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The article in the Journal of Medical Virology discusses the impact of rhinovirus (RV) on pediatric respiratory infections, highlighting the presence of viral co-detections and demographic factors. The study found that respiratory viral coinfections were present in 24% of cases, with Adenovirus being the most common co-detected virus. The research suggests that high RV viral load and underlying conditions are associated with a more severe clinical course, while bacterial coinfections were not clearly investigated. The study conducted in Italy also emphasizes the role of comorbidities in the severity of RV-associated acute respiratory infections in children. [Extracted from the article]

BACKGROUND: The human imunodeficiency virus (HIV) still continues to be a global health problem, counting more than approximately 38 million people with the infection at the end of 2020, and of these, approximately 25.4 million people appear to be currently on treatment (UNIAIDS, December 2020)1. The antiretroviral drugs used belong to the class: nucleoside analogues, nucleotide analogues, integrase inhibitors (InInt), protease inhibitors (IP) and non-nucleoside analogues. Side effects of therapy include the development of lipodystrophy, which leads to the accumulation of abdominal and dorsocervical region fat2. METHODS: The objective of the study is to evaluate in vitro the morphological and molecular effects on adipogenesis and lipogenesis, following single exposure to some drugs belonging to the class of integrase inhibitors (RAL, DTG, ELV, BIC) and combined exposure of these with tenofovir alafenamide (TAF)3, nucleotide analogue. RESULTS: In the case of single drug treatments, differentiation does not appear to be very different from that of control, although increased expression of both PPARγ and C/EBPa is observed. Instead in the combined treatment with TAF, an inhibition of adipocyte differentiation and a morphological change of the cells are evident, especially in combinations BIC+TAF and DTG+TAF; an increase in the level of PPARγ expression is observed in the early stages following induction, with a subsequent down-regulation, while the cells appear with an irregular shape and jagged contours. CONCLUSIONS: The use of some of these drugs in patients who already have a BMI above normal values and therefore a particularly present fat mass at impendenziometry, could have a role in limiting lipid accumulation and/or the differentiation of mesenchymal cells into adipocytes. [ABSTRACT FROM AUTHOR]

After an acute liver damage, tissue regeneration repairs lesions with degradation of deposed fibrotic material, while mechanisms of tissue restoration are persistently activated following several repeated injuries, inducing deposition of extracellular matrix. (ECM). Factors responsible for ECM remodeling have been identified in a pathway involving a family of zinc-dependent enzyme matrix metalloproteinases (MMPs), together with tissue inhibitor of metalloproteinases (TIMPs). Recent experimental models suggested a role of CCR5 receptor in the genesis of liver fibrosis. Drawing from these background we decided to evaluate the effects of the treatment with the CCR5 inhibitor Maraviroc on LX-2, a human hepatic stellate cell line (HSC). Treatment with Maraviroc resulted in a block in S phase of LX-2 cells with increased expression levels of cyclin D1 and p21 while the expression of p53 was reduced. Treatment with Maraviroc was also able to block the accumulation of fibrillar collagens and extracellular matrix proteins (ECM), as demonstrated by the decrease of specific markers as Collagen type I, α-SMA and TGF-β1. In addition we observed a down regulation of both metalloproteins (MMP-2, MMP-9), used for the degradation of the extracellular matrix and their inhibitors (TIMP-1, TIMP-2). The identification of a compound that may modulate the dynamic of liver fibrosis could be crucial in all chronic liver diseases. Maraviroc could play an important role because, in addition to its own anti-HIV activity, it could reduce the release of pro-inflammatory citokynes implicated in liver fibrogenesis. [ABSTRACT FROM AUTHOR]