Malignant Catarrhal Fever Induced by Alcelaphine herpesvirus 1 Is Associated with Proliferation of CD8+ T Cells Supporting a Latent Infection

Alcelaphine herpesvirus 1 (AlHV-1), carried by wildebeest asymptomatically, causes malignant catarrhal fever (WD-MCF) when cross-species transmitted to a variety of susceptible species of the Artiodactyla order. Experimentally, WD-MCF can be induced in rabbits. The lesions observed are very similar to those described in natural host species. Here, we used the rabbit model and in vivo 5-Bromo-2′-Deoxyuridine (BrdU) incorporation to study WD-MCF pathogenesis. The results obtained can be summarized as follows. (i) AlHV-1 infection induces CD8+ T cell proliferation detectable as early as 15 days post-inoculation. (ii) While the viral load in peripheral blood mononuclear cells remains below the detection level during most of the incubation period, it increases drastically few days before death. At that time, at least 10% of CD8+ cells carry the viral genome; while CD11b+, IgM+ and CD4+ cells do not. (iii) RT-PCR analyses of mononuclear cells isolated from the spleen and the popliteal lymph node of infected rabbits revealed no expression of ORF25 and ORF9, low or no expression of ORF50, and high or no expression of ORF73. Based on these data, we propose a new model for the pathogenesis of WD-MCF. This model relies on proliferation of infected CD8+ cells supporting a predominantly latent infection

Disrupting Circadian Homeostasis of Sympathetic Signaling Promotes Tumor Development in Mice

and why disruption of circadian rhythm may lead to tumorigenesis. oncogenic potential, leading to tumor development in the same organ systems in wild-type and circadian gene-mutant mice. is a clock-controlled physiological function. The central circadian clock paces extracellular mitogenic signals that drive peripheral clock-controlled expression of key cell cycle and tumor suppressor genes to generate a circadian rhythm in cell proliferation. Frequent disruption of circadian rhythm is an important tumor promoting factor

Exploring Links Between Aural Lexical Knowledge and L2 Listening in Arabic and Japanese Speakers: A Close Replication of Cheng, Matthews, Lange and McLean (2022)

Aural lexical knowledge (ALK) is crucial for second language (L2) listening. Despite its importance, there is scant research that has validly explored the relationship between ALK and L2 listening across different English as a Foreign Language (EFL) contexts. In an effort to broaden this research base, the current study closely replicates a previous study, Cheng et al. (2022), which measured single-word ALK, phrasal verb ALK and L2 listening comprehension among participants with Chinese as a first language (L1). The current study administered the same instruments but did so among 147 Japanese and 131 Arabic-speaking English language learners. Results indicated that the capacity of ALK to predict variance in L2 listening for the Japanese group (R2 = .38) was similar to that observed in the original study (R2 = .42). However, the results for the Arabic-speaking group were very different to that of the original study and showed an unexpectedly strong relationship between ALK and L2 listening (R2 = .92). Future research directions and pedagogical implications are discussed