Mechanism that Allows Shingles Virus to Spread Beyond Initial Infection Site Identified

Scientists at the University of Colorado Anschutz Medical Campus have discovered that the varicella zoster virus (VZV), which is responsible for chickenpox and shingles, employs a clever evasion strategy that allows it to spread far beyond the initial infection site.

The team honed in on a viral protein called IE62 as the key player in this process. IE62 is packaged into small extracellular vesicles (sEVs), which act as transport vehicles, carrying the protein throughout the body. Once delivered to distant cells, IE62 disables their antiviral defenses, paving the way for viral infection.

This finding is particularly significant because it explains how VZV, which affects 95% of people and can remain dormant for years, manages to reactivate and cause widespread damage. The virus's ability to hijack the body's cellular machinery for its own purposes demonstrates its sophisticated evolution.

Christy Niemeyer, lead author of the study published in the Journal of Virology, emphasized the importance of this discovery: "We've uncovered a clear mechanism that explains how this virus can affect organs far from the original infection site." This insight could lead to new therapeutic approaches for managing VZV infections and their complications.

The research also sheds light on why VZV infections are often associated with co-infections and immunosuppression. Andrew Bubak, the study’s senior author, suggested that this mechanism might be more prevalent than previously thought, potentially occurring even in the absence of visible symptoms.

There are currently no treatments targeting this newly discovered protein, and this study opens up possibilities for developing novel therapeutics that could intervene in the virus's spread and reduce its systemic impact.