Viruses-Basel最新文献

Cytomegalovirus (CMV) infection during pregnancy is the leading cause of congenital infection subsequent to viral transplacental transmission. CMV placental infection can contribute to the development of adverse outcomes likely through placental dysfunction. This case report shows the potential utility of angiogenic markers, such as placental growth factor (PlGF) and soluble fms-like tyrosine kinase-1 (sFlt-1), in assessing CMV-related placental involvement and monitoring the effect of antiviral therapy on placental function, and highlights the possibility of integrating these markers into the clinical management of CMV infection.

Pepper golden mosaic virus (PepGMV) is a bipartite begomovirus of pepper and tomato from North America. In 'Anaheim' pepper plants PepGMV-Mo strain (Mo) causes systemic yellow foliar mosaic symptoms, while PepGMV-D strain (D) causes distortion of 1st-6th expanding leaves, and asymptomatic infection of subsequently developing leaves, like other known 'recovery' phenotypes. Infections established with DNA-A Mo and D components expressing red-shifted green fluorescent protein in place of coat protein and in situ hybridization, showed PepGMV-Mo localized to phloem and mesophyll cells, while -D was mesophyll restricted. Alignment of PepGMV-Mo and -D DNA-B components revealed three indels upstream of the BC1 gene that encodes the movement protein (MP). To determine if this non-coding region (*BC1) D-strain MP putative promoter contributed to 'recovery', plants were inoculated with chimeric DNA-B Mo/D components harboring reciprocally exchanged *BC1, and wild-type DNA-A Mo and D components. Symptoms were reminiscent but not identical to wild-type -Mo or -D infection, respectively, suggesting 'recovery' cannot be attributed solely to the *BC1. Both BC1 and D*BC1 were targeted by post-transcriptional gene silencing; however, 'recovered' leaves accumulated fewer transcripts and 21-24 nt vsiRNAs. Thus, inefficient in planta movement of PepGMV-D is associated with a non-pepper-adapted 'defective' BC1 that facilitates hyper-efficient PTGS, leading to BC1 transcript degradation that in turn limits virus spread, thereby recapitulating disease 'tolerance'.

Located in the Rocky Mountains within the Arapahoe and Roosevelt National Forests, Colorado State University's Mountain Campus in Pingree Park hosted the 24th Annual Rocky Mountain Virology Association's meeting in 2024. A total of 165 participants, both regional and international, participated in the 3-day event, which consisted of 48 talks and 42 posters. These presentations discussed developments in prion research, current affairs, and novel tools in virology; investigated arboviruses and their vectors, as well as molecular foundations of viral interactions; and provided increased understanding of viral immunology and vaccines. This year's Randall Jay Cohrs keynote presentation unveiled how viral infections disrupt intestinal homeostasis via Sting-dependent NK-kB signaling. This novel research demonstrated the importance of immunological pathways in the virus-induced disruption of homeostasis. Nested in the valley of the Rocky Mountains, participants could enjoy the fall colors and partake in hiking and fishing all while discussing science and networking amongst a variety of scientists. This report encapsulates selected presentations from the 24th Annual Rocky Mountain Virology Association meeting.

Hepatitis C virus (HCV) eradication is usually associated with dyslipidemia. Most studies in this field have focused on genotype-specific direct-acting antivirals (DAAs), with research on pangenotypic DAAs being limited. This study examined how two pangenotypic DAA regimens, glecaprevir/pibrentasvir (GLE/PIB) and sofosbuvir/velpatasvir (SOF/VEL), affect lipid profiles and insulin resistance after viral eradication in chronic HCV patients. A total of 100 patients (57 with GLE/PIB and 43 with SOF/VEL) treated between September 2020 and January 2022 were included in the retrospective analysis. This study found a significant increase in LDL and TC levels after treatment (p < 0.001), but no significant changes in triglycerides, high-density lipoprotein, HbA1C, or the Homeostatic Model Assessment of Insulin Resistance. According to a logistic regression analysis, higher baseline LDL or TC and lower baseline glucose are predictors of the degree of increase in LDL or TC following a sustained virological response. Both pangenotypic DAA regimens significantly impact lipid profiles, particularly LDL and TC, but not insulin resistance. This study emphasizes the need for more research into the long-term metabolic effects of DAAs.

Chronic hepatitis B (HBV), alongside hepatitis D virus (HDV) super-/co-infection and chronic hepatitis C (HCV), are major contributors to cirrhosis, end-stage liver disease, hepatocellular carcinoma (HCC), and liver-related mortality. Despite significant progress in antiviral treatments and HBV vaccination, viral hepatitis remains a global health burden. Vulnerable populations, such as those experiencing homelessness, migrants, and economically disadvantaged groups, are disproportionately impacted by these infections, often facing barriers to care and exclusion from traditional health systems. This leads to undiagnosed cases and ongoing transmission, undermining global efforts to eliminate HBV and HCV by 2030, as outlined by the World Health Organization (WHO). Recent studies highlight the importance of tailored interventions to address health inequalities. For instance, on-site community-based screening initiatives targeting marginalized groups have shown promise, achieving higher linkage to care rates without monetary incentives. These approaches not only enhance diagnosis but also facilitate integration into healthcare systems, addressing both public health and social disparities. This review underscores the need for targeted strategies to promote the early detection and management of HBV and HCV in underserved populations. Such efforts are critical to advancing the WHO's elimination goals, improving health outcomes, and addressing the broader social determinants of health.

Porcine epidemic diarrhea virus (PEDV) is a highly contagious pathogen responsible for devastating enteric disease and lethal watery diarrhea, leading to significant economic losses in the global swine industry. Understanding the epidemiology and genetic diversity of PEDV over the past decade is crucial for the effective prevention and treatment of porcine epidemic diarrhea. In this study, 1851 fecal samples were collected from pigs exhibiting diarrhea symptoms across 11 cities in Yunnan Province between 2013 and 2022. The prevalence of PEDV, along with other common swine diarrhea viruses, including porcine transmissible gastroenteritis virus (TGEV), porcine rotavirus (PoRV), porcine Sapporo virus (PoSaV), porcine stellate virus (PaStV), and porcine delta coronavirus (PDCoV) was assessed using a polymerase chain reaction (PCR) assay. The results revealed a total detection rate of 52.94% (980/1851) for the six viruses, with PEDV accounting for 25.93% (480/1851) of cases. Further analysis showed that weaned piglets were more susceptible to PEDV than fattening pigs, with the highest prevalence observed in spring (61.52%, 275/447) and the lowest in summer (12.68%, 97/765). Dual infections were also identified, with PEDV + PoSaV being the most common combination (2.81%, 52/1851), followed by PEDV + PoRV, with a detection rate of 1.67% (31/1851). Phylogenetic analysis of the PEDV S genes revealed that the 28 epidemic strains in Yunnan Province shared a nucleotide sequence homology from 91.4% to 98.4% and an amino acid sequence homology ranging from 85.6% to 99.3%. All strains were classified as GII variant strains. This study provides a comprehensive overview of the epidemiology of PEDV and its co-infection patterns with other common diarrhea-causing viruses in the swine herds of Yunnan Province over the past decade. These findings offer valuable insights for the development of effective prevention and control strategies to mitigate the impact of PEDV and other enteroviruses on the swine industry in Yunnan Province.

The Mayaro virus (MAYV), Togaviridae family, genus Alphavirus, has caused several sporadic outbreaks, affecting countries in the Americas. Currently, there are no licensed drugs against MAYV, requiring the search for effective antiviral compounds. Thus, this study aimed to evaluate the antiviral potential of polyphenol (-)-epigallocatechin-3-gallate (EGCG) against MAYV infection, in vitro. Antiviral assays against MAYV were performed in BHK-21 and Vero E6 cells. In addition, molecular docking was performed with EGCG and the MAYV non-structural and structural proteins. EGCG showed a significant protective effect against MAYV infection in both cell lines. The virucidal assay showed an effect on extracellular viral particles at the entry stage into BHK-21 cells. Finally, it also showed significant inhibition in the post-entry stages of the MAYV replication cycle, acting on the replication of the genetic material and late stages, such as assembly and release. In addition, the MAYV proteins E1 and nsP1 were significantly inhibited by the EGCG treatment in BHK-21 cells. Molecular docking analysis also showed that EGCG could interact with MAYV Capsid and Envelope proteins (E1 and E2). Therefore, this study shows the potential of EGCG as a promising antiviral against MAYV, as it acts on different stages of the MAYV replication cycle.

Tick-borne encephalitis (TBE) is a common arbovirus infection in Croatia. The aim of the study was to analyse 17 years of data on TBE seroprevalence and acute TBE cases in correlation with winter temperature, precipitation and wildlife abundance to identify possible patterns that may be predictive indicators of TBE incidence. Clinical diagnosis of TBE was confirmed by determining IgM and IgG anti-TBE antibodies. Of the 19,094 analysed patients, 4.2% had acute TBE, significantly more often in older age (p < 0.001) and male gender (p < 0.001). Overall seroprevalence of TBE among the tested population was 5.8% and varied annually from 2.8% to 10.7%. The mean acute TBE incidence rate was 1.1/100,000 population with significant regional differences: 1.7/100,000 in the continental vs. 0.2/100,000 and 0.5/100,000 in the Mediterranean and Alpine regions, respectively. A particularly high incidence of 3.1/100,000 was recorded in northern Croatia. TBE displayed a seasonal pattern, peaking in June and July. Moderate negative correlations were observed between TBE acute cases and winter temperatures from December to February (r = -0.461; p = 0.062), relative rodent abundance (r = -0.414; p = 0.098) and yearly precipitation from one year before (r = -0.401; p = 0.123). The analysis showed that more acute TBE cases are recorded after a warmer winter and a negative correlation between the abundance of forest Apodemus sp. and the number of TBE cases in the same year.

Marek's disease (MD), characterized by the rapid onset of T-cell lymphomas in chickens, is caused by Mardivirus gallidalpha2, an oncogenic alphaherpesvirus commonly known as Marek's disease virus (MDV). MDV encodes a bZIP protein, Meq, which contains a bZIP domain (basic DNA-binding and leucine zipper dimerization domain) at the amino terminus and a transcriptional regulatory domain at the carboxyl end. Meq can transform murine and chicken fibroblasts in vitro and is essential for tumor formation in chickens. Meq homodimerization and heterodimerization through its bZIP domain are involved in Meq-mediated transformation. However, the role of Meq DNA-binding and transcriptional regulatory domains in transformation has not been investigated. In this study, we constructed recombinant Md5 (very virulent MDV) viruses expressing chimeric Meq proteins generated by swapping the DNA-binding and transcriptional regulatory domains of Meq of Md5 and vaccine (CVI988/Rispens) strains. Our results show that these recombinant viruses, rMd5-Md5/CVI-Meq (Md5 DNA-binding domain and CVI transcriptional regulatory domain) and rMd5-CVI/Md5-Meq (CVI DNA-binding domain and Md5 transcriptional regulatory domain), replicated at levels similar to parental rMd5 in cell culture and chickens and could transmit efficiently among chickens. Interestingly, parental rMd5 and chimeric viruses exhibited distinct pathogenic phenotypes in chickens: rMd5 caused 100% mortality, a moderate level of tumor incidence in visceral organs and small visceral tumors; rMd5-Md5/CVI-Meq caused 100% mortality, a high level of tumor incidence in visceral organs, and very large visceral tumors; while rMd5-CVI/Md5-Meq caused an average of 37% mortality, rarely induced tumors in visceral organs, and the visceral tumors were small. In conclusion, our study suggests that the DNA-binding domain of Meq plays an essential role in transformation (tumor incidence), while the transcriptional regulatory domain of Meq influences the distribution and size of MDV-induced tumors.

Bone marrow stromal cell antigen 2 (BST-2) is a restriction factor for human immunodeficiency virus type I (HIV-1) and plays an important role in regulating the release of viral particles. However, the antiviral efficacy of BST-2 is antagonized by the HIV-1-encoded accessory protein Vpu, which facilitates the degradation of BST-2 by recruiting E3 ubiquitin ligase β-TrCP. The involvement of deubiquitinases (DUBs) in counteracting BST-2 ubiquitination and influencing its stability during HIV-1 infection remains inadequately explored. In this study, we conducted a small interfering RNA (siRNA) screening of human DUBs and determined that OTUD1 interacts with BST-2, leading to a reduction in its K48- and K63-linked ubiquitination. This reduction increases BST-2 protein stability, and subsequently inhibits HIV-1 release. Our findings reveal a novel regulatory mechanism by which DUBs influence the stability of the HIV-1 restriction factor BST-2 to dampen viral release, providing a potential therapeutic target for HIV-1 antiviral intervention.