In this case, the diagnosis of cSLE was established based on clinical and immunological criteria as well as skin biopsy analysis. Relevant criteria are listed in the American College of Rheumatology (ACR) classification criteria of SLE; including 10 systemic or biological signs.  Other studies show a gain of sensitivity, even though with a loss of specificity, when using the Systemic Lupus International Collaborating Clinics (SLICC) for cSLE diagnosis. 
Her follow up will be based on frequent controls with her paediatrician to detect first signs of a possible complication such as lupus nephritis, gastrointestinal or neurological involvement or cardio-vascular manifestation.
As the main cause of cSLE remains uncertain, it is now admitted that a viral infection could be a trigger of the clinical manifestation. It is increasingly argued that herpesviruses like EBV or CMV are responsible for the development of autoimmune disorders. Studies show EBV and CMV DNA are found at high rates in blood samples of SLE patients. EBV serological analysis shows a higher rate of early antigen IgG and IgA in SLE patients compared to healthy EBV carriers. Cross reactions between anti EBV nuclear antigen 1 antibodies and lupus associated autoantigens were also highlighted as viral mediated autoimmunity. 
Parvovirus B19 is also known to trigger inflammatory responses with a cytokine production and high specific antibodies rate such as rheumatoid factor or antinuclear/ antiphospholipid antibodies in SLE patients. However, its role in lupus outbreak remains ambiguous. 
Similar inflammatory response and immune trigger could be expected from the recently discovered Covid-19 virus. As it became a global concern during the first half of year 2020, different studies were made on sera from patients with SARS CoV 2 infection to obtain a broader understanding of the inflammatory and immunopathogenesis of this virus.
Foremost, the fixation of coronavirus on ACE2 receptors causes the endocytosis of the virus, the downregulation of the ACE2 receptors and the rise of angiotensin II rate. As a result, an important cytokine and chemokine storm is released, especially IL 1 β, IL-4, IL-6, IL-8, IL-10, IFN γ, TNF- α, MCP1 and IP 10.   Furthermore, a study from Zhou et al showed another side to the coronavirus-linked autoimmunity; they studied blood samples from twenty Covid-19 positive patients and discovered a rise in autoimmune antibody with a prevalence of anti-52 kDa SSA/Ro antibody, anti-60 kDa SSA/Ro antibody and antinuclear antibody of 20%, 25% and 50% respectively. Other antibodies were all negative (i.e. anti-Scl-70, AntiJo-1 antibody, anticentromere B antibody, anti-SmD1 antibody, antiSSB antibody, anti-double-stranded DNA antibody, Anti-Streptolysin O antibody, the rheumatoid factor, Anti-Neutrophil Cytoplasmic Antibodies (ANCA) ), except for the anticyclic peptide containing citrulline antibodies (anti-CCP antibody) which was positive for only two patients. 
While those studies show biological evidences of inflammatory and immunity reaction triggered by SARS Cov-2 infection, other observations reported a rise in autoimmune disease in children, some of them overlapping a coronavirus infection. 
Considering all this information, the idea of a possible cSLE triggered by a Covid-19 infection is plausible but, to our knowledge, has not yet been described.
For this case’s patient, initial symptoms were consistent for a coronavirus infection.
Even though ageusia and anosmia are not commonly found in Covid-19 positive children; chemosensory disfunction is estimated to be present in up to 19.4% in adults.   In addition, a recent paper reports anosmia and ageusia as solely symptoms in 3 Covid-19 positive children.  Due to its tropism for the gastrointestinal tract and intense viral replication in the small and large intestines, SARS Cov 2 also causes digestive symptoms. A recent cohort study on children in Europe demonstrated that gastrointestinal manifestation is present in 22% of positive children. The two main symptoms were pyrexia and upper respiratory tract infection, found in 65% and 54% of patients, although 16% of positive children were asymptomatic. A great majority (87%) never needed respiratory support and, in 5% of cases, a co-infection with another virus was found. However, this European study considered patients eligible if SARS Cov 2 was detected in an RT-PCR from any clinical sample; serological testing was not taken into consideration. 
For the index patient, we faced an ambiguous situation where clinical symptoms were suspicious of a Covid-19 infection, but repeated RT-PCR were negative and serological assay was only once doubtful. Other symptoms were typical of cSLE and disappeared with adequate treatment, thus leading to the assumption that her Covid-19 presentation was probably paucisymptomatic.
As initial treatment, the patient received hydroxychloroquine (HCQ) in addition to corticoids for cSLE. As this molecule inhibits type 1 interferon, it has also been studied during the Covid-19 pandemic. Indeed, by blocking this immune response path, HCQ helps decrease viral replication and moderate the cytokine storm responsible for complicating Covid-19 clinical damages. A study by Gautret et al also reported a significant reduction of the viral carriage with HCQ in 20 patients. However, another study on 30 patients showed no superiority between HCQ versus placebo in viral clearance nor in the progression of radiological pneumonia.  With this knowledge, it is conceivable to say that treatment with HCQ for cSLE in a possible Covid-19 positive patient will, at worst have no action on Covid-19 symptoms or, at best avoid autoimmune dysregulation.