Hyeon Seon Ahn

: Hepatitis E, caused by hepatitis E virus (HEV), is a highly endemic disease with a major public health impact. In Senegal, the first HEV outbreak was identified in 2014 in Kedougou, and a recent study focusing on pregnant women showed a seroprevalence of 7.8%. Apart from these data, very little is known about its burden in Senegal, and there is no specific surveillance program. We describe HEV prevalence among acute febrile jaundice patients in Senegal. A retrospective analysis using jaundice samples (2008–2020) collected through the national yellow fever surveillance program were tested for HEV by IgM/IgG ELISA and reverse transcription polymerase chain reaction (RT-PCR). Sequencing and phylogenetic analyses were performed on RT-PCR-positive samples. Statistical tools were used to analyze the HEV prevalence. In total, 2,387 samples were tested, and 174 IgG, 135 IgM/IgG, and 29 IgM positive samples were detected. Among the IgM-positive samples, 74 were positive by RT-PCR. The results showed an overall HEV prevalence of 14% in febrile jaundice patients in Senegal. Phylogenetic analyses showed the circulation of genotype 2b. Our data confirmed the HEV outbreak in Kedougou in 2014 and showed the detection of acute cases in other regions. We also detected in these regions genotype 2b, which is usually associated with large outbreaks in many African countries, suggesting a high risk of HEV outbreak occurrence in Senegal. Finally, our data showed that the yellow fever surveillance program, which is based on jaundice and already exists in many countries, could be a valuable tool for HEV surveillance.

Chikungunya virus (CHIKV) is an alphavirus transmitted by mosquitos that poses a threat to global public health and for which there is an urgent need for widespread access to globally licensed vaccines. Here, we demonstrate that an inactivated CHIKV vaccine (BBV87) protects against systemic infection with CHIKV in a non-human primate (NHP) challenge model. Groups of five cynomolgus macaques received two doses of 20 µg BBV87 vaccine or saline alone (28 days apart). Twenty-eight days after the second immunisation, all animals were challenged with CHIKV. All controls were productively infected with detectable viremia and pathological responses following challenge, including altered thermoregulation, haematological and cytokine changes. Critically, the histopathological analysis of finger joints identified areas of inflammation in the synovium. By contrast vaccinated macaques had no detectable viremia and none of the pathological changes were reported in control animals. This study demonstrates that a 20 µg dose of BBV87 vaccine confers robust protection in vivo, both on the acquisition of infection and pathology.