HDAC1 and PRC2 mediate combinatorial control in SPI1/PU.1-dependent gene repression in murine erythroleukaemia.

Although originally described as transcriptional activator, SPI1/PU.1, a major player in haematopoiesis whose alterations are associated with haematological malignancies, has the ability to repress transcription. Here, we investigated the mechanisms underlying gene repression in the erythroid lineage, in which SPI1 exerts an oncogenic function by blocking differentiation. We show that SPI1 represses genes by binding active enhancers that are located in intergenic or gene body regions. HDAC1 acts as a cooperative mediator of SPI1-induced transcriptional repression by deacetylating SPI1-bound enhancers in a subset of genes, including those involved in erythroid differentiation. Enhancer deacetylation impacts on promoter acetylation, chromatin accessibility and RNA pol II occupancy. In addition to the activities of HDAC1, polycomb repressive complex 2 (PRC2) reinforces gene repression by depositing H3K27me3 at promoter sequences when SPI1 is located at enhancer sequences. Moreover, our study identified a synergistic relationship between PRC2 and HDAC1 complexes in mediating the transcriptional repression activity of SPI1, ultimately inducing synergistic adverse effects on leukaemic cell survival. Our results highlight the importance of the mechanism underlying transcriptional repression in leukemic cells, involving complex functional connections between SPI1 and the epigenetic regulators PRC2 and HDAC1.

Chlorophyll and pheophytin protonated and deprotonated ions: Observation and theory.

Pheophytin a and chlorophyll a have been investigated by electrospray mass spectrometry in the positive and negative modes, in view of the importance of the knowledge of their properties in photosynthesis. Pheophytin and chlorophyll are both observed intensely in the protonated mode, and their main fragmentation route is the loss of their phytyl chain. Pheophytin is observed intact in the negative mode, while under collisions, it is primarily cleaved beyond the phytyl chain and loses the attaching propionate group. Chlorophyll is not detected in normal conditions in the negative mode, but addition of methanol solvent molecule is detected. Fragmentation of this adduct primarily forms a product (-30 amu) that dissociates into dephytyllated deprotonated chlorophyll. Semi-empirical molecular dynamics calculations show that the phytyl chain is unfolded from the chlorin cycle in pheophytin a and folded in chlorophyll a. Density functional theory calculations have been conducted to locate the charges on protonated and deprotonated pheophytin a and chlorophyll a and have found the major location sites that are notably more stable in energy by more than 0.5 eV than the others. The deprotonation site is found identical for pheophytin a and the chlorophyll a-methanol adduct. This is in line with experiment and calculation locating the addition of methanol on a double bond of deprotonated chlorophyll a.

Genetic characterization of B-cell prolymphocytic leukemia: a prognostic model involving MYC and TP53.

B-cell prolymphocytic leukemia (B-PLL) is a rare hematological disorder whose underlying oncogenic mechanisms are poorly understood. Our cytogenetic and molecular assessments of 34 patients with B-PLL revealed several disease-specific features and potential therapeutic targets. The karyotype was complex (≥3 abnormalities) in 73% of the patients and highly complex (≥5 abnormalities) in 45%. The most frequent chromosomal aberrations were translocations involving MYC [t(MYC)] (62%), deletion (del)17p (38%), trisomy (tri)18 (30%), del13q (29%), tri3 (24%), tri12 (24%), and del8p (23%). Twenty-six (76%) of the 34 patients exhibited an MYC aberration, resulting from mutually exclusive translocations or gains. Whole-exome sequencing revealed frequent mutations in TP53, MYD88, BCOR, MYC, SF3B1, SETD2, CHD2, CXCR4, and BCLAF1. The majority of B-PLL used the IGHV3 or IGHV4 subgroups (89%) and displayed significantly mutated IGHV genes (79%). We identified 3 distinct cytogenetic risk groups: low risk (no MYC aberration), intermediate risk (MYC aberration but no del17p), and high risk (MYC aberration and del17p) (P = .0006). In vitro drug response profiling revealed that the combination of a B-cell receptor or BCL2 inhibitor with OTX015 (a bromodomain and extra-terminal motif inhibitor targeting MYC) was associated with significantly lower viability of B-PLL cells harboring a t(MYC). We concluded that cytogenetic analysis is a useful diagnostic and prognostic tool in B-PLL. Targeting MYC may be a useful treatment option in this disease.

Architectural and functional heterogeneity of hematopoietic stem/progenitor cells in non-del(5q) myelodysplastic syndromes.

Myelodysplastic syndromes (MDSs) are hematopoietic stem cell disorders in which recurrent mutations define clonal hematopoiesis. The origin of the phenotypic diversity of non-del(5q) MDS remains unclear. Here, we investigated the clonal architecture of the CD34+CD38- hematopoietic stem/progenitor cell (HSPC) compartment and interrogated dominant clones for MDS-initiating cells. We found that clones mainly accumulate mutations in a linear succession with retention of a dominant subclone. The clone detected in the long-term culture-initiating cell compartment that reconstitutes short-term human hematopoiesis in xenotransplantation models is usually the dominant clone, which gives rise to the myeloid and to a lesser extent to the lymphoid lineage. The pattern of mutations may differ between common myeloid progenitors (CMPs), granulomonocytic progenitors (GMPs), and megakaryocytic-erythroid progenitors (MEPs). Rare STAG2 mutations can amplify at the level of GMPs, from which it may drive the transformation to acute myeloid leukemia. We report that major truncating BCOR gene mutation affecting HSPC and CMP was beneath the threshold of detection in GMP or MEP. Consistently, BCOR knock-down (KD) in normal CD34+ progenitors modifies their granulocytic and erythroid differentiation. Clonal architecture of the HSPC compartment and mutations selected during differentiation contribute to the phenotypic heterogeneity of MDS. Defining the hierarchy of driver mutations provides insights into the process of transformation and may guide the search for novel therapeutic strategies.

Presence of atypical thrombopoietin receptor (MPL) mutations in triple-negative essential thrombocythemia patients.

Mutations in signaling molecules of the cytokine receptor axis play a central role in myeloproliferative neoplasm (MPN) pathogenesis. Polycythemia vera is mainly related to JAK2 mutations, whereas a wider mutational spectrum is detected in essential thrombocythemia (ET) with mutations in JAK2, the thrombopoietin (TPO) receptor (MPL), and the calreticulin (CALR) genes. Here, we studied the mutational profile of 17 ET patients negative for JAK2V617F, MPLW515K/L, and CALR mutations, using whole-exome sequencing and next-generation sequencing (NGS) targeted on JAK2 and MPL. We found several signaling mutations including JAK2V617F at very low allele frequency, 1 homozygous SH2B3 mutation, 1 MPLS505N, 1 MPLW515R, and 2 MPLS204P mutations. In the remaining patients, 4 presented a clonal and 7 a polyclonal hematopoiesis, suggesting that certain triple-negative ETs are not MPNs. NGS on 26 additional triple-negative ETs detected only 1 MPLY591N mutation. Functional studies on MPLS204P and MPLY591N revealed that they are weak gain-of-function mutants increasing MPL signaling and conferring either TPO hypersensitivity or independence to expressing cells, but with a low efficiency. Further studies should be performed to precisely determine the frequency of MPLS204 and MPLY591 mutants in a bigger cohort of MPN.

Acquired TET2 mutation in one patient with familial platelet disorder with predisposition to AML led to the development of pre-leukaemic clone resulting in T2-ALL and AML-M0.

Familial platelet disorder with predisposition to acute myeloid leukaemia (FPD/AML) is characterized by germline RUNX1 mutations, thrombocytopaenia, platelet dysfunction and a risk of developing acute myeloid and in rare cases lymphoid T leukaemia. Here, we focus on a case of a man with a familial history of RUNX1R174Q mutation who developed at the age of 42 years a T2-ALL and, 2 years after remission, an AML-M0. Both AML-M0 and T2-ALL blast populations demonstrated a loss of 1p36.32-23 and 17q11.2 regions as well as other small deletions, clonal rearrangements of both TCRγ and TCRδ and a presence of 18 variants at a frequency of more than 40%. Additional variants were identified only in T2-ALL or in AML-M0 evoking the existence of a common original clone, which gave rise to subclonal populations. Next generation sequencing (NGS) performed on peripheral blood-derived CD34+ cells 5 years prior to T2-ALL development revealed only the missense TET2P1962T mutation at a frequency of 1%, which increases to more than 40% in fully transformed leukaemic T2-ALL and AML-M0 clones. This result suggests that TET2P1962T mutation in association with germline RUNX1R174Q mutation leads to amplification of a haematopoietic clone susceptible to acquire other transforming alterations.

Implementation of an in-house quantitative real-time polymerase chain reaction method for Hepatitis B virus quantification in West African countries.

Hepatitis B virus (HBV) is a major cause of chronic liver disease worldwide. HBV infection is diagnosed by serological tests, while real-time polymerase chain reaction (qRT-PCR) assays are used to quantify viral load, which is a crucial parameter to determine viral replication and to monitor antiviral treatments. However, measuring viral load in resource-limited countries remains nonsystematic, due to the high cost of commercial kits. Here, we describe the development, validation and implementation of a low-cost, in-house qRT-PCR assay to monitor HBV viral load in chronic carriers enrolled in the PROLIFICA programme in the Gambia and Senegal. Over 1500 HBsAg-positive patients, including 210 chronically infected HBV patients, who were given antiviral treatment (tenofovir), were monitored by qRT-PCR using the SYBR Green- and HBV-specific primers. Twenty-four tenofovir-treated patients were followed up and their viral load was tested every 3 months over the 12-month experimental time course. Compared to commercial assays, our in-house assay was shown to be (i) highly reliable, with good intra- and interassay reproducibility over a wide range (45-4.5 × 108 copies mL-1 ), (ii) very similar in the viral loads detected (R2  = .90), (iii) highly sensitive, as it detected loads as low as 30 copies mL-1 (~5 IU mL-1 ), (iv) cheaper (2- to 3-fold), (v) easier to implement and (vi) more rapid. Based on our experience, we recommend this assay as a reliable alternative to commercial assays, for monitoring HBV viraemia in resource-limited, highly endemic countries to reduce the cost and technical obstacles associated with commercial kits.

Insights on stock structure of round sardinella Sardinella aurita off north-west Africa based on otolith shape analysis.

This study examines the geographic variability in otolith shape of round sardinella Sardinella aurita as a tool for stock discrimination. Fish were analysed from six sampling locations from Senegal to the Mediterranean coast of Morocco. A combination of otolith shape indices and elliptic Fourier descriptors was investigated by multivariate statistical procedures. Within the studied area, three distinct groups were identified with an overall correct classification of 78%. Group A: Nador (Alboran Sea), group B: Casablanca (northern Morocco) and group C: Senegalese-Mauritanian. The results of this study confirm the absence of an Atlantic Ocean-Mediterranean Sea transition for this species, the Gibraltar Strait acting as an efficient barrier for S. aurita population separation. Off north-west Africa, fish from northern Morocco form a single group which is clearly isolated from Senegalese-Mauritanian waters, confirming the existence of a distinct stock in this area. Among group C, some discontinuity exists and suggests the existence of a sedentary fraction of S. aurita in northern Mauritania (Arguin Bank). The results are discussed in relation to oceanographic features and physical barriers to dispersal and fish management strategy in the study area.

Sleep quality assessment in 35 Parkinson's disease patients in the Fann Teaching Hospital, Dakar, Senegal.

INTRODUCTION: Sleep disorders are diverse in Parkinson's disease. We aimed to assess the quality of sleep in patients with Parkinson's disease in an African population. METHODS: In a transversal and prospective study from April to June 2014, all parkinsonian patients followed at the Fann Teaching Hospital Neurology Clinic (Dakar, Senegal) were assessed using the Hoehn and Yahr's scale and filled out the following questionnaires: Parkinson's disease sleep scale (PDSS), the Pittsburgh Sleep Quality Index (PSQI), and the Epworth Sleepiness Scale (ESS). A PDSS score<82 (or a subscore<5) and a PSQI score>5 indicated poor quality or impaired sleep. An ESS score>10 indicated excessive daytime sleepiness. We used the Pearson coefficient to search for correlation between age, disease stage, disease duration, and the importance of sleep impairment. RESULTS: Hoehn and Yahr staging was 2.42±0.90 in the 35 patients (60% male, mean age 65.7±7.4years, disease duration 32.4±23.4months). The mean total PDSS score was 99.5±24.1 and 74.3% of the patients had an abnormally high PSQI score, indicating high frequency and intensity of sleep disorders. Most frequent disorders were pain or cramps interrupting sleep, night waking to urinate and fatigue or sleepiness on waking. Patients exhibited excessive diurnal sleepiness in 22.9% of the cases; they often had an abnormal PSQI score. Both the total PDSS score and the difficulty to sleep increased with disease stage, but not with age or disease duration. CONCLUSION: We found evidence of major alteration of sleep quality in Senegalese Parkinson patients.

[Epilepsy and reproductive health: Senegalese cohort]. / Épilepsie et santé de la reproduction : cohorte sénégalaise.

INTRODUCTION: Epilepsy is a public health problem in Senegal and Africa because of its severity and its social importance. It occurs at any age sparing no sex. It can influence sexual life and reciprocally. Our aims were to study the effects of antiepileptic drugs on the sexual lives of women with epilepsy, the influence of these drugs on pregnancy and breastfeeding. METHODS: We conducted a prospective study from 1st March to 31st August 2011 in the neurological department of the Fann-Dakar teaching hospital Senegal. Only women with epilepsy were included. RESULTS: We collected 120 patients aged 16-64years with a mean age of 30.58years, 45% married, 44.16% were uneducated preponderant. All patients were taking antiepileptic drugs, 89.16% was alone. Fifty-five percent of our patients had epilepsy for at least 6years; 45.83% had generalized epilepsy; 44.17% of partial seizures. In our cohort, 64.16% were under phenobarbital, 69.16% had good adherence. As side effects of drugs, 90% had sexual problems. Seventy-five percent enjoyed an active sex life. A decrease in the number of sex per week for the disease [31/55=56.66%] was noted. In addition, 51.17% were using contraception, including 38.7% of oral kind and 64.86% had noticed an increase in seizure frequency during their pregnancies. Of the 74 women who had contracted a pregnancy, 41.89% had premature infants, 16.21% have made abortions and 61.17% had psychosocial life affected. DISCUSSION AND CONCLUSION: People with epilepsy often experience sexual problems that may be caused by epilepsy, antiepileptic and/or reactions of the partner and the other facing the diagnosis of epilepsy.

Time-domain diffuse optical imaging technique for monitoring rheumatoid arthritis disease activity: theoretical development and in silico validation.

Objective.Effective early treatment-within 3-5 months of disease onset-significantly improves rheumatoid arthritis (RA) prognosis. Nevertheless, 1 in 3 patients experiences treatment failure which takes 3-6 months to detect with current monitoring techniques. The aim of this work is to develop a method for extracting quantitative features from data obtained with time-domain diffuse optical imaging (TD-DOI), and demonstrate their sensitivity to RA disease activity.Approach.80 virtual phantoms of the proximal interphalangeal joint-obtained from a realistic tissue distribution derived from magnetic resonance imaging-were created to simulate RA-induced alterations in 5 physiological parameters. TD-DOI images were generated using Monte Carlo simulations, and Poisson noise was added to each image. Subsequently, each image was convolved with an instrument response function (IRF) to mimic experimental measurements. Various spatiotemporal features were extracted from the images (i.e. statistical moments, temporal Fourier components), corrected for IRF effects, and correlated with the disease index (DI) of each phantom.Main results.Spatiotemporal Fourier components of TD-DOI images were highly correlated with DI despite the confounding effects of noise and the IRF. Moreover, lower temporal frequency components (⩽0.4 GHz) demonstrated greater sensitivity to small changes in disease activity than previously published spatial features extracted from the same images.Significance.Spatiotemporal components of TD-DOI images may be more sensitive to small changes in RA disease activity than previously reported DOI features. TD-DOI may enable earlier detection of RA treatment failure, which would reduce the time needed to identify treatment failure and improve patient prognosis.

Time-domain diffuse optical imaging technique for monitoring rheumatoid arthritis disease activity: experimental validation in tissue-mimicking finger phantoms.

Objective.Effective treatment within 3-5 months of disease onset significantly improves rheumatoid arthritis (RA) prognosis. Nevertheless, 30% of RA patients fail their first treatment, and it takes 3-6 months to identify failure with current monitoring techniques. Time-domain diffuse optical imaging (TD-DOI) may be more sensitive to RA disease activity and could be used to detect treatment failure. In this report, we present the development of a TD-DOI hand imaging system and validate its ability to measure simulated changes in RA disease activity using tissue-mimicking finger phantoms.Approach.A TD-DOI system was built, based on a single-pixel camera architecture, and used to image solid phantoms which mimicked a proximal interphalangeal finger joint. For reference,in silicoimages of virtual models of the solid phantoms were also generated using Monte Carlo simulations. Spatiotemporal Fourier components were extracted from both simulated and experimental images, and their ability to distinguish between phantoms representing different RA disease activity was quantified.Main results.Many spatiotemporal Fourier components extracted from TD-DOI images could clearly distinguish between phantoms representing different states of RA disease activity.Significance.A TD-DOI system was built and validated using finger-mimicking solid phantoms. The findings suggest that the system could be used to monitor RA disease activity. This single-pixel TD-DOI system could be used to acquire longitudinal measures of RA disease activity to detect early treatment failure.

[Spatiotemporal distribution of tuberculosis cases in the city of Saint-Louis Senegal from 2008-2011]. / Répartition spatio-temporelle des cas de tuberculose dans la ville de Saint-Louis du Sénégal entre 2008-2011.

BACKGROUND: We studied the incidence of tuberculosis in the health district of Saint-Louis, Senegal over a period of 4years (2008-2011). One thousand three hundred and eighty-six cases were identified, producing an annual standardized incidence ratio of 129 cases per 100,000 inhabitants. RESULTS: Men in the 15-24-year old age group were more likely to be affected, and diagnosis was more common in the second half of the year. Treatment compliance was excellent (96%), and the cure rate of patients with a TB-positive microscopic examination was 95%. The overall treatment failure rate was 1% and the 6-month morality was 2%. Seropositivity, measured in volunteer patients (48%) was 3%. CONCLUSION: A spatial and temporal map of tuberculosis in the city of Saint-Louis, Senegal has been established. A cluster appears to be very likely in Guet Ndar, a particularly dense population zone in a fishing area. There is also a possible secondary cluster at Pikine.

Sunitinib Treatment of VHL C162F Cells Slows Down Proliferation and Healing Ability via Downregulation of ZHX2 and Confers a Mesenchymal Phenotype.

von Hippel-Lindau (VHL) disease, due to mutations of the tumor suppressor VHL gene, is a rare hereditary syndrome with a high risk of developing clear cell renal cell carcinoma (ccRCC). We asked whether the VHL-C162F mutation interferes with proliferation, migration, healing and forming colony ability by using wild-type VHL (WT VHL) and VHL-C162F reconstituted cells. We then analyzed the in vitro impact of the sunitinib treatment on VHL-C162F cells. We showed that VHL-C162F mutations have no impact on cell morphology, colony formation and migration ability but confer a significant higher healing ability than in WT VHL cells. RNA sequencing analysis revealed that VHL-C162F mutation upregulates genes involved in hypoxia and epithelial mesenchymal transition (EMT) pathways by comparison with VHL WT cells. We next showed a decrease in healing ability in VHL-C162F cells depleting on ZHX2, an oncogenic driver of ccRCC, highlighting the potential involvement of ZHX2 in aggressiveness of the VHL-C162F cells. Moreover, we found that sunitinib treatment inhibits ZHX2 expression and induces a reduced proliferation correlating with downregulation of P-ERK. Sunitinib treatment also conferred a more mesenchymal profile to VHL-C162F cells with significant downregulation of E-cadherin and upregulation of N-cadherin, Slug and AXL. Sunitinib therapy may therefore promote disease progression in VHL-C162F patients.

FANCA deficiency promotes leukaemic progression by allowing the emergence of cells carrying oncogenic driver mutations.

Leukaemia is caused by the clonal evolution of a cell that accumulates mutations/genomic rearrangements, allowing unrestrained cell growth. However, recent identification of leukaemic mutations in the blood cells of healthy individuals revealed that additional events are required to expand the mutated clones for overt leukaemia. Here, we assessed the functional consequences of deleting the Fanconi anaemia A (Fanca) gene, which encodes a DNA damage response protein, in Spi1 transgenic mice that develop preleukaemic syndrome. FANCA loss increases SPI1-associated disease penetrance and leukaemic progression without increasing the global mutation load of leukaemic clones. However, a high frequency of leukaemic FANCA-depleted cells display heterozygous activating mutations in known oncogenes, such as Kit or Nras, also identified but at low frequency in FANCA-WT mice with preleukaemic syndrome, indicating that FANCA counteracts the emergence of oncogene mutated leukaemic cells. A unique transcriptional signature is associated with the leukaemic status of FANCA-depleted cells, leading to activation of MDM4, NOTCH and Wnt/ß-catenin pathways. We show that NOTCH signalling improves the proliferation capacity of FANCA-deficient leukaemic cells. Collectively, our observations indicate that loss of the FANC pathway, known to control genetic instability, fosters the expansion of leukaemic cells carrying oncogenic mutations rather than mutation formation. FANCA loss may contribute to this leukaemogenic progression by reprogramming transcriptomic landscape of the cells.

Acute renal failure in the postpartum due to calcified myoma: a case report.

BACKGROUND: It has been reported that delivery can be a cause of urine retention. This complication occurs especially in case which are associated with a pelvic mass like calcified uterine myoma. But this unusual aspect of myoma can make ultrasonographic traps. OBJECTIVE: To report an unusual case of calcified uterine myoma which was unnoticed during pregnancy and made so obstructive renal failure few days after the delivery. CASE REPORT: Seven days after delivery a Twenty-nine-year-old Senegalese woman was admitted at a private hospital for a slight alteration of consciousness(Glasgow Coma Scale at 12). Emergency check-up showed an acute obstructive renal failure. Biological investigations showed ascendancy of granulocytes, deterioration of renal function with creatinin in 78 mg / l and urea in 1.82 g/l. Ultrasonographic examination revealed bilateral dilatation of renal calyces and an interstitial calcified uterine myoma compressing the bladder. Management consisted on a urethral catheterization of bladder, correction of hydro-electrolytic troubles and antibiotherapy (ciprofloxacin).Global evolution leads to fast fully consciousness, with disappearance of biological and ultrasonographic disorders. CONCLUSION: Calcified myoma can look like cephalic pole during pregnancy. This unusual aspect can be sometimes source of acute obstructive renal failure requiring urinary drainage in emergency. Improvement of women's management during postpartum can prevent such complications.

PATLAB: A graphical computational software package for photoacoustic computed tomography research.

Photoacoustic tomography (PAT) provides high resolution optical images of tissue at depths of up to several centimetres. This modality has been of interest to researchers for at least 30 years and is still the subject of intensive research. However, PAT researchers lack access to a comprehensive open-source graphical simulation and reconstruction software package. In this article, we introduce PATLAB, an open-source MATLAB-based graphical software package that can perform both PAT simulation and image reconstruction. PATLAB is simple to use yet is capable of complex PAT data processing tasks and offers advanced users a framework to build and test new methods.

NF-κB signaling controls H3K9me3 levels at intronic LINE-1 and hematopoietic stem cell genes in cis.

Ionizing radiations (IR) alter hematopoietic stem cell (HSC) function on the long term, but the mechanisms underlying these effects are still poorly understood. We recently showed that IR induces the derepression of L1Md, the mouse young subfamilies of LINE-1/L1 retroelements. L1 contributes to gene regulatory networks. However, how L1Md are derepressed and impact HSC gene expression are not known. Here, we show that IR triggers genome-wide H3K9me3 decrease that occurs mainly at L1Md. Loss of H3K9me3 at intronic L1Md harboring NF-κB binding sites motifs but not at promoters is associated with the repression of HSC-specific genes. This is correlated with reduced NFKB1 repressor expression. TNF-α treatment rescued all these effects and prevented IR-induced HSC loss of function in vivo. This TNF-α/NF-κB/H3K9me3/L1Md axis might be important to maintain HSCs while allowing expression of immune genes during myeloid regeneration or damage-induced bone marrow ablation.

Demographics and outcomes of laboratory-confirmed COVID-19 cases during the first epidemic wave in Senegal.

BACKGROUND: Few studies have focused on the effects of COVID-19 on African populations. During the first epidemic wave in Senegal (May 1 to July 31, 2020), COVID-19 cases were isolated in treatment centers of epidemics (TCEs). We described the demographics and outcomes of COVID-19 cases in TCEs. PATIENTS AND METHODS: All cases with laboratory-confirmed COVID-19 in Thiès medical region of Senegal were included. RESULTS: COVID-19 was confirmed in 600 cases. Median age of cases (men: 357, 59.5%; women: 243, 40.5%) was 34.0years. The incidence was 12 per 100,000 inhabitants per month. Overall, 46 (7.7%) cases had a severe or critical form of the disease, and nine of them died. Of 455 cases quarantined in non-hospital TCEs, 340 (74.7%) had no symptom and 115 (25.3%) had mild or moderate symptoms. CONCLUSION: In this African retrospective cohort, COVID-19 cases were young and mostly asymptomatic with a low case fatality rate.