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<p>Post COVID-19 Condition (PCC) remains a complex and enigmatic condition despite substantial research progress. The direct impact of SARS-CoV-2 on different cell types is critical in the physiopathology, with the severity of damage being affected by factors such as viral load and the virus's ability to enter cells. Certain tissues, such as the lungs and brain, can retain viral proteins post-recovery, leading to persistent symptoms associated with PCC. Besides, the virus disrupts hormonal pathways, including the renin–angiotensin–aldosterone system (RAAS), creating a pro-inflammatory environment. Altered neurotransmitter regulation and immune responses are also common. The dysregulation of both innate and adaptive immune systems plays a key role, with hyperinflammatory responses and lymphocyte depletion contributing to severe outcomes. Endothelial dysfunction leads to vascular complications, while neuroinflammation from the virus’s neurotropic abilities causes varied neurological symptoms. The brainstem's vulnerability to the virus may further exacerbate neurological issues. Understanding the pathophysiology of PCC is vital for developing effective treatments and improving patient outcomes.</p>

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Unravelling the complex and unexpected physiopathology of the post COVID-19 condition: a narrative review

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年5月7日

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  • Felipe González-Alvarez,
  • Jose de Jesus Aceves-Buendia,
  • M. Lizeth Padilla-Jaimes,
  • Kassandra M. Noé-Zendejas,
  • Cuahutemoc Alejandro Alvarez-De La Cruz,
  • Alfredo Rojas-Maya,
  • Sthefany Anahi Bringas-Ortiz,
  • Andrea Diusdedith Gómez-santana,
  • Karla Maria Tamez-Torres,
  • José Sifuentes-Osornio,
  • Eduardo Peña,
  • Bruno Estañol

摘要

Post COVID-19 Condition (PCC) remains a complex and enigmatic condition despite substantial research progress. The direct impact of SARS-CoV-2 on different cell types is critical in the physiopathology, with the severity of damage being affected by factors such as viral load and the virus's ability to enter cells. Certain tissues, such as the lungs and brain, can retain viral proteins post-recovery, leading to persistent symptoms associated with PCC. Besides, the virus disrupts hormonal pathways, including the renin–angiotensin–aldosterone system (RAAS), creating a pro-inflammatory environment. Altered neurotransmitter regulation and immune responses are also common. The dysregulation of both innate and adaptive immune systems plays a key role, with hyperinflammatory responses and lymphocyte depletion contributing to severe outcomes. Endothelial dysfunction leads to vascular complications, while neuroinflammation from the virus’s neurotropic abilities causes varied neurological symptoms. The brainstem's vulnerability to the virus may further exacerbate neurological issues. Understanding the pathophysiology of PCC is vital for developing effective treatments and improving patient outcomes.