Our results demonstrated that older age was independently associated with prolonged SARS-CoV-2 RNA shedding. Previous studies have shown that older age is a risk factor for SARS-CoV-2 infection and has been associated with a greater risk of development of acute respiratory distress syndrome and mortality [8, 12]. Our findings further contribute to the literature by addressing the association between age and SARS-CoV-2 RNA shedding. One possible explanation would be that older patients typically generate less robust innate and adaptive immune responses, limiting the viral clearance, which predisposes to prolonged duration of viral shedding [13]. Of interest, a previous study of SARS-CoV has shown that the polymorphism of genes involved in innate immunity (i.e. interleukin-18, interleukin-1A and fibrinogen-like protein 2), which could be regulated in an age- and sex-dependent manner, was associated with viral load during the initial stage of the disease [14]. This highlights the importance of host genetic factors in the process of viral infections and merits further investigations in COVID-19.