HERV-K10 as a mediator of immune modulation in hepatitis infections.

Although the increase in HERV-K10 expression in chrHBV patients did not reach statistical significance, likely due to limited sample size, we observed a clear trend toward upregulation compared to healthy controls ( Figure 4G ).

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Although the LTR5 group—encompassing HERV-K10 loci—did not reach statistical significance at the group level, locus-specific analysis identified two individual HERV-K10 loci on chromosome 1 that were significantly upregulated upon HBV infection ( Figure 2B ).

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