The entire world has been impacted by the ongoing SARS-CoV2 pandemic. Introduction of vaccinations have helped reduce the spread and hospitalisations; however, it is inevitable that SARS-CoV2 will become endemic. In Australia, we were uniquely poised to uncover how a single infection, without background community spread, impacts the immune system over an extended period. We recruited 69 COVID convalescent patients and studied them prospectively with longitudinal samples taken at 12-, 16- and 24-weeks post infection. PBMC were isolated and immune phenotyped using flow cytometry. Unbiased tSNE approaches and a deep hierarchical gating strategy were used to identify over 130 common and rare cell populations and subtypes of the immune compartment. Perturbations occurred in both innate and adaptive immune arms including neutrophils, monocytes and NK cells as well as B cells, T follicular helpers, T helpers and many subtypes of Tregs. There was a larger proportion of innate immune cells expressing CXCR3, and a larger proportion of CXCR3+ T follicular helpers (TfH1 cells) in COVID convalescent patients compared with pre-COVID, anti-SARS-CoV2 IgG antibody negative, healthy controls. There was also an observed proportional increase in CCR10 expressing T helper central memory subtypes (Th22cm, Th2/22cm) and a proportional decrease in CCR10 expressing Treg subtypes (ThR22, ThR2/22) compared with healthy controls. These alterations returned to pre-COVID healthy control levels by 24 weeks post infection. Investigations are currently underway to determine functional and transcriptional impacts COVID infection may have on these cell types. Understanding how exposure to the virus impacts immunological programs in the long-term may reveal treatments for COVID infection or long-haul COVID symptoms.