ABSTRACT
Background and Aims Viral infections occur acutely but can also progress chronically, with the immune system having a central role in immunopathoge-nesis. The question arises whether all alterations in immune responses are reversible after viral elimination (spontaneously or by therapy). Therefore, the aim of this study is to compare soluble infammatory markers (SIM) during and after infection with SARS-CoV-2 and acute and chronic HCV-infections. Patients and Method Patients with acute HCV (n = 29), chronic HCV (n = 54), SARS-CoV-2 (n = 39) and 31 healthy-controls were included. Blood samples were tested at baseline, end of treatment/infection, and follow-up ( >= 9 months after baseline). IL-12p70, IL-1b, IL-4, IL-5, IL-6, IL-8, TNF, IFN-g, IL-10, IL-22, CXCL-10, MCP-1, MIP-1b, ITAC were quantified using the HD-SP-X Imaging and Analysis SystemTM. Results SIM profiles in patients with acute HCV were substantially elevated at baseline and the decrease during follow-up was considerably less compared to the SARS-CoV-2 cohort. In chronic HCV-patients, viral elimination by therapy resulted in a decrease in SIM, although not always to those of controls. Cirrhotic HCV patients had higher SIM levels after HCV elimination than non-cirrhotic chronic HCV-patients. In the SARS-CoV-2 cohort, most SIM returned to levels of controls 3 months after baseline. Conclusions SIM profiles and kinetics after viral elimination difer between blood-borne acute and chronic HCV- and respiratory SARS-CoV-2-infections. The immunologic imprint 9 months after cured HCV-infection (both acute and chronic) appears to be more pronounced than after SARS-CoV-2-infection. Further analysis is needed to correlate the SIM profle with the clinical pheno-type (long-HepC vs. long-COVID-19).
ABSTRACT
Background and aims: The global pandemic has inevitably diverted resources away from management of chronic diseases, including cirrhosis, where up to 40% of patients are readmitted with new cirrhosis decompensation events. Whilst there is increasing knowledge on COVID-19 infection in liver cirrhosis, little is described on the impact of the pandemic on decompensated cirrhosis admissions and outcomes, which was the aim of this study. Method: A single-centre, retrospective study, evaluated decompensated cirrhosis admissions to a tertiary London hepatology and transplantation centre, from October 2018 to February 2021. Patients were included if they had an admission with cirrhosis decompensation defined as new onset jaundice or ascites, infection, encephalopathy, portal hypertensive bleeding or renal dysfunction. Admissions were excluded if they lasted <24 hours,were elective or occurred post liver-transplant. Results: Therewere 351 admissions in the pre-COVID period (October 2018 to February 2020) and 240 admissions during the COVID period (March 2020 to February 2021), with an average of 20.4 admissions per month throughout. Patients transferred in from secondary centres had consistently higher severity scores during the COVID period (UKELD 58 versus 54;p = 0.007, MELD Na 22 versus 18;p = 0.006, AD score 55.0 versus 51.0;p = 0.055). The proportion of ITU admissions pre versus during-COVID stayed constant (22.9% versus 19.2%), but there was a trend towards increased ICU admissions with acute-on-chronic liver failure (ACLF) (73.9% versus 63.8% prepandemic). Of those admitted to the intensive care without ACLF, there was a significant increase in EF-CLIF acute decompensation (AD) scores during the COVID period (58 versus 48, p = 0.009). In addition, there was a trend towards increased hospital re-admission rates during the COVID period (29.5% versus 21.5%, p = 0.067). When censored at 30 days, time to death post discharge was significantly reduced during the COVID period (p < 0.05) with a median time to death of 35 days compared to 62 days pre-COVID.(Figure Presented)Conclusion: This study provides a unique perspective on the impact that the global pandemic had on the clinical course and characteristics of decompensated cirrhosis admissions. The findings of increased early mortality and re-admissions, and higher AD scores, indicating increased disease morbidity, highlight the need to maintain resourcing on providing high-level hepatology care. Given that COVID-19 will likely be a chronic issue, alternative care pathways such as remote monitoring may need adoption to facilitate continuity of care post-discharge and to reduce readmission rates and morbidity in the future
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World Health Organization (WHO) has assessed that coronavirus disease 2019 (COVID-19) as an epidemic. However, an effective antiviral for COVID-19 is still uncertain. Since the onset of the outbreak, the scientific and clinical community keep proposing many agents that would have efficacy against COVID-19. Arbidol is an indole core with proven effectiveness against influenza over the past few years apart from critics. The concrete hypothesis of arbidol interaction with spike glycoprotein prevents the entry of virus. Further, demonstrated clinical efficiency of arbidol against RNA virus and broad-spectrum inhibition of influenza A and B virus, adenovirus, and other viruses, including hepatitis C virus, drives us to seek more understating of the molecule and its clinical possibilities. In this review, we attempt to describe the many possible hypotheses of arbidol against Covid-19.
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BACKGROUND: Garlic (Allium sativum L.) is a common herb consumed worldwide as functional food and traditional remedy for the prevention of infectious diseases since ancient time. Garlic and its active organosulfur compounds (OSCs) have been reported to alleviate a number of viral infections in pre-clinical and clinical investigations. However, so far no systematic review on its antiviral effects and the underlying molecular mechanisms exists. SCOPE AND APPROACH: The aim of this review is to systematically summarize pre-clinical and clinical investigations on antiviral effects of garlic and its OSCs as well as to further analyse recent findings on the mechanisms that underpin these antiviral actions. PubMed, Cochrane library, Google Scholar and Science Direct databases were searched and articles up to June 2020 were included in this review. KEY FINDINGS AND CONCLUSIONS: Pre-clinical data demonstrated that garlic and its OSCs have potential antiviral activity against different human, animal and plant pathogenic viruses through blocking viral entry into host cells, inhibiting viral RNA polymerase, reverse transcriptase, DNA synthesis and immediate-early gene 1(IEG1) transcription, as well as through downregulating the extracellular-signal-regulated kinase (ERK)/mitogen activated protein kinase (MAPK) signaling pathway. The alleviation of viral infection was also shown to link with immunomodulatory effects of garlic and its OSCs. Clinical studies further demonstrated a prophylactic effect of garlic in the prevention of widespread viral infections in humans through enhancing the immune response. This review highlights that garlic possesses significant antiviral activity and can be used prophylactically in the prevention of viral infections.
ABSTRACT
Naive CD4+ T cells can differentiate into different cell subsets after receiving antigen stimulation, which secrete corresponding characteristic cytokines and thereby exert biological effects in various diseases. Th22 cells, a novel subset of CD4+ T cells, are different from Th1, Th2, Th17, and Treg cell subsets, which have been discovered in recent years. They can express CCR4, CCR6, and CCR10 molecules and secrete IL-22, IL-13, and TNF-α. They are not able to secrete IL-17, IL-4, and interferon-γ (IFN-γ). IL-22 is considered as a major effector molecule of Th22 cells whose functions and mechanisms of regulating cell differentiation have been constantly improved. In this review, we provide an overview of the origin, differentiation of Th22 cells. Moreover, we also describe the interrelationships between Th22 cells and Th17, Th1, and Th2 cells. Additionally, the role of Th22 cells were discussed in human diseases with virus infection, which will provide novel insight for the prevention and treatment of viral infection in human.