Unnatural Host Research Articles

Host specificity of two co‐occurring nesting‐forms of the bag‐shelter moth Ochrogaster lunifer (Lepidoptera: Notodontidae) is congruent with there being cryptic species

AbstractThe Bag‐shelter moth, Ochrogaster lunifer (Lepidoptera: Notodontidae), is an Australian endemic species of Thaumetopoeinae with a univoltine life cycle and gregarious, herbivorous larvae. It is variable throughout its range across the continent, most noticeably by the species of host tree used and nest‐building behaviour. It has long been considered a species complex by some taxonomists, and the lack of gene flow between populations of ground‐nesters and above‐ground nesters at the same sites provides strong evidence for at least two species. We tested the specificity of host use and nesting behaviour of ground‐nesting and trunk‐nesting forms of O. lunifer by transplanting field‐collected egg masses to the other form's host, either in their natural position or in the position used by the other form. At the study site, ground‐nesting and trunk‐nesting (tree‐hugger) O. lunifer coexist. Ground‐nesting larvae are found on Acacia spp., and egg masses are laid at the base of host tree trunks where nests develop whereas tree‐hugger larvae are found on Blakella tessellaris, egg masses are laid in the outer canopy, and nests develop on the trunk or large branches. Of the 47 egg masses of O. lunifer transplanted to the unnatural host, only one cohort of tree‐hugger larvae developed through to adult moths. Placing an egg mass in its unnatural position on its natural host did not prevent the larvae from developing and successfully establishing nests for either nesting‐form, although all the ground‐nesters moved position (from the canopy to the ground) and the tree‐huggers mostly did not (from the ground to the canopy). Only the tree‐hugger form of O. lunifer developed a viable nest on the unnatural host species, established a nest at the unnatural oviposition site, and shared that nest with larvae of the other nesting‐form, suggesting tree‐hugger larvae are somewhat plastic in their behaviour and ecology. Our findings add to previous studies indicating that Acacia is likely the ancestral host of O. lunifer though large areas of its range remain unstudied.

Sea anemone-anemonefish symbiosis: Behavior and mucous protein profiling.

Fish species of the genus Amphiprion (Perciformes: Pomacentridae) seek protection from predators among the tentacles of sea anemones as their natural habitat, where they live essentially unharmed from stinging by the host's nematocysts. The skin mucus of these anemonefish has been suggested as a protective mechanism that prevents the discharge of the nematocysts upon contact. Whereas some anemonefish species seem to produce their own protective mucous coating, others may acquire mucus (or biomolecules within) from the sea anemone during an acclimation period. In controlled experiments, we show that Amphiprion ocellaris acclimated successfully to their natural host anemone species Stichodactyla gigantea, and also to Stichodactyla haddoni, and in some cases Heteractis crispa, neither of which are natural host species. No symbiosis was observed for three other anemone species tested, Entacmaea quadricolor, Macrodactyla doreensis, and Heteractis malu. We explored the skin mucous protein profile from naive and experienced A. ocellaris during their acclimation to natural and unnatural host anemones. We confidently report the presence of metabolic and structural proteins in the skin mucus of all samples, likely involved in immunological defense, molecular transport, stress response, and signal transduction. For those anemonefish that established symbiosis, there was a clear increase in ribosomal-type proteins. We additionally provide evidence for the presence of anemone proteins only in the skin mucus of individuals that established symbiosis. Our results support previous speculation of the role of skin mucous-associated proteins in anemonefish-anemone symbiosis. Further exploration of these mucosal proteins could reveal the mechanism of anemonefish acclimation to host anemones.

Expressing Parasitoid Venom Protein VRF1 in an Entomopathogen Beauveria bassiana Enhances Virulence toward Cotton Bollworm Helicoverpa armigera.

Despite entomopathogenic fungi being used in various insect pest control, it is recognized that they could replace more chemical insecticides if they were more efficient. We have found that cotton bollworm Helicoverpa armigera responded to the infection of entomopathogenic fungus Beauveria bassiana by activating the Toll pathway. Koinobiont wasps also regulate host immunity and development to ensure the survival of their progeny. Previously, venom protein VRF1 was identified in Microplitis mediator. It enters H. armigera hemocytes, suppresses the expression of antimicrobial peptides (AMPs) by inhibiting the Toll pathway, and prevents parasite offspring from being encapsulated. With this in mind, we thought that it might be feasible to increase the virulence of B. bassiana by embedding VRF1 into its genome. Compared with that of wild-type (WT) B. bassiana, the median lethal dose (LD50) of the transformant expressing VRF1 (named BbVRF1) decreased approximately 2.36-fold, and the median time to lethality (LT50) was shortened to 84% when infecting H. armigera (a natural host of M. mediator). The AMP expression level of hemocytes in H. armigera infected with BbVRF1 strain was significantly downregulated compared to that in the control group infected with the WT. In addition, the LD50 of BbVRF1 against the fall armyworm Spodoptera frugiperda (an unnatural host of M. mediator) was decreased 3.45-fold and the LT50 was shortened to 73%, showing a greater virulence. Our research indicated that BbVRF1, an engineered strain of B. bassiana, has greater efficacy against pest insects both within and outside its host range (M. mediator), expanding the utilization of parasitoid wasp virulence effectors. IMPORTANCE Mycoinsecticides are essential for the development of integrated pest management as substitutes to chemical insecticides, but their usage is limited by their inferior virulence. Thus, genetically engineered bioinsecticides, including recombinant entomopathogenic fungi, have been regarded as a breakthrough to rapidly control pests. Deep knowledge of parasitoid wasps allows us to take advantage of this natural enemy of pest insects beyond raising them for field release. Our transformant BbVRF1 (Beauveria bassiana integrated with a venom protein VRF1 from Microplitis mediator) showed a higher virulence in H. armigera and S. frugiperda, demonstrating its potential for managing natural or unnatural hosts of M. mediator. This result provides a new strategy regarding which venom protein of parasitoid wasps can become part of the arsenal with which to equip entomopathogenic fungi. Utilizing parasitoid wasps with this approach could easily overcome the difficulties of artificial culture and enhance the virulence of other biocontrol agents.

Killing effect of fish serum and mucus on Gyrodactylus cichlidarum (Platyhelminthes, Monogenea) mediated by complement

Gyrodactylids mainly parasitizing on the skin and fins of fishes, represent an ongoing challenge of farmed fishes. Evidences from previous studies suggested that complement system play important role in fish against gyrodactylids. Through a series of parasite killing experiments with fish sera and mucus, the present study revealed the role of Oreochromis niloticus complement in killing Gyrodactylus cichlidarum. The killing effect on G. cichlidarum was observed in serum and mucus of O. niloticus, which was markedly weakened after the complement inhibition by heat treatment and C3 antibody neutralization. Scanning electron microscopy (SEM) revealed various injuries on the tegument of G. cichlidarum exposed to O. niloticus serum. After inhibiting the alternative complement pathway (ACP) by zymosan, the killing activity of O. niloticus serum to G. cichlidarum was significantly attenuated (P < 0.01). The inhibition (by adding EGTA or l-lysine) to the classical complement activation pathway (CCP) also resulted a weak suppression on the killing effect. The results demonstrated the indispensable role of O. niloticus complement in killing G. cichlidarum, mainly via the ACP and with the involvement of CCP as well. In addition, complement in serum of an unnatural host (Ctenopharyngodon idella) of G. cichlidarum showed highly significantly weaker killing effect to G. cichlidarum than that of O. niloticus (P < 0.01), which needs further study for its mechanism. These findings provided new evidences about the immune mechanism of fish against gyrodactylids, and are reference for the study on the control of gyrodactyliasis.

Peste Des Petits Ruminants in Atypical Hosts and Wildlife: Systematic Review and Meta-Analysis of the Prevalence between 2001 and 2021.

Peste des petits ruminants (PPR) or goat plague is considered a leading, highly contagious, and most lethal infectious viral disease of small ruminants affecting the worldwide livestock economy and international animal trade. Although sheep and goats are the primarily affected, the PPR Virus (PPRV) host range has expanded to other livestock (large ruminants) and wildlife animals over the last few decades, resulting in serious concern to the ongoing PPR global eradication program, which is primarily optimized, designed, and targeted towards accessible sheep and goat population. A systematic review and meta-analysis study was conducted to estimate the prevalence and spill-over infection of PPRV in large ruminants (bovine and camel) and wildlife. Published articles from 2001 to October 2021 on the "PPR" were searched in four electronic databases of PubMed, Scopus, Science direct, and Google Scholars. The articles were then selected using inclusion criteria (detection/prevalence of PPRV in bovine, camel, and wildlife population), exclusion criteria (only sheep or goats, lack of prevalence data, experimental trial, test evaluation, and reviews written in other languages or published before 2001), and the prevalence was estimated by random effect meta-analysis model. In the current study, all published articles belonged to Africa and Asia. The overall pooled prevalence of PPR estimates was 24% (95% CI: 15-33), with 30% in Asia (95% CI: 14-49) and 20% in Africa (95% CI: 11-30). The overall estimated pooled prevalence at an Africa-Asia level in bovine and camel was 13% (95% CI: 8-19), and in wildlife, it was 52% (95% CI: 30-74) with significant heterogeneity (I2 = 97%) in most pooled estimates with a high prevalence in atypical hosts and wildlife across Asia and Africa. Over the last two decades, the host range has increased drastically in the wildlife population, even for prevalent PPR in the unnatural hosts only for a short time, contributing to virus persistence in multi-host systems with an impact on PPR control and eradication program. This observation on the epidemiology of the PPRV in unnatural hosts demands appropriate intervention strategies, particularly at the livestock-wildlife interface.

​Dermal Response to Experimental Orfvirus (ORFV) Infection in Goats, Mice and Rabbit

Background: During a study on the outbreak of orf in goats, it was intended to study the disease transmissibility in different hosts from field samples and ascertain the infective potential of the agent in laboratory animals compared to goats. Methods: Cutaneous clinical materials from orf virus (ORFV) infected goats was used to experimentally infect naive goats, rabbits and mice and ascertain its infective potential and transmissibility in different hosts. The processed inoculum was applied topically to mimic a natural transmission through injured skin. Regular skin biopsies were taken that revealed characteristic macroscopic and microscopic lesions typical of orf. Result: Virus inoculum applied on abraded skin in goats successfully established the lesions of orf. A parallel inoculation in rabbit and mice could not successfully reproduce the disease in these unnatural hosts beyond a subtle vesicular stage on 3 dpi with subsequent healing by 7 dpi. The lesions in goats regressed spontaneously by 28 days post-infection (dpi). Intracytoplasmic inclusions were associated only in the vesicular stage. Immunopathological progression was observed by immunoperoxidase staining of CD4+ and CD8+ T-cells which were found to appear by day 5 in the dermis and became more abundant and distributed by day 8, but subsequently reduced in number by 15 dpi. CD4+ cells were found to be more numerous and widespread. Viral antigen in tissues could be demonstrated by 4 dpi by immunohistological methods that increased in signal intensity progressively and disappear by 28 dpi. Similarly, viral nucleic acid in the skin could be detected on day 8 dpi but not on 28 dpi by PCR. The present experiment depicts the ease of disease transmissibility through traumatized skin in the primary hosts, but establishment in unnatural hosts may not be readily achieved. The infection was self-limiting with possibly no virus latency as indicated by immunofluorescence and PCR studies.

Escaping the evolutionary trap: Can size-related contest advantage compensate for juvenile mortality disadvantage when parasitoids develop in unnatural invasive hosts?

The quality of hosts for a parasitoid wasp may be influenced by attributes such as host size or species, with high quality for successful development usually coincident with high quality for larger offspring. This is not always the case: for the Scelionid wasp Trissolcus basalis, oviposition in eggs of the Brown Marmorated Stink Bug, Halyomorpha halys, rather than of the normal host, the Southern Green Stink Bug, Nezara viridula, leads to lower offspring survival, but survivors can be unusually large. Adult female T. basalis engage in contests for host access. As larger contestants are typically favoured in contests between parasitoids, the larger size of surviving offspring may compensate for the mortality of others. We construct a general game-theoretic model to explore whether size advantage can sustain a maternal preference to utilize a more deadly host species. We find that size advantage alone is unlikely to sustain a shift in host preference, yet such an outcome is possible when size asymmetries act simultaneously with advantages in host possession (ownership effect). Halyomorpha halys is an invasive pest of major agro-economic importance in Europe and the Americas, and use of its eggs as hosts by native parasitoids such as T. basalis has been seen as an evolutionary trap due to their high developmental mortality. Our model suggests that the recently discovered effect of host choice on offspring size may provide an escape from the trap via effects on contest biology of T. basalis which could foster a more stable association with H. halys. An evolutionary shift in the reproductive value of H. halys could increase the efficiency of T. basalis as a biological control agent of this invasive stink bug pest.

Examination of the APOBEC3 Barrier to Cross Species Transmission of Primate Lentiviruses.

The transmission of viruses from animal hosts into humans have led to the emergence of several diseases. Usually these cross-species transmissions are blocked by host restriction factors, which are proteins that can block virus replication at a specific step. In the natural virus host, the restriction factor activity is usually suppressed by a viral antagonist protein, but this is not the case for restriction factors from an unnatural host. However, due to ongoing viral evolution, sometimes the viral antagonist can evolve to suppress restriction factors in a new host, enabling cross-species transmission. Here we examine the classical case of this paradigm by reviewing research on APOBEC3 restriction factors and how they can suppress human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV). APOBEC3 enzymes are single-stranded DNA cytidine deaminases that can induce mutagenesis of proviral DNA by catalyzing the conversion of cytidine to promutagenic uridine on single-stranded viral (−)DNA if they escape the HIV/SIV antagonist protein, Vif. APOBEC3 degradation is induced by Vif through the proteasome pathway. SIV has been transmitted between Old World Monkeys and to hominids. Here we examine the adaptations that enabled such events and the ongoing impact of the APOBEC3-Vif interface on HIV in humans.

Emerging Haemosporidian Infections in Village Chickens (&amp;lt;i&amp;gt;Gallus gallus domesticus&amp;lt;/i&amp;gt;) in Yobe State, Nigeria

In some parts of Nigeria, studies have revealed avian haemosporidian infections in village chickens, some of which are considered emerging parasitic infections because chickens are unnatural hosts. Infections may have occurred as a result of accidental cross-infection via infected haemophagus arthropod vectors. This study was carried out to determine the emerging avian haemosporidian infections in Village chickens in Yobe State, Nigeria using microscopy. Blood samples were collected from 2100 Village chickens in 7 Local Government Areas of Yobe State. Microscopy revealed an overall prevalence of 13.8% (290/2100) for avian haemosporidians comprising of <i>Plasmodium</i> with 13.9% (198/2100) and <i>Haemoproteus</i> 2.4% (55/2100) as single infections. Mixed infection of <i>Plasmodium</i> and <i>Haemoproteus</i> had a prevalence of 1.8% (37/1820). Male (9.9%) had a higher prevalence of avian haemosporidian infections than female chickens (4.0%). Adults (10.4%) had a higher prevalence than growers chickens (3.4%), and prevalence was higher in the rainy (9.3%) than the dry (4.5%) season of the study period. Detection of <i>Haemoproteus</i> specie in chickens in Yobe State is considered an emergent infection because chickens are not natural host to the parasite. It is therefore recommended that Village chicken producers should be educated on the risk factors and impacts of avian haemosporidian on bird productivity through frequent agricultural extension services. More research is needed to assess the frequency of avian haemosporidian infections in other poultry species in Nigeria, in order to better understand the disease's epidemiology and develop effective management and prevention strategies.

Bile Acid Binding Protein Functionalization Leads to a Fully Synthetic Rhodopsin Mimic.

Rhodopsins are photoreceptive proteins using light to drive a plethora of biological functions such as vision, proton and ion pumping, cation and anion channeling, and gene and enzyme regulation. Here we combine organic synthesis, NMR structural studies, and photochemical characterization to show that it is possible to prepare a fully synthetic mimic of rhodopsin photoreceptors. More specifically, we conjugate a bile acid binding protein with a synthetic mimic of the rhodopsin protonated Schiff base chromophore to achieve a covalent complex featuring an unnatural protein host, photoswitch, and photoswitch-protein linkage with a reverse orientation. We show that, in spite of its molecular-level diversity, light irradiation of the prepared mimic fuels a photochromic cycle driven by sequential photochemical and thermal Z/E isomerizations reminiscent of the photocycles of microbial rhodopsins.

Host choice and fitness of anemonefish Amphiprion ocellaris (Perciformes: Pomacentridae) living with host anemones (Anthozoa: Actiniaria) in captive conditions.

In this study, we investigated the host choice of naïve Amphiprion ocellaris, a specialist, at two different stages of development (newly settling juveniles and post‐settlement juveniles). The fish were exposed to their natural and unnatural host species in the laboratory and their fitness was assessed in terms of activity and growth rate. Newly settling juveniles exhibited little host preference, while post‐settlement juveniles immediately associated with their most common host in the wild. The analysis of fish activity confirmed that A. ocellaris is diurnal; they are most active in the morning, less at midday and barely move at night. The average travelling distance of juveniles was shorter in the groups living with their natural host, increasing in the groups living with an unnatural host and was highest in groups that did not become associated with any other unnatural host species. Post‐settlement juveniles living with the natural host species grew better than those living with unnatural hosts or without anemone contact. These results suggest that the welfare of A. ocellaris in captivity will be optimized by keeping them with their natural anemone host species, although more generalist Amphiprion species may survive in association with other hosts.

Reduced red blood cell deformability in Plasmodium knowlesi malaria

AbstractThe simian parasite Plasmodium knowlesi can cause severe and fatal human malaria. However, little is known about the pathogenesis of this disease. In falciparum malaria, reduced red blood cell deformability (RBC-D) contributes to microvascular obstruction and impaired organ perfusion. In P knowlesi infection, impaired microcirculatory flow has been observed in Macaca mulatta (rhesus macaques), unnatural hosts who develop severe and fatal disease. However, RBC-D has not been measured in human infection or in the natural host M fascicularis (long-tailed macaques). Using ektacytometry, we measured RBC-D in adults with severe and non-severe knowlesi and falciparum malaria and in healthy controls. In addition, we used micropipette aspiration to determine the relative stiffness of infected RBCs (iRBCs) and uninfected RBCs (uRBCs) in P knowlesi–infected humans and M fascicularis. Ektacytometry demonstrated that RBC-D overall was reduced in human knowlesi malaria in proportion to disease severity, and in severe knowlesi malaria, it was comparable to that of severe falciparum malaria. RBC-D correlated inversely with parasitemia and lactate in knowlesi malaria and HRP2 in falciparum malaria, and it correlated with hemoglobin nadir in knowlesi malaria. Micropipette aspiration confirmed that in humans, P knowlesi infection increased stiffness of both iRBCs and uRBCs, with the latter mostly the result of echinocytosis. In contrast, in the natural host M fascicularis, echinocyte formation was not observed, and the RBC-D of uRBCs was unaffected. In unnatural primate hosts of P knowlesi, including humans, reduced deformability of iRBCs and uRBCs may represent a key pathogenic mechanism leading to microvascular accumulation, impaired organ perfusion, and anemia.

Endogenous RGS14 is a cytoplasmic-nuclear shuttling protein that localizes to juxtanuclear membranes and chromatin-rich regions of the nucleus.

Regulator of G protein signaling 14 (RGS14) is a multifunctional scaffolding protein that integrates G protein and H-Ras/MAPkinase signaling pathways to regulate synaptic plasticity important for hippocampal learning and memory. However, to date, little is known about the subcellular distribution and roles of endogenous RGS14 in a neuronal cell line. Most of what is known about RGS14 cellular behavior is based on studies of tagged, recombinant RGS14 ectopically overexpressed in unnatural host cells. Here, we report for the first time a comprehensive assessment of the subcellular distribution and dynamic localization of endogenous RGS14 in rat B35 neuroblastoma cells. Using confocal imaging and 3D-structured illumination microscopy, we find that endogenous RGS14 localizes to subcellular compartments not previously recognized in studies of recombinant RGS14. RGS14 localization was observed most notably at juxtanuclear membranes encircling the nucleus, at nuclear pore complexes (NPC) on both sides of the nuclear envelope and within intranuclear membrane channels, and within both chromatin-poor and chromatin-rich regions of the nucleus in a cell cycle-dependent manner. In addition, a subset of nuclear RGS14 localized adjacent to active RNA polymerase II. Endogenous RGS14 was absent from the plasma membrane in resting cells; however, the protein could be trafficked to the plasma membrane from juxtanuclear membranes in endosomes derived from ER/Golgi, following constitutive activation of endogenous RGS14 G protein binding partners using AlF4¯. Finally, our findings show that endogenous RGS14 behaves as a cytoplasmic-nuclear shuttling protein confirming what has been shown previously for recombinant RGS14. Taken together, the findings highlight possible cellular roles for RGS14 not previously recognized that are distinct from the regulation of conventional GPCR-G protein signaling, in particular undefined roles for RGS14 in the nucleus.

How to develop viruses into anticancer weapons.

Viruses have shaped human history through devastating infections. In addition, virus infection may be responsible for up to 15% of cancer deaths [1]. Nevertheless, certain viruses can be our “friends.” At the end of the 18th century, Edward Jenner used cowpox to protect humans against infection with a lethal pathogen, smallpox. Based on the effectiveness of this “vaccination” process, in the 1960s, the World Health Organization mounted a global vaccination campaign that resulted in the eradication of smallpox [2]. In the mid-20th century, the principle of virus attenuation through adaptation to unnatural hosts was extended to cultured cells: cells from different species were used to select viruses with multiple mutations, reducing replication speed and allowing the immune system to control viral infection. Based on such a “live-attenuated” vaccine, global eradication of another viral disease, rinderpest, was recently achieved [3]. Other global vaccination campaigns, including those against polio and measles, are progressing. In addition, subunit vaccines are proving to be effective against virus-induced cancers, preventing hepatitis B virus–induced hepatocellular carcinoma and human papilloma virus–induced cervical cancer [2, 4]. A new frontier is to develop viruses into anticancer weapons. Many cancers remain incurable despite recent advances in radio-, chemo-, and immunotherapy. Based on their preferential replication in tumor cells, viruses from nine families have progressed to clinical trials of oncolysis: DNA viruses include Adenoviridae, Herpesviridae, Parvoviridae, and Poxviridae and RNA viruses Paramyxoviridae, Picornaviridae, Reoviridae, Retroviridae, and Rhabdoviridae [5, 6]. Recently, a genetically modified herpes simplex virus 1–based oncolytic vector, named talimogene laherparepvec (T-VEC), was approved as cancer therapeutic in the United States and Europe [7]. What are the mechanisms supporting cancer therapy with viruses, and how can oncolytic virotherapy be improved?

A review of piroplasmid infections in wild carnivores worldwide: importance for domestic animal health and wildlife conservation.

Piroplasmids are tick-borne protozoan parasites that infect blood cells (erythrocytes, lymphocytes or other leukocytes) or endothelial cells of numerous wild and domestic vertebrates worldwide. They cause severe disease in livestock, dogs, cats, wild mammals and, occasionally, in humans. Piroplasmid infections are prevalent in wild carnivores worldwide although there is limited information about their clinical and epidemiological importance. There are currently nine recognized species of Babesia, two of Theileria, two of Cytauxzoon and one of Rangelia infecting captive and wild carnivores, including members of Canidae, Felidae, Mustelidae, Procyonidae, Ursidae, Viverridae, Hyaenidae and Herpestidae in the Americas, Eurasia and Africa. However, the number of piroplasmid species is likely higher than currently accepted due to the reported existence of DNA sequences that may correspond to new species and the lack of studies on many host species and biogeographical areas. Indeed, many species have been recognized in the last few years with the advancement of molecular analyses. Disease and mortality have been documented in some wild carnivores, whereas other species appear to act as natural, subclinical reservoirs. Various factors (e.g. unnatural hosts, stress due to captivity, habitat degradation, climate fluctuation or immunosuppression) have been associated with disease susceptibility to piroplasmid infections in some species in captivity. We aimed to review the current knowledge on the epidemiology of piroplasmid infections in wild carnivores and associated tick vectors. Emphasis is given to the role of wild carnivores as reservoirs of clinical piroplasmosis for domestic dogs and cats, and to the importance of piroplasmids as disease agents for endangered carnivores.

Incidence of mango leaf cutting weevil,Deporaus marginatusPascal on cashew plant,Anacardium occidentaleL. and its induced oviposition

The study was conducted under laboratory conditions by maintaining a temperature between 30–32°c and a humidity range between 80–85%, on D. marginatus, exposed to young plants of cashew with tender leaves. the weevil was induced to oviposit on the tender leaves of cashew followed by the cutting of the leaves. the eggs laid on such unnatural host (cashew leaves) developed normally into adult weevil. this constitutes first report of D. marginatus feeding and laying eggs on cashew leaves in the laboratory and its subsequent development on tender cashew leaves. no oviposition and cutting of tender leaves was found on cashew plants in field.

Phylogenetic Analysis of Viral Protein 2 of Bluetongue Virus

Bluetongue is a highly infectious vector born viral disease, and it is a disease of wild and domestic animals (ruminants). Bluetongue is a non-contagious disease of animals and spread by the biting midges (Sperlova. A. and Zendulkova. D. 2011). The name Bluetongue is given by Spreull in 1905 (Spreull, 1905). Bluetongue disease is mild in goats and severe in sheep as sheep is the primary host of bluetongue virus. Cattle act as the reservoir of bluetongue virus (Browne, 1971). The Bluetongue virus is first reported by hutcheon in 1881 During the introduction of European sheep breeds in Southern Africa (Hutcheon, 1902). Later in 1948 it was reported in North America as a sore muzzle disease (Hardy and Price, 1952).). Spare in 1964 reported outbreak of bluetongue disease in India (Spare, 1964). There are several clinical symptoms of Bluetongue disease have been found in ruminants like fever, viraemia, sore muzzle, facial oedema, hyperaemia and congestion, erosion of mucous membrane, haemorrhages, vascular permeability (OIE, 2014). Symptoms are more severe and easily detectable in sheep and these signs are high fever upto 5–7 days, loss of wool, depression and haemorrhages in the coronary band, difficulty in standing and lameness because of painful hoof, excessive salivation, swollen tongue, swelling in nasal and buccal mucosa, pneumonia and death (Tabachnick et.al., 2009). The Severity of clinical signs of bluetongue disease in sheep influenced by the type and strain of infecting virus (Verwoerd & Erasmus, 2004; OIE, 2014). The bluetongue virus is hypervariable in nature therefore, there are 24 serotypes of bluetongue virus are well recognised with two newly proposed serotypes BTV 25 from Switzerland and BTV 26 from Kuwait. In India 22 serotypes have been reported of Bluetongue virus (Prasad et al., 2009; Kumar, 2009). Bluetongue virus belongs to family Reoviridae and genus Orbivirus (Tabachnick et al., 2009). Blue-tongue has a serious economic impact on dairy and wool industry mainly due to high morbidity, mortality and mandatory trade barrier on the movement of BT infected livestock and germ-plasm. BT is evolving into newer challenges and poses ever increasing the threat to associated environment. An Unnatural host like canines have in the past contracted BT infections. Many species of Culicoides have been reported to spread infections. Recently BT has been categorized as multispecies disease by OIE (2014).

Efficacy of a virus-vectored vaccine against human and bovine respiratory syncytial virus infections.

Human respiratory syncytial virus (HRSV) is a major cause of lower respiratory tract disease in children and the elderly for which there is still no effective vaccine. We have previously shown that PanAd3-RSV, which is a chimpanzee adenovirus-vectored vaccine candidate that expresses a secreted form of the HRSV F protein together with the N and M2-1 proteins of HRSV, is immunogenic in rodents and nonhuman primates, and protects mice and cotton rats from HRSV challenge. Because the extent to which protection demonstrated in rodent models will translate to humans is unclear, we have exploited the calf model of bovine RSV (BRSV) infection, which mimics HRSV disease in children more closely than do experimental models of unnatural laboratory hosts, to evaluate the safety and efficacy of the PanAd3-RSV vaccine. We show that PanAd3-RSV alone and in combination with a modified vaccinia Ankara expressing the same HRSV antigens (MVA-RSV) induced neutralizing antibodies and cellular immunity in young seronegative calves and protected against upper and lower respiratory tract infection and pulmonary disease induced by heterologous BRSV challenge. There was no evidence either of enhanced pulmonary pathology or of enhanced respiratory disease in vaccinated calves after BRSV challenge. These findings support the continued evaluation of the vectored RSV vaccines in man.

Biology of Trypanosoma (Trypanozoon) evansi in experimental heterologous mammalian hosts.

Trypanosoma (Trypanozoon) evansi is a causative agent of the dreadful mammalian disease trypanosomiasis or 'Surra' and carried as a latent parasite in domestic cattle but occasionally proves fatal when transmitted to horses and camel. Sporadic outbreak of 'Surra' to different animals (beside their natural hosts) reminds that T. evansi may be zoonotic, as their close relative cause sleeping sickness to human being. This haemoflagellate is mechanically transmitted by horse fly and its effect on different host varies depending on certain factors including the effectiveness of transmission by mechanical vector, the suitability and susceptibility of the host as well as most importantly the ability of the disease establishment of parasite to adapt itself to the host's resistance, etc. The course of the disease caused by T. evansi is similar to that of human sleeping sickness caused by T. (T.) brucei gambiense. The target organs and symptoms show close similarity. T. evansi can successfully be transmitted among unnatural hosts i.e., other classes of vertebrates, like chicken. In transmission experiments, the unnatural hosts may sometimes induce profound changes in the biology of trypanosomes. Hence, in present study the observations are the biology of different morphological changes of T. evansi as well as its ability of disease formation within some heterologous mammal viz., albino rat, guineapig, bandicoot, mongoose, domestic cat and common monkey. Blood smears of infected albino rats, bandicoot, and mongoose revealed only monomorphic form. Interestingly, blood smears of infected cat and monkey, T. evansi shows slender trypomastigote form and short intermediate form whereas organ smears shows other two forms of haemoflagellate viz., sphaeromastigote and amastigote form. The haemoflagellate maintains a common reproductive cycle in all the experimental heterologous hosts whereas disease symptoms differ. T. evansi infected cat and monkey shows nervous symptoms. Infected monkey expresses some symptoms similar to that of human sleeping sickness disease. Thus the paper highlights zoonotic potentialities of T. evansi.

Adaptation to the Interferon-Induced Antiviral State by Human and Simian Immunodeficiency Viruses

The production of type I interferon (IFN) is an early host response to different infectious agents leading to the induction of hundreds of IFN-stimulated genes (ISGs). The roles of many ISGs in host defense are unknown, but their expression results in the induction of an "antiviral state" that inhibits the replication of many viruses. Here we show that prototype primate lentiviruses human immunodeficiency virus type 1 (HIV-1) and simian immunodeficiency virus of macaques (SIV(MAC) and SIV(MNE)) can replicate in lymphocytes from their usual hosts (humans and macaques, respectively), even when an antiviral state is induced by IFN-α treatment. In contrast, HIV-1 and SIV(MAC)/SIV(MNE) replication was hypersensitive to IFN-α in lymphocytes from unnatural hosts, indicating that the antiviral state can effectively curtail the replication of primate lentiviruses in hosts to which they are not adapted. Most of the members of a panel of naturally occurring HIV-1 and HIV-2 strains behaved like prototype strains and were comparatively insensitive to IFN-α in human lymphocytes. Using chimeric viruses engineered to overcome restriction factors whose antiretroviral specificities vary in a species-dependent manner, we demonstrate that differential HIV-1 and SIV(MAC) sensitivities to IFN-α in lymphocytes from humans and macaques could not be ascribed to TRIM5, APOBEC3, tetherin, or SAMHD1. Single-cycle infection experiments indicated that at least part of this species-specific, IFN-α-induced restriction of primate lentivirus replication occurs early in the retroviral life cycle. Overall, these studies indicate the existence of undiscovered, IFN-α-inducible antiretroviral factors whose spectrum of activity varies in a species-dependent manner and to which at least some HIV/SIV strains have become adapted in their usual hosts.