Chandelier
Senior Member (Voting Rights)
SARS-CoV-2 spike-driven reactivation of latent herpesviruses as a mechanistic link to post-viral diseases
Jana, Manoj K.; Nora-Krukle, Zaiga; Prusty, Bhupesh K.
Emerging evidence suggests that the severe acute respiratory syndrome coronavirus 2 spike protein can perturb innate immune signalling and cellular metabolism, conditions known to disrupt herpesvirus latency.
We propose that spike-induced immune-metabolic stress may facilitate the reactivation of neurotropic herpesviruses such as human herpesvirus 6, human herpesvirus 7, and Epstein–Barr virus, thereby sustaining immune dysregulation and cellular dysfunction.
This virus–virus interaction framework provides a plausible mechanistic explanation for the biology of chronic post-viral disease and highlights herpesvirus reactivation as a potential target for biomarker development and therapeutic intervention.
In this review, we examine the evidence that spike-induced immune and metabolic remodelling facilitates the reactivation of latent neurotropic herpesviruses, particularly human herpesvirus 6 (HHV-6), HHV-7, and Epstein–Barr virus, amplifying immune dysregulation through viral proteins and host–pathogen interactions that perturb mitochondrial function, innate immune responses, and neuroimmune communication.
We discuss how this virus–virus interaction represents a biologically plausible pathway linking chronic SARS-CoV-2 infection to downstream cellular dysfunction.
By integrating emerging evidence on spike persistence with established principles of herpesvirus latency biology, we argue that herpesvirus reactivation serves as a mechanistic consequence of SARS-CoV-2 infection.
Understanding how the spike protein perturbs cellular homeostasis and triggers latent virus reactivation may reveal biomarkers of reactivation and inform targeted therapeutic strategies to interrupt this cascade in post-infectious disease states.
Web | DOI | Trends Open | Open Access
Jana, Manoj K.; Nora-Krukle, Zaiga; Prusty, Bhupesh K.
Significance
Persistent symptoms following viral infections are increasingly recognized, yet the biological mechanisms driving long-term disease remain poorly defined.Emerging evidence suggests that the severe acute respiratory syndrome coronavirus 2 spike protein can perturb innate immune signalling and cellular metabolism, conditions known to disrupt herpesvirus latency.
We propose that spike-induced immune-metabolic stress may facilitate the reactivation of neurotropic herpesviruses such as human herpesvirus 6, human herpesvirus 7, and Epstein–Barr virus, thereby sustaining immune dysregulation and cellular dysfunction.
This virus–virus interaction framework provides a plausible mechanistic explanation for the biology of chronic post-viral disease and highlights herpesvirus reactivation as a potential target for biomarker development and therapeutic intervention.
Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is increasingly associated with long-term biological perturbations that persist beyond the acute phase of the disease.In this review, we examine the evidence that spike-induced immune and metabolic remodelling facilitates the reactivation of latent neurotropic herpesviruses, particularly human herpesvirus 6 (HHV-6), HHV-7, and Epstein–Barr virus, amplifying immune dysregulation through viral proteins and host–pathogen interactions that perturb mitochondrial function, innate immune responses, and neuroimmune communication.
We discuss how this virus–virus interaction represents a biologically plausible pathway linking chronic SARS-CoV-2 infection to downstream cellular dysfunction.
By integrating emerging evidence on spike persistence with established principles of herpesvirus latency biology, we argue that herpesvirus reactivation serves as a mechanistic consequence of SARS-CoV-2 infection.
Understanding how the spike protein perturbs cellular homeostasis and triggers latent virus reactivation may reveal biomarkers of reactivation and inform targeted therapeutic strategies to interrupt this cascade in post-infectious disease states.
Web | DOI | Trends Open | Open Access
