First described in 1958, the human monkeypox virus (hMPXV) is a neglected zoonotic pathogen closely associated with the smallpox virus. The virus usually spreads via close contact with the infected animal or human and has been endemic mostly in parts of the African continent. However, with the recent increase in trade, tourism, and travel, the virus has caused outbreaks in countries outside Africa. The recent outbreak in 2022 has been puzzling given the lack of epidemiological connection and the possible sexual transmission of the virus. Furthermore, there is limited understanding of the structural and pathogenetic mechanisms that are employed by the virus to invade the host cells. Henceforth, it is critical to understand the working apparatus governing the viral-immune interactions to develop effective therapeutical and prophylactic modalities. Hence, in the present short communication, we summarize the previously reported research findings regarding the virology of the human monkeypox virus.

The human microbiota is a variety of different microorganisms. The composition of microbiota varies from host to host, and it changes during the lifetime. It is known that microbiome may be changed because of a diet, bacteriophages and different processes for example, such as inflammation. Like all other areas of medicine, there is a continuous growth in the area of microbiology. Different microbes can reside in all sites of a human body, even in locations that were previously considered as sterile; for example, liver, pancreas, brain and adipose tissue. Presently one of the etiological factors for liver disease is considered to be pro-inflammatory changes in a host’s organism. There are lot of supporting data about intestinal dysbiosis and increased intestinal permeability and its effect on development of liver disease pointing to the gut–liver axis. The gut–liver axis affects pathogenesis of many liver diseases, such as chronic hepatitis B, chronic hepatitis C, alcoholic liver disease, non-alcoholic liver disease, non-alcoholic steatohepatitis, liver cirrhosis and hepatocellular carcinoma. Gut microbiota has been implicated in the regulation of brain health, emphasizing the gut–brain axis. Also, experiments with mice showed that microorganisms have significant effects on the blood–brain barrier integrity. Microbiota can modulate a variety of mechanisms through the gut–liver axis and gut–brain axis. Normal intestinal flora impacts the health of a host in many positive ways, but there is now significant evidence that intestinal microbiota, especially altered, have the ability to impact the pathologies of many diseases through different inflammatory mechanisms. At this point, many of the pathophysiological reactions in case of microbial disbyosis are still unclear.

Sciendo provides publishing services and solutions to academic and professional organizations and individual authors. We publish journals, books, conference proceedings and a variety of other publications.

Sciendo provides publishing services and solutions to academic and professional organizations and individual authors. We publish journals, books, conference proceedings and a variety of other publications.

The One Health concept is an integrated, interdisciplinary approach that recognises the interconnection between human, animal, and environmental health. Initially, it focused on zoonotic infections, but has since evolved into a comprehensive framework addressing global health challenges, including antimicrobial resistance, emerging infectious diseases, food safety, climate change, and environmental degradation. This article reviews the historical development of One Health as a concept, from its early foundations to its recognition as an international strategy supported by major global organisations. Particular attention is given to six priority areas: laboratory diagnostics and surveillance, zoonotic disease control, neglected tropical diseases, antimicrobial resistance, food safety, and environmental health. The importance of interdisciplinary collaboration, integrated surveillance systems, and coordinated preventive strategies is emphasised. Recent international and European initiatives are discussed, highlighting efforts to translate One Health principles into practical actions. Developments in Latvia are also presented as examples of emerging interdisciplinary cooperation. Successful implementation of One Health requires coordinated policies, multidisciplinary research, sustainable funding, and active collaboration across sectors. Addressing increasingly interconnected health threats requires a comprehensive approach guided by the principle of thinking globally and acting locally.

Objectives: This study aimed to assess the dynamics of liver tests (LT) and detect signs of liver fibrosis and steatosis 2.5 years after the first COVID-19 episode in patients without pre-existing liver-related conditions. Methods: The study included 65 adult patients hospitalized with COVID-19 (including 18 with severe or critical illness) in 2020. After 2.5 years, in addition to regular LT, liver health status was assessed by the FIB-4 index, hyaluronic acid, cytokeratin 18 fragment M30 (serum, ELISA), cardiometabolic risk factors, and the multiparametric ultrasound examination. Results: LT abnormalities in the acute COVID-19 period were observed more frequently (p = 0.036) in patients with severe or critical COVID-19 (83%) than in patients with non-severe COVID-19 (55%). LT dynamics in 2.5 years showed an improvement of liver health status in most patients (p = 0.006). Persistent LT abnormalities were associated with LT abnormalities during hospitalization (p = 0.021). After 2.5 years, the presence of cardiometabolic risk factors and signs of liver fibrosis were associated with the severity of the first COVID-19 episode. However, regression analyses did not support disease severity as a predictor for LT abnormalities and liver stiffness. The latter was predicted by cardiovascular diseases in the anamnesis. Conclusions: In most patients, LT normalized despite potential risk factors. Simultaneously, in some patients, signs of liver fibrosis after COVID-19 might be stimulated by COVID-19-related metabolic dysfunction and the presence of cardiovascular diseases.