I n tropical countries, including India, acute febrile illnesses (AFIs) constitute a group of infections with similar manifestations, such as fever, malaise, body aches, chills, hepatic and renal dysfunction, and central nervous system effects. The causative agents of AFI can be bacterial (e.g., Orientia tsutsugamushi, Leptospira, and Salmonella enterica serovar Typhi), parasitic (protozoans of the apicomplexa family), or viral (e.g., dengue virus [DENV], chikungunya virus [CHIKV], influenza A[H1N1] virus) (1-4). Distinguishing between the causative agents of AFIs can be difficult. In tropical climates, several AFI pathogens,

Current understanding of flagellum biogenesis during the cell cycle in trypanosomatids is limited to a few pathogenic species, including Trypanosoma brucei, Trypanosoma cruzi, and Leishmania spp. The most notable characteristics of trypanosomatid flagella studied so far are the extreme stability and lack of ciliary disassembly/absorption during the cell cycle. This is different from cilia in Chlamydomonas and mammalian cells, which undergo complete absorption prior to cell cycle initiation. In this study, we examined flagellum duplication during the cell cycle of Leptomonas pyrrhocoris. With the shortest duplication time documented for all Trypanosomatidae and its amenability to culture on agarose gel with limited mobility, we were able to image these cells through the cell cycle. Rapid, cell cycle-specific flagellum disassembly different from turnover was observed for the first time in trypanosomatids. Given the observed length-dependent growth rate and the presence of different disassembly mechanisms, we proposed a min-max model that can account for the flagellar length variation observed in L. pyrrhocoris.

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SARS-CoV-2 has infected millions of individuals across the globe and has killed over 2.7 million people. Even though vaccines against this virus have recently been introduced, the antibody generated in the process has been reported to decline quickly. This can reduce the efficacy of vaccines over time and can result in re-infections. Thus, drugs that are effective against COVID-19 can provide a second line of defence and can prevent occurrence of the severe form of the disease. The interaction between SARS-CoV2 S-protein and human ACE2 (hACE2) is essential for the infection of the virus. Thus, drugs that block this interaction could potentially inhibit SARS-CoV-2 infection into the host cells. To identify such drugs, we first analyzed the recently published crystal structure of S-protein-hACE2 complex and identified essential residues of both S-protein and hACE2 for this interaction. We used this knowledge to virtually dock a drug library containing 4115 drug molecules against S-protein for repurposing drugs that could inhibit binding of S-protein to hACE2. We identified several potential inhibitors based on their docking scores, pharmacological effects and ability to block residues of S protein required for interaction with hACE2. The top inhibitors included drugs used for the treatment of hepatitis C (velpatasvir, pibrentasvir) as well as several vitamin D derivatives. Several molecules obtained from our screen already have good experimental support in published literature. Thus, we believe that our results will facilitate the discovery of an effective drug against COVID-19.