Diabetes is the most frequent comorbidity among patients with COVID-19. COVID-19 patients with diabetes have a more severe prognosis than patients without diabetes. However, the etiopathogenetic mechanisms underlying this more unfavorable outcome in these patients are not clear. Probably the etiopathogenetic mechanisms underlying diabetes could represent a favorable substrate for a greater development of the inflammatory process already dysregulated in COVID-19 with a more severe evolution of the disease. In the attempt to shed light on the possible etiopathogenetic mechanisms, we wanted to evaluate the possible role of mTOR (mammalian Target Of Rapamycin) pathway in this context.We searched the PubMed and Scopus databases to identify articles involving diabetes and the mTOR pathway in COVID-19.The mTOR pathway could be involved in this etiopathogenetic mechanism, in particular, the activation and stimulation of this pathway could favor an inflammatory process that is already dysregulated in itself, while its inhibition could be a way to regulate this dysregulated inflammatory process. However, much remains to be clarified about the mechanisms of the mTOR pathway and its role in COVID-19.The aim of this review is to to understand the etiopathogenesis underlying COVID-19 in diabetic patients and the role of mTOR pathway in order to be able to search for new weapons to deal with this disease.

Introduction: Disease modifying treatments are commonly used in the treatment of multiple sclerosis. As different opportunistic infections have been reported, concerns are also raised regarding the risk of invasive fungal infections.Areas covered: Both clinical trials and observational studies on safety and efficacy of diseases modifying treatment for multiple sclerosis were reviewed and data regarding the occurrence of invasive fungal infections were reported. Papers evaluating the following drugs were reviewed: rituximab, ocrelizumab, alemtuzumab, fingolimod, natalizumab, dimethyl fumarate, interferon, glatiramer acetate, cladribine, teriflunomide.Expert opinion: Overall, the occurrence of invasive fungal infections was low, with most infective events reported among patients treated with monoclonal antibodies and fingolimod. Aspergillosis and cryptococcal meningitidis were the most representative fungal infections. Although not common, these infections may be difficult to diagnose and their fatality rate is often high. For this reason, screening protocols for fungal infections must be implemented in the clinical practice when managing patients with MS.

Introduction Pseudomonas aeruginosa (PA) is a known cause of skin and soft tissue infections (SSTIs). Therapeutic options against multidrug-resistant (MDR) and extensively drug-resistant (XDR) strains of PA are limited, especially in patients with impaired renal function. Ceftolozane/tazobactam (C/T) is a novel beta-lactam/beta-lactamase inhibitor with powerful anti-PA activity. Thanks to its characteristics, it appears to be the best available anti-pseudomonal drug in many clinical scenarios. A case series of four adult patients followed between January 2018 and May 2019 is reported. All subjects presented complicated SSTIs by MDR- or XDR-PA and were affected by chronic kidney disease. Results C/T was used as a monotherapy in three cases and in combination regimen in the remaining case. In two cases, C/T was the first-line option, in the remaining ones was the salvage treatment. All patients were successfully treated without worsening of renal function and without any other adverse events. Conclusions C/T may represent a useful option against MDR- and XDR-PA strains responsible of complicated SSTIs in patients affected by impaired renal function.

Hepatitis C virus (HCV) is estimated to chronically infect about 160,000,000 people in the world and to be responsible for more than 360,000 deaths a year [1, 2]. HCV is a non-stable virus. In fact it is currently classified in 7 major genotypes (identified with numbers 1 to 7) and in 67 subtypes [3]. Finally, HCV is detected in a single host as a mix of closely related viral populations called quasispecies. The biological explanation for this huge genomic instability lies in the lack of a proofcorrection activity of the viral RNA-dependent RNA polymerase. HCV is acquired through blood transfusion before 1990s, use of glass syringes, unsafe sexual intercourse, invasive medical procedures, tattooing, and intravenous drug use [4-11]. After its entry in the human host, HCV produces an acute infection that becomes chronic in a high percentage of cases (54-86%), likely due to the high viral heterogeneity that allows its escape from host immune system [12-14]. Once hepatitis becomes chronic, it entails a high risk of developing liver cirrhosis. In fact, 15-56% of patients with chronic hepatitis C develop a liver cirrhosis. This wide range of disease progression is due to the presence or absence of factors that contribute to a higher and quicker progression such as alcohol intake, iron overload, steatosis, HBV or HIV co-infection [2, 12, 14-20]. Actually, the incidence of new infections is declining at-least in developed countries [11, 2123]. However, due to the large amount of people infected in past decades, it is expected that the number of patients with an advanced disease will increase in the next years [9]. With the exception of extrahepatic diseases (such as mixed cryoglobulinemia, Sjögren syndrome, non-Hodgkin lymphoma [14, 24-28]), all the severe consequences of HCV infection and the total burden of death occur only in presence of liver cirrhosis. Complications include hepatocellular carcinoma development, ascites, variceal bleeding, jaundice and endstage liver disease. Therefore the presence of cirrhosis is a threshold with a high negative prognostic value [29]. It is demonstrated that the natural history of the disease can be halted or even reversed in case of a successful viral eradication by antiviral therapy [30-36]. Antiviral therapy currently consists in the combination of pegylated-interferon and ribavirin. In case of patients infected with HCV genotype 1, a third drug (namely, a protease inhibitor boceprevir or telaprevir) is often added to increase the rate of viral clearance [37-42]. Viral clearance is obtained if HCV-RNA persists undetectable for 6 months after therapy withdrawal. This is called Sustained Virological Response (SVR) and represents the surrogate endpoint in clinical trials concerning anti-HCV drugs [30]. In fact, patients who maintain an Rassegna