Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV) -2 infection induces an exacerbated inflammation driven by innate immunity components . Dendritic cells (DCs) play a key role in the defense against viral infections, for instance plasmacytoid DCs (pDCs), have the capacity to produce vast amounts of interferon-alpha (IFN-α). In COVID-19 there is a deficit in DC numbers and IFN-α production, which has been associated with disease severity . In this work, we described that in addition to the DC deficiency, several DC activation and homing markers were altered in acute COVID-19 patients, which were associated with multiple inflammatory markers . Remarkably, previously hospitalized and non-hospitalized patients remained with decreased numbers of CD1c+ myeloid DCs and pDCs seven months after SARS-CoV-2 infection . Moreover, the expression of DC markers as CD86 and CD4 were only restored in previously non-hospitalized patients while integrin β7 and indoleamine 2,3- dyoxigenase (IDO) no restoration was observed . These findings contribute to a better understanding of the immunological sequelae of COVID-19.