Role of S100A8/S100A9 in Human Herpesvirus 6 Replication

人疱疹病毒6 （HHV-6）在体内和体外主要在cd4阳性淋巴细胞中复制，并可能在单核细胞/巨噬细胞谱系中建立潜伏感染。已证实HHV-6B是麻疹的病原，而HHV-6A尚未与任何人类疾病相关。在这里，我们发现HHV-6在HHV-6感染的CD4+ T细胞中诱导了S100A8和S100A9的表达。此外，我们发现S100A9与HHV-6B U83相互作用。S100A9显著增强HHV-6的复制。这些发现提示S100A8/S100A9可能在HHV-6的复制和发病机制中起重要作用。

Human herpesvirus 6 (HHV-6) replicates predominantly in CD4-positive lymphocytes in vivo and in vitro and may establish latent infection in the monocyte/macrophage-lineage cells. It has been proved that HHV-6B is the etiologic agent of exanthem subitum, whereas HHV-6A has not yet been associated with any human diseases. Here, we showed that HHV-6 induced the expression of S100A8 and S100A9 in HHV-6 infected CD4+ T cells. Furthermore, we found that S100A9 interacted with HHV-6B U83. S100A9 significantly enhanced the HHV-6 replication. These findings suggest the S100A8/S100A9 may have an important role in the HHV-6 replication and pathogenesis.