These first results i) confirm that a certain level of “basal” HERV expression is a physiological phenomenon, and should be considered when investigating HERV upregulation in a diseased context to avoid overinterpreted conclusions; and ii) suggest that it is unlikely that HIV infection can lead to an unspecific upregulation of HML2 sequences or to the general activation of any other HERV group. Here, CLEC10A is linked to HIV infectious disease.