The mitochondrial activity of leukocytes from Artibeus jamaicensis bats remains unaltered after several weeks of flying restriction.

Bats are the only flying mammals known. They have longer lifespan than other mammals of similar size and weight and can resist high loads of many pathogens, mostly viruses, with no signs of disease. These distinctive characteristics have been attributed to their metabolic rate that is thought to be the result of their flying lifestyle. Compared with non-flying mammals, bats have lower production of reactive oxygen species (ROS), and high levels of antioxidant enzymes such as superoxide dismutase. This anti-oxidative vs. oxidative profile may help to explain bat's longer than expected lifespans. The aim of this study was to assess the effect that a significant reduction in flying has on bats leukocytes mitochondrial activity. This was assessed using samples of lymphoid and myeloid cells from peripheral blood from Artibeus jamaicensis bats shortly after capture and up to six weeks after flying deprivation. Mitochondrial membrane potential (Δψm), mitochondrial calcium (mCa2+), and mitochondrial ROS (mROS) were used as key indicators of mitochondrial activity, while total ROS and glucose uptake were used as additional indicators of cell metabolism. Results showed that total ROS and glucose uptake were statistically significantly lower at six weeks of flying deprivation (p < 0.05), in both lymphoid and myeloid cells, however no significant changes in mitochondrial activity associated with flying deprivation was observed (p > 0.05). These results suggest that bat mitochondria are stable to sudden changes in physical activity, at least up to six weeks of flying deprivation. However, decrease in total ROS and glucose uptake in myeloid cells after six weeks of captivity suggest a compensatory mechanism due to the lack of the highly metabolic demands associated with flying.

First evidence of bovine immunodeficiency virus infection in Mexican cattle.

This study set out to identify the presence of bovine immunodeficiency virus (BIV) in animals geographically located in Mexico. BIV was first discovered in the United States in a dairy cow with persistent lymphocytosis, lymphoid hyperplasia and lymphocytic encephalitis. Many studies indicate that BIV infection is globally distributed, but its presence in Mexico remains unknown. We collected 1,168 heparinized blood samples from cattle in ten states across the Mexican Republic, then separated plasma using centrifugation and tested for antibodies against BIV. We used an indirect ELISA based on the use of a synthetic peptide derived from transmembrane glycoprotein (gp45/TM). In order to identify the viral genome, we designed a synthetic gene as a PCR control, as well as a pair of oligonucleotides for amplifying a 519 bp product of the env gene which encodes the surface protein. Positive amplicons were purified and subjected to nucleotide sequencing. A total of 189 (28.94%) tested plasma samples suggest the presence of specific anti-BIV antibodies in all states studied except for Chiapas. Additionally, PCR results identified six positive cows in the states of Puebla and Coahuila. BIV in these cows was confirmed via nucleotide sequencing and in silico analysis of these samples. This is the first report of the presence of BIV in Mexican cattle.