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). 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

Reproductive control of vampire bat (Desmodus rotundus): An environmentally friendly alternative

Vampire bat control strategies have not changed in México for more than 40 years. Anticoagulants and strychnine are frequently used to reduce bat populations and the prevalence of rabies. Despite these control efforts, vampire bat-borne rabies continues to have a significant economic impact. A new control method is being developed that takes advantage of the reproductive changes induced by phytoestrogens in mammals. In this study, we fed bats the phytoestrogen coumestrol, for 30 days and examined its effect on the reproductive organs of male and female vampire bats in laboratory tests. For males, coumestrol resulted in an increase in weight and loss of the typical histological structure of testes. Treated females had no corpora lutea in their ovaries and fewer primordial folliculi were observed. These results suggest that coumestrol might be a candidate replacement for anti-coagulants used for vampire bat control

Vampire Bat Rabies: Ecology, Epidemiology and Control

Extensive surveillance in bat populations in response to recent emerging diseases has revealed that this group of mammals acts as a reservoir for a large range of viruses. However, the oldest known association between a zoonotic virus and a bat is that between rabies virus and the vampire bat. Vampire bats are only found in Latin America and their unique method of obtaining nutrition, blood-feeding or haematophagy, has only evolved in the New World. The adaptations that enable blood-feeding also make the vampire bat highly effective at transmitting rabies virus. Whether the virus was present in pre-Columbian America or was introduced is much disputed, however, the introduction of Old World livestock and associated landscape modification, which continues to the present day, has enabled vampire bat populations to increase. This in turn has provided the conditions for rabies re-emergence to threaten both livestock and human populations as vampire bats target large mammals. This review considers the ecology of the vampire bat that make it such an efficient vector for rabies, the current status of vampire-transmitted rabies and the future prospects for spread by this virus and its control

Differential infection patterns and recent evolutionary origins of equine hepaciviruses in donkeys

The hepatitis C virus (HCV) is a major human pathogen. Genetically related viruses in animals suggest a zoonotic origin of HCV. The closest relative of HCV is found in horses (termed equine hepacivirus [EqHV]). However, low EqHV genetic diversity implies relatively recent acquisition of EqHV by horses, making a derivation of HCV from EqHV unlikely. To unravel the EqHV evolutionary history within equid sister species, we analyzed 829 donkeys and 53 mules sampled in nine European, Asian, African, and American countries by molecular and serologic tools for EqHV infection. Antibodies were found in 278 animals (31.5%), and viral RNA was found in 3 animals (0.3%), all of which were simultaneously seropositive. A low RNA prevalence in spite of high seroprevalence suggests a predominance of acute infection, a possible difference from the mostly chronic hepacivirus infection pattern seen in horses and humans. Limitation of transmission due to short courses of infection may explain the existence of entirely seronegative groups of animals. Donkey and horse EqHV strains were paraphyletic and 97.5 to 98.2% identical in their translated polyprotein sequences, making virus/host cospeciation unlikely. Evolutionary reconstructions supported host switches of EqHV between horses and donkeys without the involvement of adaptive evolution. Global admixture of donkey and horse hepaciviruses was compatible with anthropogenic alterations of EqHV ecology. In summary, our findings do not support EqHV as the origin of the significantly more diversified HCV. Identification of a host system with predominantly acute hepacivirus infection may enable new insights into the chronic infection pattern associated with HCV

Evidence for novel hepaciviruses in rodents

CITATION: Drexler, J. F. et al. 2013. Evidence for novel hepaciviruses in rodents. PLoS Pathogens, 9(6): e1003438, doi:10.1371/journal.ppat.1003438.The original publication is available at http://journals.plos.org/plospathogensHepatitis C virus (HCV) is among the most relevant causes of liver cirrhosis and hepatocellular carcinoma. Research is complicated by a lack of accessible small animal models. The systematic investigation of viruses of small mammals could guide efforts to establish such models, while providing insight into viral evolutionary biology. We have assembled the so-far largest collection of small-mammal samples from around the world, qualified to be screened for bloodborne viruses, including sera and organs from 4,770 rodents (41 species); and sera from 2,939 bats (51 species). Three highly divergent rodent hepacivirus clades were detected in 27 (1.8%) of 1,465 European bank voles (Myodes glareolus) and 10 (1.9%) of 518 South African four-striped mice (Rhabdomys pumilio). Bats showed anti-HCV immunoblot reactivities but no virus detection, although the genetic relatedness suggested by the serologic results should have enabled RNA detection using the broadly reactive PCR assays developed for this study. 210 horses and 858 cats and dogs were tested, yielding further horse-associated hepaciviruses but none in dogs or cats. The rodent viruses were equidistant to HCV, exceeding by far the diversity of HCV and the canine/equine hepaciviruses taken together. Five full genomes were sequenced, representing all viral lineages. Salient genome features and distance criteria supported classification of all viruses as hepaciviruses. Quantitative RT-PCR, RNA in-situ hybridisation, and histopathology suggested hepatic tropism with liver inflammation resembling hepatitis C. Recombinant serology for two distinct hepacivirus lineages in 97 bank voles identified seroprevalence rates of 8.3 and 12.4%, respectively. Antibodies in bank vole sera neither cross-reacted with HCV, nor the heterologous bank vole hepacivirus. Co-occurrence of RNA and antibodies was found in 3 of 57 PCR-positive bank vole sera (5.3%). Our data enable new hypotheses regarding HCV evolution and encourage efforts to develop rodent surrogate models for HCV.http://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1003438Publisher's versio