2Division of Neurotherapeutics, Massachusetts General Hospital, Harvard Medical School, Boston, MA, United States.1PolyBio Research Foundation, Kenmore, WA, United States.Certain Human Genome Variants and/or Herv Activity May Facilitate Pasc DevelopmentДЄmy D.SARS-CoV-2 and/or Related Inflammatory Insults May Disrupt Brainstem Signaling.SARS-CoV-2 May Promote Extended вЂњAutoantibodyвЂќ Production, Often via Molecular Mimicry.Microbiome Dysbiosis Can Disrupt Host Metabolic and Neuroendocrine Signaling and/or Epithelial Barrier Function.SARS-CoV-2 May Dysregulate Host Microbiome/Virome Balance by Facilitating Pathobiont Virulence.SARS-CoV-2 or Reactivated Pathogens May Induce Pathological Immune Cell Signaling or Prime Glia.Reactivated Viruses and COVID-19 Associated Myocarditis.The Activity of Persistent Pathogens Can Serve as a Form of Predisposition to COVID-19.Functional Redundancy in Pathogen-Driven Processes Can Facilitate Chronic Symptom Development.SARS-CoV-2 May Impact the Activity of Bacteria, Fungi, and Parasites.

Immune Dysregulation Promoted by SARS-CoV-2 Can Lead to Reactivation of Already Acquired Neurotrophic Pathogens Such as Herpesviruses.

SARS-CoV-2 Appears Capable of Persistence in Certain Tissues.

SARS-CoV-2 Can Cause Injury to One or Multiple Organs or Tissues.

The Neuroinvasive and Neurotrophic Potential of SARS-CoV-2.

The editor and reviewers' affiliations are the latest provided on their Loop research profiles and may not reflect their situation at the time of review. Texas Christian University, United States

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