heart rate regulation, not to mention sleep disturbance with altered rapid eye movement sleep and cognitive deficit in the short term, and even as a consequence of long COVID. The current opinion piece aims to promote future angles of science and research in order to further elucidate the not entirely known initiating pathophysiology of SARS-CoV-2 infection. |
| format | Article |
| id | doaj-art-2c7f85420ba3473aab6f4bd5720531e6 |
| institution | Kabale University |
| issn | 2073-4409 |
| language | English |
| publishDate | 2025-07-01 |
| publisher | MDPI AG |
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| series | Cells |
| spelling | doaj-art-2c7f85420ba3473aab6f4bd5720531e62025-08-20T04:00:54ZengMDPI AGCells2073-44092025-07-011415118210.3390/cells14151182Underlying Piezo2 Channelopathy-Induced Neural Switch of COVID-19 InfectionBalázs Sonkodi0Department of Health Sciences and Sport Medicine, Hungarian University of Sports Science, 1123 Budapest, HungaryThe focal “hot spot” neuropathologies in COVID-19 infection are revealing footprints of a hidden underlying collapse of a novel ultrafast ultradian Piezo2 signaling system within the nervous system. Paradoxically, the same initiating pathophysiology may underpin the systemic findings in COVID-19 infection, namely the multiorgan SARS-CoV-2 infection-induced vascular pathologies and brain–body-wide systemic pro-inflammatory signaling, depending on the concentration and exposure to infecting SARS-CoV-2 viruses. This common initiating microdamage is suggested to be the primary damage or the acquired channelopathy of the Piezo2 ion channel, leading to a principal gateway to pathophysiology. This Piezo2 channelopathy-induced neural switch could not only explain the initiation of disrupted cell–cell interactions, metabolic failure, microglial dysfunction, mitochondrial injury, glutamatergic synapse loss, inflammation and neurological states with the central involvement of the hippocampus and the medulla, but also the initiating pathophysiology without SARS-CoV-2 viral intracellular entry into neurons as well. Therefore, the impairment of the proposed Piezo2-induced quantum mechanical free-energy-stimulated ultrafast proton-coupled tunneling seems to be the principal and critical underlying COVID-19 infection-induced primary damage along the brain axes, depending on the loci of SARS-CoV-2 viral infection and intracellular entry. Moreover, this initiating Piezo2 channelopathy may also explain resultant autonomic dysregulation involving the medulla, hippocampus and heart rate regulation, not to mention sleep disturbance with altered rapid eye movement sleep and cognitive deficit in the short term, and even as a consequence of long COVID. The current opinion piece aims to promote future angles of science and research in order to further elucidate the not entirely known initiating pathophysiology of SARS-CoV-2 infection.https://www.mdpi.com/2073-4409/14/15/1182neuroCOVIDPiezo2 channelopathymetabolic switchmicrogliaglutamatergic synapse lossautonomic dysregulation |
| spellingShingle | Balázs Sonkodi Underlying Piezo2 Channelopathy-Induced Neural Switch of COVID-19 Infection Cells neuroCOVID Piezo2 channelopathy metabolic switch microglia glutamatergic synapse loss autonomic dysregulation |
| title | Underlying Piezo2 Channelopathy-Induced Neural Switch of COVID-19 Infection |
| title_full | Underlying Piezo2 Channelopathy-Induced Neural Switch of COVID-19 Infection |
| title_fullStr | Underlying Piezo2 Channelopathy-Induced Neural Switch of COVID-19 Infection |
| title_full_unstemmed | Underlying Piezo2 Channelopathy-Induced Neural Switch of COVID-19 Infection |
| title_short | Underlying Piezo2 Channelopathy-Induced Neural Switch of COVID-19 Infection |
| title_sort | underlying piezo2 channelopathy induced neural switch of covid 19 infection |
| topic | neuroCOVID Piezo2 channelopathy metabolic switch microglia glutamatergic synapse loss autonomic dysregulation |
| url | https://www.mdpi.com/2073-4409/14/15/1182 |
| work_keys_str_mv | AT balazssonkodi underlyingpiezo2channelopathyinducedneuralswitchofcovid19infection |