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COVID‐19 is currently pandemic and the detection of SARS‐CoV‐2 variants in wastewater is causing widespread concern. Herein, cold atmospheric plasma (CAP) is proposed as a novel wastewater disinfection technology that effectively inactivates SARS‐CoV‐2 transcription‐ and replication‐competent virus‐like particles, coronavirus GX_P2V, pseudotyped SARS‐CoV‐2 variants, and porcine epidemic diarrhoea virus in a large volume of water within 180 s (inhibition rate > 99%). Further, CAP disinfection did not adversely affect the viability of various human cell lines. It is identified that CAP produced peroxynitrite (ONOO−), ozone (O3), superoxide anion radicals (O2−), and hydrogen peroxide (H2O2) as the major active substances for coronavirus disinfection. Investigation of the mechanism showed that active substances not only reacted with the coronavirus spike protein and affected its infectivity, but also destroyed the nucleocapsid protein and genome, thus affecting virus replication. This method provides an efficient and environmentally friendly strategy for the elimination of SARS‐CoV‐2 and other coronaviruses from wastewater. [ABSTRACT FROM AUTHOR]

[Display omitted] • The structural characteristics of EV71 and the mechanism of infection were reviewed. • Anti-EV71 drug candidates for different targets based on in vitro , animal, and clinical data were summarized. • The main therapeutic approaches for EV71 infection were discussed, and suggestions were made for further drug development. Enterovirus A71 (EV-A71) is capable of causing hand, foot and mouth disease (HFMD), which may lead to neurological sequelae and even death. As EV-A71 is resistant to environmental changes and mutates easily, there is still a lack of effective treatments or globally available vaccines. For more than 50 years since the HFMD epidemic, related drug research has been conducted. Progress in this area can promote the further application of existing potential drugs and develop more efficient and safe antiviral drugs, and provide useful reference for protecting the younger generation and maintaining public health security. At present, researchers have identified hundreds of EV-A71 inhibitors based on screening repurposed drugs, targeted structural design, and rational modification of previously effective drugs as the main development strategies. This review systematically introduces the current potential drugs to inhibit EV-A71 infection, including viral inhibitors targeting key sites such as the viral capsid, RNA-dependent RNA polymerase (RdRp), 2C protein, internal ribosome entry site (IRES), 3C proteinase (3Cpro), and 2A proteinase (2Apro), starting from each stage of the viral life cycle. Meanwhile, the progress of host-targeting antiviral drugs and their development are summarized in terms of regulating host immunity, inhibiting autophagy or apoptosis, and regulating the cellular redox environment. In addition, the current clinical methods for the prevention and treatment of HFMD are summarized and discussed with the aim of providing support and recommendations for the treatment of enterovirus infections including EV-A71. [ABSTRACT FROM AUTHOR]

A recent study published in MedComm highlights the characteristics of the SARS-CoV-2 Omicron BA.2.86 subvariant and its potential to cause a future pandemic. The BA.2.86 lineage, derived from the Omicron BA.2 variant, exhibits a high propensity to infect lung cells and has distinct antigenic epitopes. Additionally, its sublineage JN.1 demonstrates even greater immune escape ability. The BA.2.86 variant shows enhanced binding to ACE2 and increased membrane fusion capacity in lung cells. It also exhibits resistance to many monoclonal antibodies, indicating its evolving immune escape capacity. The JN.1 variant, which has stronger lung infection ability, is spreading rapidly worldwide. Further monitoring of its evolution is necessary. [Extracted from the article]

A study published in the journal MedComm found that a specific mutation in the viral nucleoprotein of avian influenza A viruses (IAVs) allows them to evade the butyrophilin subfamily 3 member A3 (BTN3A3) restriction on virus replication. This mutation, along with other substitutions in the nucleoprotein, enables IAVs to escape from BTN3A3 and potentially increase their zoonotic potential. The research highlights the importance of surveillance for IAV variations associated with BTN3A3 evasion in order to assess the risk of influenza pandemics and protect global public health. The study also identifies other host factors, such as interferon-stimulated genes, that play a role in controlling IAV infection. [Extracted from the article]