Virus infection can trigger extrinsic apoptosis. Cell-surface death receptors of the tumor necrosis factor family mediate this process. They either assist persistent viral infection or elicit the elimination of infected cells by the host. Death receptor-mediated apoptosis plays an important role in viral pathogenesis and the host antiviral response. Many viruses have acquired the capability to subvert death receptor-mediated apoptosis and evade the host immune response, mainly by virally encoded gene products that suppress death receptor-mediated apoptosis. In this review, we summarize the current information on virus infection and death receptor-mediated apoptosis, particularly focusing on the viral proteins that modulate death receptor-mediated apoptosis.

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This randomized controlled-feeding trial aimed to determine the impact of fried meat intake on the gut microbiota and fecal cometabolites and whether such impacts influenced host glucose homoeostasis, intestinal endotoxin levels, and systemic inflammation. RESEARCH DESIGN AND METHODSA total of 117 overweight adults were randomized into two groups. Fifty-nine participants were provided fried meat four times per week, and 58 participants were restricted from fried meat intake, while holding food group and nutrient compositions constant, for 4 weeks. The gut microbiota was analyzed by 16S rRNA sequencing. Glucose and insulin concentrations at 0, 30, 60, and 120 min of an oral glucose tolerance test, fecal microbiota-host cometabolite levels, and intestinal endotoxin and inflammation serum biomarker levels were measured. The area under the curve (AUC) for insulin, insulinogenic index (IGI), and muscle insulin resistance index (MIRI) were calculated. RESULTSThe participants who consumed fried meat had lower IGI values than the control subjects, but they had higher MIRI and AUC values of insulin and lipopolysaccharide (LPS), TNF-a, IL-10, and IL-1β levels (P < 0.05). Fried meat intake lowered microbial community richness and decreased Lachnospiraceae and Flavonifractor abundances while increasing Dialister, Dorea, and Veillonella abundances (P FDR <0.05), provoking a significant shift in the fecal cometabolite profile, with lower 3-indolepropionic acid, valeric acid, and butyric acid concentrations and higher carnitine and methylglutaric acid concentrations (P FDR <0.05). Changes in these cometabolite levels were significantly associated with changes in IGI and MIRI values and LPS, FGF21, TNF-a, IL-1β, and IL-10 levels (P < 0.05). CONCLUSIONSFried meat intake impaired glucose homoeostasis and increased intestinal endotoxin and systemic inflammation levels by influencing the gut microbiota and microbial-host cometabolites.

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Dibromoacetic acid (DBA), a by-product of disinfection, develops in drinking water during chlorination or ozonation processes. Water intake is the main source of DBA exposure in humans, which is potentially neurotoxic. The present study investigated the neurotoxic effects of DBA by assessing the behavioral and biochemical characteristics of Sprague Dawley rats intragastrically treated with DBA at concentrations of 20, 50 and 125 mg kg body weight for 28 consecutive days. The results indicated that animal weight gain and food consumption were not significantly affected by DBA. However, shuttle box tests showed increases in mistake frequency and reaction latency between the control and high-dose group. We found significant changes in hippocampal neurons by histomorphological observation. Additionally, biochemical analysis indicated enhanced production of reactive oxygen species (ROS) resulting in disruption of cellular antioxidant defense systems including decreased mitochondrial superoxide dismutase (SOD) activity and release of cytochrome c (cyt-c) from mitochondria into the cytosol, which can induce neuronal apoptosis. Furthermore, the increase of cyt-c in the cytosol enhanced caspase-3 and caspase-9 activity, which was confirmed by poly ADP-ribose polymerase-1 (PARP-1) cleavage to its signature fragment of 85 kDa and decreased levels of protein kinase C-δ (PKC-δ) in the hippocampus. Meanwhile, DBA treatment caused differential modulation of apoptosis-associated proteins and mRNAs for phosphorylated apoptosis signal regulating kinase 1 (p-ASK-1), phosphorylated c-jun N-terminal kinase (p-JNK), cyt-c, Bax, Bcl-2, caspase-9 and cleaved caspase-3 accompanied by DNA damage. Taken together, these data indicate that DBA may induce neurotoxicity via caspase-3-dependent apoptosis involving mitochondrial translocation of cyt-c in the rat hippocampus.

Context Emerging evidence suggests that not only the quantity but also the quality and food sources of macronutrients plays an important role in CVD. However, limited studies have examined the association of meal timing of different quality of macronutrients with CVD risk. Objective This study aimed to examine the association of subtypes of macronutrient consumption at dinner vs breakfast with cardiovascular diseases (CVD). Methods A total of 27 911 participants from the National Health and Nutrition Examination Survey (2003-2016) were included. The differences of subtypes of macronutrients at dinner vs breakfast (Δratio) were categorized into quintiles. Multiple logistic regression models and isocaloric substitution effects of subtypes were performed. Results After adjustment of a variety of covariates, participants in the highest quintile of the Δratio of low-quality carbohydrates had a higher risk of angina (odds ratio [OR] = 1.63; 95% CI, 1.16-2.29) (Pfor trend = .007) and heart attack (OR = 1.47; 95% CI, 1.13-1.93) (Pfor trend = .068) compared with the lowest quintile. The highest quintile of the Δratio of animal protein had a higher risk of coronary heart disease (OR = 1.44; 95% CI, 1.06-1.95) (Pfor trend = .014) and angina (OR = 1.44; 95% CI, 1.01-2.07) (Pfor trend = .047). For the Δratio of unsaturated fatty acid (USFA), the highest quintile of the Δratio of USFA was related to lower stroke risk (OR = 0.76; 95% CI, 0.58-0.99) (Pfor trend = .049). Isocaloric substitution of low-quality carbohydrates/animal protein by high-quality carbohydrates/plant protein at dinner reduced CVD risk by around 10%. Conclusion This study indicated that overconsumption of low-quality carbohydrates and animal protein at dinner rather than breakfast was significantly associated with higher CVD risk and USFA consumption at dinner related to lower CVD risk among US adults. Substitution of low-quality carbohydrates or animal protein by high-quality carbohydrates or plant protein at dinner could reduce CVD risk.