Scientists discover “migrions,” structures that amplify infections

Scientists discover “migrions,” structures that amplify infections

Photo: depositphotos

Scientists have identified previously unknown structures that resemble hybrids of cells and viruses and help pathogens spread faster and more aggressively by moving together with migrating cells, according to SciTechDaily.

Viruses rely on movement between cells to establish infection and drive disease progression. Unlike bacteria, they cannot replicate independently and must enter host cells, making the mode of intercellular transmission a key factor in infection severity.

Researchers from Peking University Health Science Center and the Harbin Veterinary Research Institute have now uncovered an unexpected pathway used by vesicular stomatitis virus (VSV) to move from one cell to another. They found that infected cells actively transport viral genetic material and proteins into migrasomes — recently identified cellular structures that form during cell migration.

Migrasomes typically facilitate cell-to-cell communication by releasing packets of biological material as cells move. However, the researchers observed that some migrasomes were loaded with viral nucleic acids and displayed the VSV surface protein VSV-G. The team named these virus-carrying structures “migrions.”

Migrions are larger than individual virus particles and function as virus-like entities rather than conventional free virions. When VSV spreads via migrions, viral replication begins more rapidly than during infection by free virus particles, likely because multiple copies of the viral genome are delivered simultaneously.

The scientists also found that migrions can carry more than one type of virus at the same time, enabling the co-transmission of heterologous viruses.

According to the researchers, migrions represent a new paradigm of intercellular viral transmission that directly links viral spread to cell migration. The discovery challenges traditional models of viral dissemination by introducing a migration-dependent mechanism that exploits the host’s migratory machinery to drive systemic infection.

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