Nanotechnologies for the Diagnosis and Treatment of SARS-CoV-2 and Its Variants.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), responsible for the global coronavirus disease 2019 (COVID-19) pandemic, has caused well over 750 million infections and 6.8 million deaths. Rapid diagnosis and isolation of infected patients are the primary aims of the concerned authorities to minimize the casualties. The endeavor to mitigate the pandemic has been impeded by the emergence of newly identified genomic variants of SARS-CoV-2. Some of these variants are considered as serious threats because of their higher transmissibility and potential immune evasion, leading to reduced vaccine efficiency. Nanotechnology can play an important role in advancing both diagnosis and therapy of COVID-19. In this review, nanotechnology-based diagnostic and therapeutic strategies against SARS-CoV-2 and its variants are introduced. The biological features and functions of the virus, the mechanism of infection, and currently used approaches for diagnosis, vaccination, and therapy are discussed. Then, nanomaterial-based nucleic acid- and antigen-targeting diagnostic methods and viral activity suppression approaches that have a strong potential to advance both diagnostics and therapeutics toward control and containment of the COVID-19 pandemic are focused upon.

Social isolation-related depression accelerates ethanol intake via microglia-derived neuroinflammation.

Social isolation is common in modern society and is a contributor to depressive disorders. People with depression are highly vulnerable to alcohol use, and abusive alcohol consumption is a well-known obstacle to treating depressive disorders. Using a mouse model involving isolation stress (IS) and/or ethanol intake, we investigated the mutual influence between IS-derived depressive and ethanol-seeking behaviors along with the underlying mechanisms. IS increased ethanol craving, which robustly exacerbated depressive-like behaviors. Ethanol intake activated the mesolimbic dopaminergic system, as evidenced by dopamine/tyrosine hydroxylase double-positive signals in the ventral tegmental area and c-Fos activity in the nucleus accumbens. IS-induced ethanol intake also reduced serotonergic activity, via microglial hyperactivation in raphe nuclei, that was notably attenuated by a microglial inhibitor (minocycline). Our study demonstrated that microglial activation is a key mediator in the vicious cycle between depression and alcohol consumption. We also propose that dopaminergic reward might be involved in this pathogenicity.