Introduction

Respiratory syncytial virus (RSV), first characterized in 19561, often causes lower respiratory tract infections in infants. It is the second leading cause of bronchiolitis and pneumonia, particularly during the winter months in temperate countries and during the rainy season in tropical countries 2-6. RSV was estimated to be responsible for more than 90 million deaths worldwide between 1995-2010, including 20 million in sub-Saharan Africa alone7,8.
RSV belongs to the order Mononegavirales , the familyPneumoviridae , the genus Orthopneumovirus and the speciesHuman orthopneumovirus . It is an enveloped virus, with a linear, negative-sense RNA genome of about 15 000 base pairs (bp). The genome contains 10 genes that code for 11 proteins: the NS1, NS2, N, P, M, SH, G, F, M1-2, M2-2 and L proteins 5. The surface glycoproteins G and F are the main targets of neutralising antibodies9. The F protein governs the fusion of the viral envelope with the cell membrane. The glycoprotein G is involved in the attachment of the virus to the CX3CR1 chemokine receptor expressed on epithelial cells and facilitates the penetration of the virus into the host cell 10. The variability of the G protein facilitates evasion of the immune response, allowing re-infections throughout life and complicates vaccine development11.
Epidemiological and molecular studies on the antigenic and genetic variability of the G protein have classified RSV into two highly divergent phylogenetic sub-groups A and B 3,12,13. To date, there are 15 genotypes in the RSV-A sub-group (GA1-GA7, SAA1-SAA2, CB-A, NA1-NA4, and ON1) and 37 genotypes in the B sub-group (GB1-GB13, SAB1-SAB4, URU1-URU2, CB1, CBB, JAB1, THB and BA1-BA14)14-17. In the RSV-A sub-group, the ON1 genotype was first described in 2010 in Canada and is the most frequent RSV-A genotype to date. It contains a 72 nucleotide (nt) duplication in the gene sequence corresponding to the C-terminal region of the G protein, the largest known duplication 2,4. In RSV-B, the BA genotypes, first detected in 1999, have now become the predominant RSV-B circulating worldwide and carry a 60 nt duplication18,19.
In Central African Republic (CAF), a preliminary study reported RSV in 3.0% (10/329) of children aged 0-15 years enrolled from January to December 2010 20. Here, we analysed epidemiological and clinical data and characterised RSV strains from children under 5 years of age, hospitalized or not, recruited in 5 sentinel sites and provide first insights into RSV prevalence, seasonality and disease severity in CAF.