Immune-endocrine interactions in treated and untreated cats naturally infected with FIV

Feline immunodeficiency virus (FIV) is a lentivirus that causes a progressive disruption of immune function in cats. The neuroendocrine and immune systems communicate bidirectionally, mediated by cytokines such as tumour necrosis factor-α (TNF), several interleukins (IL-1, IL-6, IL-10), and through signals induced by the ratio of IL-10 to IL-12. FIV can affect both pituitary adrenal and thyroid axis function. Twenty FIV-infected cats in similar stages of the disease were evaluated for six months. A cross-sectional study in which the twenty cats were divided into two groups was performed. Ten were treated with Zidovudine (ZDV: 5mg/kg/d, PO, q12h, for six months) and 10 were untreated. Plasma concentrations of adrenocorticotropic hormone (ACTH), cortisol, T4, FT4, T3, IL-10, IL-12 and viral load (VL) were evaluated after six months. ACTH was found in significantly lower concentrations (p<0.0001) in the treated group whereas cortisol did not show significant differences between the two groups. Both T4 and FT4 had high values in untreated individuals (p<0.001) compared with Zidovudine treated cats. T3 did not show significant differences between the two groups. Both IL-10 and IL-12 were found in significantly higher concentrations in ZDV treated cats (p<0.001). By contrast, the IL10/IL-12 ratio values were significantly lower in untreated cats. Viral load was significantly lower in the treated cats after six months of therapy, compared with values detected pre-treatment (p<0.002). Untreated cats showed a significant increase of VL (p<0.04) compared with the values at the beginning of the study. In treated cats, VL showed lower numbers of viral copies than in untreated cats (p<0.01). In summary, Zidovudine treatment appeared to contribute to the normalization of both the adrenal and thyroid axes. This effect could be attributed to the decrease observed in VL, resulting in a change in cytokine patterns.     

Punctodera achalensis n. sp. (Nematoda: Punctoderidae), a new cyst nematode from Argentina

European Journal of Plant Pathology - Trichoderma aggressivum, a mycopathogen causing green mould disease, is a major problem in Agaricus bisporus cultivation due to crop loss, and resistance to...     

Drought as a modulator of plant–virus–vector interactions: Effects on symptom expression,plant immunity and vector behaviour

Plant–virus interactions are affected by environmental conditions that determine plant vulnerability to pathogens and the population dynamics of insect vectors. We hypothesize that drought enhances horizontal transmission by dampening the basal immunity of plants, which triggers symptom expression and vector manipulation. The potato yellow vein virus (PYVV) causes potato yellow vein disease (PYVD), a re-emerging epidemic of potato crops in South America, and is transmitted horizontally by the greenhouse whitefly (GWF), Trialeurodes vaporariorum (Hemiptera: Aleyrodidae), or vertically through infected seed tubers. We investigated the role of drought and temperature as modulators of PYVD symptom expression, plant immune response, and vector survival, development and host preference. We found that drought induced symptom expression, suppressed the salicylic acid pathway and increased PYVV replication. GWF survival was reduced on PYVV-infected hosts and development was slowest when they fed on plants with PYVD symptoms, which also triggered adults’ attraction to PYVV-infected plants. However, adults previously fed on infected plants showed the opposite effect, being more attracted to PYVV-free plants. We propose a theoretical model that explains the role of drought in modulating potato–PYVV–GWF interactions and provides new insights into plant–virus–vector coevolution.