Human coronaviruses (HCoVs) are known respiratory pathogens associated with a range of respiratory outcomes. In the past 14 years, the onset of severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV) have thrust HCoVs into spotlight of the research community due to their high pathogenicity in humans. The study of HCoV-host interactions has contributed extensively to our understanding of HCoV pathogenesis. In this review, we discuss some of the recent findings of host cell factors that might be exploited by HCoVs to facilitate their own replication cycle. We also discuss various cellular processes, such as apoptosis, innate immunity, ER stress response, mitogen-activated protein kinase (MAPK) pathway and nuclear factor kappa B (NF-κB) pathway that may be modulated by HCoVs.

Traditional drug development and discovery has not kept pace with threats from emerging and re-emerging diseases such as Ebola virus, MERS-CoV and more recently, SARS-CoV-2. Among other reasons, the exorbitant costs, high attrition rate and extensive periods of time from research to market approval are the primary contributing factors to the lag in recent traditional drug developmental activities. Due to these reasons, drug developers are starting to consider drug repurposing (or repositioning) as a viable alternative to the more traditional drug development process. Drug repurposing aims to find alternative uses of an approved or investigational drug outside of its original indication. The key advantages of this approach are that there is less developmental risk, and it is less time-consuming since the safety and pharmacological profile of the repurposed drug is already established. To that end, various approaches to drug repurposing are employed. Computational approaches make use of machine learning and algorithms to model disease and drug interaction, while experimental approaches involve a more traditional wet-lab experiments. This review would discuss in detail various ongoing drug repurposing strategies and approaches to combat the current COVID-19 pandemic, along with the advantages and the potential challenges.

COVID-19 was declared a pandemic by the World Health Organization on March 11, 2020. This novel coronavirus disease, caused by the SARS-CoV-2 virus, has resulted in severe and unprecedented social and economic disruptions globally. Since the discovery of COVID-19 in December 2019, numerous antivirals have been tested for efficacy against SARS-CoV-2 in vitro and also clinically to treat this disease. This review article discusses the main antiviral strategies currently employed and summarizes reported in vitro and in vivo efficacies of key antiviral compounds in use.

COVID-19, the disease caused by SARS-CoV-2 (1), was declared a pandemic by the World Health Organization (WHO) in March 2020 (2). While awaiting a vaccine, several antivirals are being used to manage the disease with limited success (3, 4). To expand this arsenal, we screened 4 compound libraries: a United States Food and Drug Administration (FDA) approved drug library, an angiotensin converting enzyme-2 (ACE2) targeted compound library, a flavonoid compound library as well as a natural product library. Of the 121 compounds identified with activity against SARS-CoV-2, 7 were shortlisted for validation. We show for the first time that the active form of Vitamin D, calcitriol, exhibits significant potent activity against SARS-CoV-2. This finding paves the way for consideration of host-directed therapies for ring prophylaxis of contacts of SARS-CoV-2 patients.

Three patients with cutaneous T-cell lymphoma (CTCL) are reported who had concurrent B-cell chronic lymphocytic leukaemia (B-CLL). The separate lineage and clonal nature of the individual lymphoid malignancies were confirmed by gene-rearrangement analysis. The chronology of the illnesses did not support the hypothesis that CTCL predisposes to the development of B-cell proliferative disorders. There was no clear association with immunosuppressive therapy, and HTLV-1 studies were negative in all patients. Consequently, we speculate that a lymphoid stem cell defect, which may lead to the development of either aberrant B- or T-cell clones, may be responsible for such cases of dual lymphoid neoplasia.