Primary cultures of rat and mouse sensory neurons were used to study the entry of herpes simplex virus type 1 (HSV-1). Soluble, truncated nectin-1 but not HveA prevented viral entry. Antibodies against nectin-1 also blocked infection of rat neurons. These results indicate that nectin-1 is the primary receptor for HSV-1 infection of sensory neurons.Herpes simplex virus type 1 (HSV-1) has a broad host range, and recent studies have identified a number of cell surface proteins that serve as receptors for viral entry (reviewed in reference 18). It appears that the abundance of the different receptors varies with the cell type, and this variation might influence the course of HSV-1 infection (4). The envelope of HSV-1 contains several glycoproteins, and studies with mutant virus have shown that the glycoproteins gB, gD, and gH are required for infection of rat neurons (1). An essential event in virus cell interaction is the binding of viral glycoprotein D (gD) to a cellular receptor. Glycoprotein D interacts with at least three structurally unrelated receptors: HveA (12, 13, 21), nectin-1 (4, 7), and 3-O-sulfated heparan sulfate (16). HveA, also known as HVEM, is a member of the tumor necrosis factor receptor superfamily. HveA mRNA is expressed in lymphoid cells and fibroblasts but only weakly in human brain tissue (8,12). Nectin-1, also called HveC, is a member of the immunoglobulin superfamily. Nectin-1 is found at cellular junctions and is involved in cell-cell adhesion (14, 19) and in synapse formation (11). High levels of nectin-1 mRNA are expressed in the human central nervous system (2), in neuronal cell lines (4), and in mouse sensory, sympathetic, and parasympathetic neurons (5). Nectin-1 protein is found in abundance in rat sensory neurons but not in rat motor neurons (9). Wilcox and Johnson developed a model of HSV-1 latency in primary sensory neurons (22,23). This model reproduces many of the characteristic features of a natural human HSV-1 latent infection, including restricted viral gene expression (3) and reactivation, to produce infectious virus (17,23). Using this model and functional assays to measure virus entry, evidence was obtained that HSV-1 entry into rodent sensory neurons is mediated by nectin-1.Effects of soluble HveA or nectin-1 receptors on HSV-1 entry. Neuronal cultures were prepared from dorsal root ganglia of embryonic day 15 rats or mice as previously described (22, 23). Dulbecco's Eagle's medium-F12 (supplemented with 10% newborn bovine serum, 100 ng of 2.5-S mouse nerve growth factor/ml, and 20 M 5-fluoro-2Ј-deoxyuridine to inhibit growth of nonneuronal cells) was used to establish neuronal cultures (neuronal maintenance medium). Rats and mice were treated according to institutional guidelines for animal use. Primary rat fibroblasts and HeLa cells were cultured in Dulbecco's Eagle's medium with 5% fetal bovine serum. For infection, a recombinant HSV-1 (17 ϩ strain) expressing green fluorescent protein (GFP) fused to the C terminus of the immediate-early gene product ICP4 was used....

Curcumin (Cur), a polyphenolic compound extracted from spice and common food colourant turmeric, contains versatile bio-activities. Monoacetylcurcumin (MAC), a structural analogue of Cur, differs from Cur by acetyl modification, but retains enone groups. Comparative analysis revealed MAC effectively inhibited influenza virus infection (IAV) to a similar extent as, if not superior to, curcumin. Both compounds mildly reduced viral NA activity. Surprisingly, unlike Cur, the MAC inhibition of IAV did not occur through the blocking of HA activity. However, MAC strongly dampened Akt phosphorylation, the prerequisite signalling for efficient IAV propagation. A much stronger inhibition effect on IAV infection was observed when MAC treatment was in combination with Cur. Collectively, MAC demonstrated clear antiviral activity, and likely inhibited IAV via multiple mechanisms that were not identical to Cur. Importantly, Cur and MAC in combination synergistically inhibited IAV infection.

Autophagy participates in multiple fundamental physiological processes, including survival, differentiation, development, and cellular homeostasis. It eliminates cytoplasmic protein aggregates and damaged organelles by triggering a series of events: sequestering the protein substrates into double-membrane vesicles, fusing the vesicles with lysosomes, and then degrading the autophagic contents. This degradation pathway is also involved in various disorders, for instance, cancers and infectious diseases. This paper provides an overview of modulation of autophagy in the course of reovirus infection and also the interplay of autophagy and reovirus.

After adjustments, results showed that moderate-to-vigorous physical activity (MVPA) was inversely associated with WBC count (b = - .03; 95% CI [ - 0.04, - 0.006; p = .01), and WBC count (b = .10; 95% CI [0.009, 0.18; p = .04) was positively associated with PSA. Both the Sobel (coef. = - .004, SE = .002; z = - 2.0; p = .03) and the Aroian (coef. = - .004, SE = .002; z = - 1.9; p = .03) tests demonstrated that WBC mediated the relationship between physical activity and PSA. Additionally, among 107 participants with prostate cancer, survivors engaging in more MVPA had lower levels of WBC (b = - .04; 95% CI [ - 0.09, - 0.0009; p = .04). Conclusion Physical activity may influence PSA levels through WBC modulation; however, future research is needed to determine the direction of causality. Additionally, prostate cancer survivors engaging in higher levels of MVPA had lower levels of WBC, underscoring the importance of promoting physical activity among prostate cancer survivors.

Termite control costs $1.5 billion per year in the United States alone, and methods for termite control usually consist of chemical pesticides. However, these methods have their drawbacks, which include the development of resistance, environmental pollution, and toxicity to other organisms. Biological termite control, which employs the use of living organisms to combat pests, offers an alternative to chemical pesticides. This study highlights the discovery of a fungus, termed “APU strain,” that was hypothesized to be pathogenic to termites. Phylogenetic and morphological analysis showed that the fungus is a strain of Aspergillus sclerotiorum, andexperiments showed that both western drywood (Incisitermes minor) and western subterranean (Reticulitermes hesperus) termites die in a dose-dependent manner exposed to fungal spores of A. sclerotiorum APU strain. In addition, exposure to the A. sclerotiorum Huber strain elicited death in a similar manner as the APU strain. The mechanism by which the fungus caused termite death is still unknown and warrants further investigation. While these results support that A. sclerotiorum is a termite pathogen, further studies are needed to determine whether the fungal species has potential as a biological control agent.