The biology of acquired immune deficiency (AIDS) is yet to be completely understood partly because it is complicated by the manifestation of various viral infections and associated pathogenesis. Virus entry into target cells is a key step in the virus replication cycle which is characterized by intricate and complex interactions between virus and host cells. Analyses of virus entry are always hampered to some extent due to the inability to mimic in vivo conditions. Emphasis has been placed on understanding what the virus does during the entry process; for example the signaling it mediates during entry, or identifying the cellular receptors with which the virus interact. Often, the role of the cellular environment that is critical for the complex process of virus uptake has taken a back stage. Interestingly, most of the viruses associated with AIDS cause tumors. In a recently concluded study, we identified a role for intracellular oncogenic (Raf) signaling in human herpesvirus-8 (HHV-8/KSHV) infection of target cells. In this review we present an update on entry of various viruses commonly associated with AIDS and yet another novel way of analyzing virus entry.
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Plant Dis
January 2025
INRA Bordeaux, UMR 1332 Biologie du Fruit et Pathologie, INRA - Université de Bordeaux, CS20032, Villenave d'Ornon , France, 33882 cedex;
Privet leaf blotch-associated virus (PLBaV) is an Idaeovirus discovered by high-throughput sequencing (HTS) in privet (Ligustrum japonicum L) in southern Italy in 2017 (Navarro et al., 2017). In privet, it causes a leaf blotch disease with yellowish or whitish chlorotic blotches or ringspots.
View Article and Find Full Text PDFAnnu Rev Entomol
January 2025
Department of Entomology and Nematology, University of Florida, Gainesville, Florida, USA; email:
The point of entry for the majority of arthropod pathogens and arthropod-vectored pathogens of plant, animal, and human health importance is the arthropod midgut. Pathogen interaction with the midgut therefore represents a primary target for intervention to prevent pathogen infection and transmission. Despite this key role in pathogen invasion, relatively little is known of the specific molecular interactions between pathogens and the surface of the arthropod gut epithelium, with few pathogen receptors having been definitively identified.
View Article and Find Full Text PDFMicrobiol Spectr
January 2025
Office of Vaccine Research and Review, Center for Biologics Evaluation and Research, US Food and Drug Administration, Silver Spring, Maryland, USA.
Although much has been learned about the entry mechanism of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), many details of the entry mechanisms of seasonal human coronaviruses (HCoVs) remain less well understood. In the present study, we used 293T cell lines stably expressing angiotensin converting enzyme (ACE2), aminopeptidase N (APN), or transmembrane serine protease 2 (TMPRSS2), which support high-level transduction of lentiviral pseudoviruses bearing spike proteins of seasonal HCoVs, HCoV-NL63, -229E, or -HKU1, respectively, to compare spike processing and virus entry pathways among these viruses. Our results showed that the entry of HCoV-NL63, -229E, and -HKU1 pseudoviruses into cells is sensitive to endosomal acidification inhibitors (chloroquine and NHCl), indicating entry via the endocytosis route.
View Article and Find Full Text PDFCurr Diabetes Rev
January 2025
Department of Pharmacology, Central University of Punjab, Ghudda, Bathinda, 151401, India.
The connection between COVID-19 and DM unveils a multifaceted interplay that significantly impacts disease severity and management strategies. Initial studies reveal that people with DM had higher severity rates of COVID-19 due to the infection by SARS-CoV-2. The virus solely induces hyperglycemia and, at the same time, profoundly influences the immune and inflammatory reactions, increasing the rate of severe complications and death among diabetes patients.
View Article and Find Full Text PDFJ Cachexia Sarcopenia Muscle
February 2025
Meakins-Christie Laboratories and Translational Research in Respiratory Diseases Program, Research Institute of the McGill University Health Centre, Montreal, Quebec, Canada.
Background: COVID-19 has been associated with both respiratory (diaphragm) and non-respiratory (limb) muscle atrophy. It is unclear if SARS-CoV-2 infection of skeletal muscle plays a role in these changes. This study sought to: 1) determine if cells comprising skeletal muscle tissue, particularly myofibres, express the molecular components required for SARS-CoV-2 infection; 2) assess the capacity for direct SARS-CoV-2 infection and its impact on atrophy pathway genes in myogenic cells; and 3) in an animal model of COVID-19, examine the relationship between viral infection of skeletal muscle and myofibre atrophy within the diaphragm and limb muscles.
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