Surge in the jellyfish population of a tropical monsoonal estuary: A boon or bane to its plankton community dynamics?

Recurrent jellyfish blooms and their impacts on ecosystem deliverables of coastal habitats have become a major ecological concern. In view of this, repercussions of a surge in the jellyfish population on the plankton community were studied in Cochin estuary (CE), the largest tropical estuary along the southwest coast of India. Evaluation of hydrographic attributes and plankton community of the CE during early and late pre-monsoon revealed a marked disparity in its hydrography which favoured an increase in jellyfish abundances during late pre-monsoon, eliciting distinct impacts on the plankton community. The escalation in the jellyfish abundance and their subsequent predation on the crustacean plankton released the phytoplankton community from the grazing pressure resulting in a trophic cascade in the planktonic food web. The indiscriminate feeding of jellyfishes on the ichthyoplankton, decapod larvae, and Copepoda, the primary diet component of forage fishes evoked a potent threat to the fishery potential of CE.

Drug repurposing screen identifies masitinib as a 3CLpro inhibitor that blocks replication of SARS-CoV-2 in vitro

There is an urgent need for anti-viral agents that treat SARS-CoV-2 infection. The shortest path to clinical use is repurposing of drugs that have an established safety profile in humans. Here, we first screened a library of 1,900 clinically safe drugs for inhibiting replication of OC43, a human beta-coronavirus that causes the common-cold and is a relative of SARS-CoV-2, and identified 108 effective drugs. We further evaluated the top 26 hits and determined their ability to inhibit SARS-CoV-2, as well as other pathogenic RNA viruses. 20 of the 26 drugs significantly inhibited SARS-CoV-2 replication in human lung cells (A549 epithelial cell line), with EC50 values ranging from 0.1 to 8 micromolar. We investigated the mechanism of action for these and found that masitinib, a drug originally developed as a tyrosine-kinase inhibitor for cancer treatment, strongly inhibited the activity of the SARS-CoV-2 main protease 3CLpro. X-ray crystallography revealed that masitinib directly binds to the active site of 3CLpro, thereby blocking its enzymatic activity. Mastinib also inhibited the related viral protease of picornaviruses and blocked picornaviruses replication. Thus, our results show that masitinib has broad anti-viral activity against two distinct beta-coronaviruses and multiple picornaviruses that cause human disease and is a strong candidate for clinical trials to treat SARS-CoV-2 infection.