COVID-19 is a devastating global pandemic around the world. While the majority of infected cases appear mild, in some cases individuals present respiratory complications with possible serious lung damage. There are no specific treatments for COVID-19 as yet, though a number are under evaluation, including experimental antivirals. Sofosbuvir, the clinically approved anti-hepatitis C virus (HCV) drug, is also capable of suppressing other families of positive-strand RNA viruses; Flaviviridae and Togaviridae. Coronaviruses are a family of positive-strand RNA viruses with conserved polymerase, so SARS-CoV-2 RdRp is very likely to be effectively inhibited by sofosbuvir. More importantly, sofosbuvir is safe and well tolerated at 400 mg daily in a 24 week therapeutic regimen. Sofosbuvir active metabolite, however, shows an extremely high intracellular stability So, it is hypothesized that SARS-CoV-2 infection could also be susceptible to sofosbuvir and we were convinced to design and run a clinical trial to evaluate the effect of sofosbuvir 400 mg (in combination with velpatasvir 100 mg, as add-on treatment, in addition to standard of care) on the COVID-19. However, we believe that this manuscript/ correspondence should be made available to the international scientific community as soon as possible, with the help of this esteemed journal. Ó 2020 IMSS.

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COVID-19 is a devastating global pandemic around the world. While the majority of infected cases appear mild, in some cases, individuals present respiratory complications with possible serious lung damage. There are no specific treatments for COVID-19 as yet. Many repurposed antiviral drugs have had disappointing outcomes. Angiotensin-converting enzyme 2 (ACE2), an enzyme that physiologically counters renin–angiotensin–aldosterone system activation, functions as a receptor for both SARS viruses. The current study discusses on vague role of ACE2 under physiologic/pathologic conditions. The catalytically inactive hrsACE2 has been also proposed as an efficient treatment of SARS-CoV-2 infection. Electronic supplementary material The online version of this article (10.1007/s13738-020-02049-z) contains supplementary material, which is available to authorized users.

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Radiotherapy is an inevitable choice for cancer treatment that is applied as combinatorial therapy along with surgery and chemotherapy. Nevertheless, radiotherapy at high doses kills normal and tumor cells at the same time. In addition, some tumor cells are resistant to radiotherapy. Recently, many researchers have focused on high‐Z nanomaterials as radiosensitizers for radiotherapy. Among them, gold nanoparticles (GNPs) have shown remarkable potential due to their promising physical, chemical, and biological properties. Although few clinical trial studies have been performed on drug delivery and photosensitization with lasers, GNPs have not yet received Food and Drug Administration approval for use in radiotherapy. The sensitization effects of GNPs are dependent on their concentration in cells and x‐ray energy deposition during radiotherapy. Notably, some limitations related to the properties of the GNPs, including their size, shape, surface charge, and ligands, and the radiation source energy should be resolved. At the first, this review focuses on some of the challenges of using GNPs as radiosensitizers and some biases among in vitro/in vivo, Monte Carlo, and clinical studies. Then, we discuss the challenges in the clinical translation of GNPs as radiosensitizers for radiotherapy and proposes feasible solutions. And finally, we suggest that certain areas be considered in future research.This article is categorized under: Therapeutic Approaches and Drug Discovery > NA

We read with great interest the inspiring paper by Monteil et al. [Inhibition of SARS-CoV-2 infections in engineered human tissues using clinical-grade soluble human ACE2, DOI: 10.1016/j.cell.2020.04.004]. Their paper aimed to prove that human recombinant soluble ACE2 (hrsACE2) reduces SARS-CoV-2 recovery, in vitro, and also shows that SARS-CoV-2 can directly infect engineered human blood vessel/kidney organoids, which can be inhibited by this enzyme. The respectful authors expressed that hrsACE2 can block early entry of SARS-CoV-2 infections in various host cells, especially alveolar epithelial type II cells, as a viral reservoir and stated that they cannot make any predictions with respect to the effect of the recombinant protein on the later stages of COVID-19 and, also, honestly mentioned the study limitations. They also stated further (in vitro, pre-clinical and clinical) studies are needed to address the effect of hrsACE2 at later stages of SARS-CoV-2 infection. In the critical situation, these days, where hundreds of thousands of world population are diagnosed as COVID-19 confirmed cases and tens of thousands have lost their lives so far, and on the other hand, since we do not have the facilities to achieve our opinion in the laboratory; we share this opinion with you; dear editor, respectful authors of the above article and all my colleagues around the world.

Severe acute respiratory syndrome coronavirus 2 (SARS- CoV-2) and its related disease, COVID-19 is terribly spreading to 202 countries, areas or territories. Till March 29th, 2020 the values of confirmed cases and total deaths were more than 575,000 and ~ 26,500. Due to epithelial injury, as a critical event both in early stages of the disease and specifically in the development of acute respiratory distress syndrome (ARDS), patients encounter rapid vasoconstriction in the pulmonary circulation, followed by ventilation/perfusion mismatch. Acetazolamide-medaited carbonic anhydrase (CA) inhibition may attenuate the effects of hyperventilation-induced respiratory alkalosis. The evidences on chronic obstructive pulmonary disease (COPD) and acute mountain sickness (AMS) support our proposition that low doses of acetazolamide appear to stimulate ventilation in stable patients with COVID-19.