This paper describes the effects of murine norovirus (MNV) infection on oxidative stress and histopathological changes in mice. This study uses histopathological assays, enzymatic and non-enzymatic antioxidant markers, and total oxidative status and capacity (TOS, TAC). The results suggest that MNV infection can lead to significant changes with respect to the above-mentioned parameters in various organs. Specifically, reduced superoxide dismutase (SOD), Mn superoxide dismutase (MnSOD), catalase (CAT), and glutathione reductase (GR) activities were observed in liver tissues, while higher MnSOD activity was observed in kidney tissues of MNV-infected mice when compared to the control. GR activity was lower in all tissues of MNV-infected mice tested, with the exception of lung tissue. This study also showed that norovirus infection led to increased TOS levels in the brain and liver and TAC levels in the brain, while TOS levels were significantly reduced in the kidneys. These changes may be due to the production of reactive oxygen species (ROS) caused by the viral infection. ROS can damage cells and contribute to oxidative stress. These studies help us to understand the pathogenesis of MNV infection and its potential effects on oxidative stress and histopathological changes in mice, and pave the way for further studies of the long-term effects of MNV infection.

Human adenovirus 36 (HAdV-D36) is presently the sole virus identified to be associated with an elevated risk of obesity in both humans and animals. However, its impact on embryonated chicken eggs (ECEs) remains unexplored. This study endeavoured to examine the influence of HAdV-D36 on embryonic development by utilizing embryonated chicken eggs as a dynamic model. To simulate various infection routes, the allantoic cavity and the yolk sac of ECEs were inoculated with HAdV-D36. Subsequently, embryos from both the experimental (inoculated with virus) and control (inoculated with PBS) groups were weighed and subjected to daily histological examination. The daily embryo weights were assessed and compared between groups using the Shapiro–Wilk test. Histopathological changes in tissues were examined and compared between the tested and control groups to ascertain physiological alterations induced by the virus. Our study confirmed a significant increase in the body weight of ECEs. However, this phenomenon was not attributable to adipose tissue development; rather, it was characterized by an augmented number of cells in all observed tissues compared to control subjects. We posit that HAdV-D36 may impact developing organisms through mechanisms other than enhanced adipose tissue development. Specifically, our findings indicate an increased number of cells in all tissues, a phenomenon that occurs through an as-yet-unexplored pathway.

Norovirus (NoV) is a symptomatic virus that is the leading cause of gastrointestinal disease. It spreads easily through the fecal–oral route and contact with contaminated food or surfaces. Maintaining a high level of hygiene in food industry settings and refocusing food production on isolating and testing natural compounds that exhibit antimicrobial and antioxidant properties are important elements in preventing NoVs infection. This study evaluated plant extracts prepared by cold brew and cold concentrate techniques for their antioxidant and antiviral activity. The extracts obtained demonstrated high antioxidant activity, with notable variation depending on the plant material, ranging from moderate to very strong levels. Correspondingly, high antiviral potential was observed, reaching the nearly complete inactivation of the virus. Remarkably, the highest virucidal effects were already achieved at relatively elevated, but not maximal, antioxidant activity levels. The results of the study indicate that cold water extraction techniques allow for the obtention of plant extracts showing strong virus-inactivating activity and favorable antioxidant activity.

Background: Healthcare workers (HCWs) are more exposed to influenza infection, and the influenza vaccination is recommended each year, to reduce the risk of influenza infection and prevent influenza transmission. This study is a cross-sectional study and the objectives were to determine the rate of influenza virus infection among HCWs in the 2019–2020 influenza season. Methods: Between January and March 2020, a survey was carried out in 2 hospitals and 15 primary health-care settings (PHCS) in Wroclaw (Poland). The novel point-of-care testing Flu SensDx device was used, which detects the M1 protein of the influenza virus using electrochemical impedance spectroscopy from biological material (throat/nasal swabs). Results: A total of 150 samples were collected. The majority of participating HCWs by profession were 83 physicians (55.3%) and half (51.3%) of the participating HCWs worked in PHCS. Influenza vaccination coverage was 61.3% in 2019–2020 and 46.0% in the 2018–2019 season for all participants. Of the participating HCWs, 44.0% were positive tested by the Flu SensDx device. There were no statistically significant differences among the positive tested HCWs, their influenza immunization history, and the presence of symptoms of influenza-like illness (p > 0.05). Conclusion: Although the results of the present study suggest that influenza vaccination does not reduce the frequency of influenza virus detection by Flu SensDx testing in the HCWs participants, larger studies are needed to estimate the incidence of influenza virus infection among HCWs to understand the underlying mechanism and fine-tune policies aimed at reducing nosocomial infections.

Human adenovirus 36 (HAdV-D36) is the only currently known infectious agent capable of promoting obesity in humans and animals, but the effects on the embryonated chicken egg (ECE) have not been described yet. In our study, we used ECEs as a model of a dynamically developing organism. The allantoic cavity and the yolk sack of ECEs was inoculated with HAdV-D36 to simulate the different routes of infection. Each day, a part of the embryos was weighed and histologically examined and compared to the controls to analyze pathological changes induced by the virus. Our study confirmed a significant increase in the ECEs body weight; however, this process was not caused by adipose tissue development, but increased cell proliferation of all tissues. We suggest that HAdV-D36 must affect the developing organisms via another mechanism inducing enhanced the ECEs growth.