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Mitochondrial DNA sequence divergence among greenbug (Homoptera: aphididae) biotypes: evidence for host-adapted races.

The full complement of known greenbug, Schizaphis graminum (Rondani), biotypes found in the USA were subjected to a molecular phylogenetic analysis based on a 1.2-kb portion of the cytochrome oxidase I mitochondrial gene. In addition to these nine biotypes (B, C, E, F, G, H, I, J and K), a probable isolate of the enigmatic biotype A (NY), a 'new biotype' collected from Elymus canadensis (L.) (CWR), and an isolate from Germany (EUR) were included. Schizaphis rotundiventris (Signoret) was included as an outgroup. Genetic distances among S. graminum biotypes ranged from 0.08% to 6.17% difference in nucleotide substitutions. Neighbour-joining, maximum parsimony and maximum likelihood analyses all produced dendrograms revealing three clades within S. graminum. Clade 1 contained the 'agricultural' biotypes commonly found on sorghum and wheat (C, E, K, I, plus J) and there were few substitutions among these biotypes. Clade 2 contained F, G and NY, and Clade 3 contained B, CWR and EUR, all of which are rarely found on crops. The rarest biotype, H, fell outside the above clades and may represent another Schizaphis species. S. graminum biotypes are a mixture of genotypes belonging to three clades and may have diverged as host-adapted races on wild grasses.

Adaptation, Biological↗

Lung surfactant proteins (SP-A and SP-D) in non-adaptive host responses to infection.

The lung surfactant proteins A and D (SP-A and SP-D) are collectins composed of C-type lectin domains attached to collagen regions. SP-A and SP-D are mainly found in the surfactant covering the pulmonary epithelial cells, but are also produced by cells lining the gastrointestinal tract. The main role of SP-A and SP-D is to interact directly with carbohydrate on the surface of microbial pathogens, thereby initiating a variety of effector mechanisms. This review focuses on the non-adaptive host responses of SP-A and SP-D to infection. Interaction of SP-A and SP-D with phagocytes is discussed and the structure and function of the putative receptors for SP-A and SP-D is presented. SP-A and SP-D seem to be regulated in a way similar to acute-phase proteins in the course of inflammation and evidence for the involvement of SP-A and SP-D as immunomodulators as well as their role in clearing allergens and modulating effector mechanisms in allergic reactions is discussed.

Adaptation, Physiological↗

Molecular evolution and host adaptation of Bordetella spp.: phylogenetic analysis using multilocus enzyme electrophoresis and typing with three insertion sequences.

A total of 188 Bordetella strains were characterized by the electrophoretic mobilities of 15 metabolic enzymes and the distribution and variation in positions and copy numbers of three insertion sequences (IS). The presence or absence of IS elements within certain lineages was congruent with estimates of overall genetic relationships as revealed by multilocus enzyme electrophoresis. Bordetella pertussis and ovine B. parapertussis each formed separate clusters, while human B. parapertussis was most closely related to IS1001-containing B. bronchiseptica isolates. The results of the analysis provide support for the hypothesis that the population structure of Bordetella is predominantly clonal, with relatively little effective horizontal gene flow. Only a few examples of putative recombinational exchange of an IS element were detected. Based on the results of this study, we tried to reconstruct the evolutionary history of different host-adapted lineages.

Adaptation, Biological↗

Molecular characterization of microsporidia indicates that wild mammals Harbor host-adapted Enterocytozoon spp. as well as human-pathogenic Enterocytozoon bieneusi.

Over 13 months, 465 beavers, foxes, muskrats, otters, and raccoons were trapped in four counties in eastern Maryland and examined by molecular methods for microsporidia. A two-step nested PCR protocol was developed to amplify a 392-bp fragment of the internal transcribed spacer region of the rRNA gene of Enterocytozoon spp., with the use of primers complementary to the conserved regions of published nucleotide sequences. Fifty-nine PCR-positive samples were sequenced. Multiple alignments of these sequences identified 17 genotypes of Enterocytozoon spp. (WL1 to WL17); of these, 15 have not been reported before. Most of the genotypes were found in multiple species of wildlife and belonged to a major group consisting of all the previously described Enterocytozoon bieneusi genotypes from human and domestic animals. Some of the isolates from muskrats and raccoons formed two distinct groups. Results of this study indicate that fur-bearing mammals, especially those closely associated with surface water, can be a potential source of human-pathogenic E. bieneusi. However, there are also host-adapted Enterocytozoon genotypes in wildlife, which may represent species different from E. bieneusi and have no apparent public health significance. This is the first report of E. bieneusi in wildlife.

Animals↗

A population genetic study of Borrelia burgdorferi sensu stricto from eastern Long Island, New York, suggested frequency-dependent selection, gene flow and host adaptation.

Eastern Long Island, New York, is one of the major foci of Lyme disease in the United States. As in almost all other parts of North America, Lyme disease in this region is caused by a single genomic species of spirochete, Borrelia burgdorferi sensu stricto. For three consecutive years, natural populations of Lyme Borrelia in this region were sampled and studied for gene flow among different locations, changes in population structure over time, and selective forces. The genetic diversity of Borrelia populations was measured at the outer surface protein A (ospA) locus using Cold Single-Stranded Conformation Polymorphism (Cold SSCP) analysis. The Borrelia populations were found to be highly polymorphic within any of thirteen local populations. Ewens-Watterson tests of neutrality revealed that the high level of genetic diversity within local Borrelia populations is maintained by balancing selection. Frequency-dependent selection for the different strains distinguished by the ospA alleles is likely the mechanism of the balancing selection. Allele frequency distributions of Borrelia populations were homogeneous across the region in any particular year, although different infection rates of local tick (Ixodes scapularis) populations suggested that the Borrelia populations were at least partially isolated. Since the allele frequency distribution changed over time, while remaining homogeneous over space, the nearly uniform allele frequency distribution across the region cannot be explained by recent geographic expansion from a single population. This uniform distribution across the region thus may be maintained by selection, or by a significant amount of migration or both. The genetic structure of B. burgdorferi sensu stricto also differed between spirochetes infecting nymphal ticks and those infecting adult ticks. Since larval and nymphal ticks have distinctly different host feeding preferences, host adaptation of spirochete populations is implied. This distinction and an animal study using chipmunks suggest that ticks infected by Borrelia as larvae may have high mortality in the wild. This study represents a genetic analysis of local populations of a bacterial species.

Alleles↗

Replication of Potato spindle tuber viroid in cultured cells of tobacco and Nicotiana benthamiana: the role of specific nucleotides in determining replication levels for host adaptation.

We have developed an electroporation protocol to inoculate cultured cells of tobacco and Nicotiana benthamiana with in vitro transcripts of Potato spindle tuber viroid (PSTVd) to characterize viroid structural features that determine replication efficiency at the cellular level. Both (+)- and (-)-strands of PSTVd were detected by Northern blots as early as 6 h postinoculation (h.p.i.). Accumulation of the (+)-circular PSTVd increased very rapidly starting at 24 h.p.i. and continued beyond 6 days postinoculation. Viroid accumulation in individual cells was visualized by in situ hybridization, which showed that 60-70% of the cells were infected. Previous work showed that C259 --> U substitution converted tomato isolate PSTVd(KF440-2) into a strain that is infectious on tobacco (M. Wassenegger, R. L. Spieker, S. Thalmeir, F.-U. Gast, L. Riedel, and H. L. Sänger, 1996. Virology 226, 191-197). Similarly, C259 --> U or U257 --> A substitution in the Intermediate strain (PSTVd(Int)) conferred infectivity in tobacco (Y. Zhu, Y. Qi, Y. Xun, R. Owens, and B. Ding, 2002. Plant Physiol. 130, 138-146). Our replication assays in tobacco-cultured cells demonstrated that U257 --> A and C259 --> U substitutions each enhanced PSTVd replication by 5- to 10-fold. Replacement of U257 with C, but not with G, also led to enhanced replication in tobacco cells. Replacement of C259 with nucleotide A or G did not enhance replication. Elevated accumulation of the (-)- and (+)-strands of these mutants was in part due to enhanced transcription. Interestingly, all of the nucleotide changes did not alter PSTVd replication levels in N. benthamiana cells. These results provide insights about PSTVd structures that modulate replication efficiency in adapting to a specific host.

Base Sequence↗

Host-adapted Borrelia burgdorferi in mice expresses OspA during inflammation.

Antibody responses to outer surface protein A (OspA) of Borrelia burgdorferi may occur during periods of arthritis late in the clinical course of untreated Lyme disease. These antibody responses are paradoxical, given the conclusive evidence demonstrating that B. burgdorferi transmitted to the mammalian host expresses little or no OspA. The parallel occurrence of OspA antibodies and arthritic episodes suggests that OspA expression is upregulated during infection with B. burgdorferi. We hypothesized that this was due to the inflammatory environment caused by the immune response to the spirochete. To test our hypothesis, we adapted an in vivo model that mimics the host-pathogen interaction. Dialysis chambers containing B. burgdorferi were implanted into the peritoneal cavities of mice in the presence or absence of zymosan, a yeast cell wall extract that induces inflammation. Spirochetes were harvested 2 days later, and OspA expression was assessed at the protein and transcription level by Western blotting and real-time reverse transcription-PCR, respectively. Flow cytometry was also utilized to evaluate OspA protein expression on individual spirochetes. B. burgdorferi maintained in an inflammatory in vivo environment show an increased OspA expression relative to B. burgdorferi kept under normal in vivo conditions. Furthermore, host-adapted B. burgdorferi with a low OspA phenotype upregulates OspA expression when transferred to an inflammatory in vivo environment. The results obtained by these techniques uniformly identify inflammation as a mediator of in vivo OspA expression in host-adapted B. burgdorferi, providing insights into the behavior of live spirochetes in the mammalian host.

Adaptation, Physiological↗

Complementable and noncomplementable host adaptation defects in bipartite geminiviruses.

Members of the geminvirus group of plant viruses collectively infect a broad spectrum of species. Individual viruses which are genetically very similar may nevertheless have distinct host ranges. Two such geminiviruses are tomato golden mosaic virus (TGMV) and been golden mosaic virus (BGMV), for which common hosts have not previously been reported. Each virus has two genome components, designated A and B. The A component is capable of autonomous replication and encapsidation, whereas the B component provides viral functions required for the spread of infection in plants. To investigate the basis for the distinctive host ranges of BGMV and TGMV, we have introduced plasmids containing cloned viral genome components into Nicotiana benthamiana, a good host for TGMV, and bean, Phaseolus vulgaris, a good host for BGMV. We found that TGMV has a low specific infectivity for bean and is virulent, whereas BGMV has a high specific infectivity for N. benthamiana, but infections are asymptomatic and viral DNA accumulation is low. To investigate which viral functions were defective in the poor host in each case, we attempted to complement them by co-inoculation with the well-adapted virus. After inoculation of beans with both viruses, only BGMV was detected. Thus, TGMV exhibits a noncomplementable host adaptation defect in beans. This suggests that the defect has a cis-acting or virus-specific trans-acting genetic basis. In contrast, the BGMV phenotype of low DNA accumulation in N. benthamiana was partially complemented by TGMV A alone and complemented further by the complete TGMV genome. This suggests that a virus nonspecific, trans-acting factor encoded by the BGMV A component is poorly adapted to N. benthamiana. The results of this study indicate that bipartite geminivirus host range may be limited by defective virus-host interactions of more than one kind.

DNA, Viral↗

Adaptive host preference and the dynamics of host-parasitoid interactions.

Models of two independent host populations and a common parasitoid are investigated. The hosts have density-dependent population growth and only interact indirectly by their effects on parasitoid behavior and population dynamics. The parasitoid is assumed to experience a trade-off in its ability to exploit the two hosts. Three alternative types of parasitoid are investigated: (i) fixed generalists whose consumption rates are those that maximize fitness; (ii) "ideal free" parasitoids, which modify their behavior to maximize their rate of finding unparasitized hosts within a generation; and (iii) "evolving" parasitoids, whose capture rates change between generations based on quantitative genetic determination of the relative attack rates on the two hosts. The primary questions addressed are: (1) Do the different types of adaptive processes stabilize or destabilize the population dynamics? (2) Do the adaptive processes tend to equalize or to magnify differences in host densities? The models show that adaptive behavior and evolution frequently destabilize population dynamics and frequently increase the average difference between host densities.

Adaptation, Biological↗

Crystal structure of Swine vesicular disease virus and implications for host adaptation.

Swine vesicular disease virus (SVDV) is an Enterovirus of the family Picornaviridae that causes symptoms indistinguishable from those of foot-and-mouth disease virus. Phylogenetic studies suggest that it is a recently evolved genetic sublineage of the important human pathogen coxsackievirus B5 (CBV5), and in agreement with this, it has been shown to utilize the coxsackie and adenovirus receptor (CAR) for cell entry. The 3.0-A crystal structure of strain UK/27/72 SVDV (highly virulent) reveals the expected similarity in core structure to those of other picornaviruses, showing most similarity to the closest available structure to CBV5, that of coxsackievirus B3 (CBV3). Features that help to cement together and rigidify the protein subunits are extended in this virus, perhaps explaining its extreme tolerance of environmental factors. Using the large number of capsid sequences available for both SVDV and CBV5, we have mapped the amino acid substitutions that may have occurred during the supposed adaptation of SVDV to a new host onto the structure of SVDV and a model of the SVDV/CAR complex generated by reference to the cryo-electron microscopy-visualized complex of CBV3 and CAR. The changes fall into three clusters as follows: one lines the fivefold pore, a second maps to the CAR-binding site and partially overlaps the site for decay accelerating factor (DAF) to bind to echovirus 7 (ECHO7), and the third lies close to the fivefold axis, where the low-density lipoprotein receptor binds to the minor group of rhinoviruses. Later changes in SVDV (post-1971) map to the first two clusters and may, by optimizing recognition of a pig CAR and/or DAF homologue, have improved the adaptation of the virus to pigs.

Adaptation, Physiological↗

Host-adaptive antigenic variation in Bunyaviruses.

Bunyamwera virus and snowshoe have virus (family Bunyaviridae) were passaged up to six times through mosquito cells in culture and the resultant viruses were compared to the input, mammalian cell-passed virus using monoclonal antibodies raised against the input virus. The mosquito cell-adapted virus population consisted of mutants which were better adapted to replication in the new host than was the input mammalian cell-passed virus and were differentially susceptible to neutralization by antibody.

Aedes↗

Immune evasion by tickborne and host-adapted Borrelia burgdorferi.

Immune sera from mice infected with the Lyme disease spirochete, Borrelia burgdorferi, have strong biologic activity against spirochetes cultured in vitro. Recent studies with rodents and ticks infected with B. burgdorferi indicate that spirochetes undergo major changes in protein expression as they adapt to the diverse environments encountered by a vectorborne pathogen. The purpose of this study was to explore the susceptibility of three different adaptive forms of B. burgdorferi (in vitro cultured, host-derived, and tickborne) to immune sera. Passive transfer of immune sera protected mice when they were challenged with spirochetes cultured in vitro. Immune sera did not protect mice from tickborne spirochetes or spirochetes derived from infected mice. These results indicate that spirochetes that have adapted within either the feeding tick or host are relatively invulnerable to the protective effects of immune sera, unlike spirochetes grown in vitro, which are highly susceptible.

Animals↗

Host adaptation of pigeon isolates of Salmonella enterica subsp. enterica serovar Typhimurium variant Copenhagen phage type 99 is associated with enhanced macrophage cytotoxicity.

Phage type 99 of Salmonella enterica subsp. enterica serovar Typhimurium variant Copenhagen strains isolated from pigeons were examined for the presence of genotypic and phenotypic characteristics. The pulsed-field gel electrophoresis patterns obtained with XbaI and BlnI from 38 pigeon strains were compared with those obtained from 89 porcine, poultry, and human strains of variant Copenhagen. Identical patterns with XbaI and four closely related patterns with BlnI were obtained with the pigeon strains, whereas 16 XbaI patterns were found with the other strains. The XbaI patterns of the pigeon strains showed a low genetic similarity to the patterns of the porcine, poultry, and human strains and invariably showed a low-molecular-weight band that was absent in the majority of the other strains. The virulence genes shdA, spvR, pefA, sopE, and spvB were uniformly present in six pigeon isolates representing the genetic diversity found with BlnI. These six pigeon-derived strains were highly cytotoxic for pigeon macrophages compared to three porcine strains. After experimental infection of pigeons with a pigeon strain, clinical symptoms, fecal shedding, and colonization of internal organs were more pronounced than those after infection with a porcine strain. These data suggest that the phage type 99 strains used in this study are highly adapted to pigeons and should be classified as a host-restricted lineage of the serovar Typhimurium.

Adaptation, Physiological↗

Effects of the trematode Maritrema novaezealandensis on the behaviour of its amphipod host: adaptive or not?

There are many recorded cases of parasites that are capable of altering the behaviour of their host to enhance their transmission efficiency. However, not all of these cases are necessarily the results of the parasites actively manipulating host behaviour; they may rather be the 'by-products' of pathology caused by the parasite's presence. This study investigates the effect of the microphallid trematode Maritrema novaezealandensis on the behaviour of one of its crustacean intermediate hosts, the amphipod Paracalliope novizealandiae. Uninfected amphipods were experimentally infected by exposure to M. novaezealandensis cercariae. The activity level and vertical position of experimentally infected amphipods were compared with uninfected amphipods at 2 weeks and 6 weeks post-infection, i.e. both before and after the parasite achieved infectivity to its definitive host. Infected amphipods were found to exhibit significantly lower levels of activity and to occur significantly lower in the water column than uninfected controls during both periods. Based on the timing of the change in behaviour exhibited by infected amphipods, the results suggest that the altered behaviour exhibited by P. novizealandiae infected with M. novaezealandensis is most likely due to pathology caused by the parasite rather than a case of active, and adaptive, behavioural manipulation.

Adaptation, Physiological↗

Insights into the selective pressures restricting Pelargonium flower break virus genome variability: Evidence for host adaptation.

The molecular diversity of Pelargonium flower break virus (PFBV) was assessed using a collection of isolates from different geographical origins, hosts, and collecting times. The genomic region examined was 1,828 nucleotides (nt) long and comprised the coding sequences for the movement (p7 and p12) and the coat (CP) proteins, as well as flanking segments including the entire 3' untranslated region (3' UTR). Some constraints limiting viral heterogeneity could be inferred from sequence analyses, such as the conservation of the amino acid sequences of p7 and of the shell domain of the CP, the maintenance of a leucine zipper motif in p12, and the preservation of a particular folding in the 3' UTR. A remarkable covariation, involving five specific amino acid sites, was found in the CP of isolates largely propagated in the local lesion host Chenopodium quinoa and in the progeny of a PFBV variant subjected to serial passages in this host. Concomitant with this covariation, up to 30 nucleotide substitutions in a 1,428-nt region of the viral RNA could be attributable to C. quinoa-specific adaptation, representing one of the most outstanding cases of host-driven genome variation for a plant virus. Globally, the results indicate that the selective pressures exerted by the host play a critical role in shaping PFBV populations and that these populations are likely being selected for at both protein and RNA levels.

3' Untranslated Regions↗

Lineage-specific decay of folate biosynthesis genes suggests ongoing host adaptation in phytoplasmas.

Phytoplasmas are nonculturable cell wall-less, obligate intracellular pathogens of plants and insect vectors. In their descent from walled bacterial ancestors, phytoplasmas underwent massive genome reduction, resulting in some of the smallest cellular genomes known in nonsymbiotic bacteria. While requirements for in vitro culture of phytoplasmas remain unknown, two opposing reports have appeared concerning genes encoding the ability of phytoplasmas to synthesize folates de novo. One study found pseudogene homologs of folP and folK, obviating folate synthesis in "Candidatus Phytoplasma asteris"-related strain CPh, whereas, a separate study found intact genes encoding a complete folate biosynthesis pathway in "Ca. Phytoplasma asteris"-related strain OY. To resolve the apparent conflict, we hypothesized that evolutionary adaptation to the availability of folate and/or other metabolites in host cells is an ongoing process in the phytoplasma clade that is reflected in part by differences among phytoplasmas in the status of genes of the folate biosynthesis pathway. By studying folP and folK loci in 11 closely related phytoplasmas, we determined that these essential folate biosynthesis genes are intact in some phytoplasmas but are deteriorating in closely related strains. We suggest that the status of the folate biosynthesis pathway and the course of gene decay are lineage-specific, predicting the eventual, lineage-related loss of recognizable folP and folK homologs in phytoplasma genomes.

Adaptation, Physiological↗

In vivo recognition by the host adaptive immune system of microencapsulated xenogeneic cells.

BACKGROUND: Microencapsulation is under consideration as a means of enabling pancreatic islet transplantation. To understand better the ongoing destructive host response, we examined whether the adaptive immune system of the recipient recognized polymer-encapsulated xenogeneic cells implanted intraperitoneally. METHODS: Balb/c mice were implanted with xenogeneic Chinese hamster ovary cells, inside and outside poly(hydroxyethyl methacrylate-methyl methacrylate) microcapsules, and responses were compared with xenografted Chinese hamster skin (positive control). Capsules were localized within an agarose rod. Splenocyte proliferation upon rechallenge in vitro, antibody titer in serum, and Th1/2 polarization (assessed by interleukin-4 and interferon-gamma in supernatants of antigen-challenged splenocytes and immunoglobulin [Ig]G1 and IgG2a antibody isotypes in serum) were measured. RESULTS: Encapsulation did not prevent a strong recipient antibody response. Splenocyte proliferation in vitro did not differ after priming by implanted cells, inside or outside capsules. Thus, the capsule membrane did not prevent indirect recognition of shed antigens. However, after 10 days of implantation, proliferation was lower than that induced by skin grafts, although this difference disappeared by 2 months. This transient T-cell suppression was unexpected because encapsulated cell viability was already compromised by 10 days. The influence of Th1/2 bias did not explain the observed suppression. Cells inside capsules elicited a consistent Th2 response, whereas cells outside capsules elicited a mixed response, and skin xenografts showed an initial Th2 response that became mixed by 2 months. CONCLUSIONS: Encapsulation does not prevent host immune responses, but the inflammatory response to the implanted biomaterials or xenogeneic cells may be responsible both for encapsulated cell death and transient T-cell suppression.

Animals↗

Ruminal and host adaptations to changes in frequency of protein supplementation.

The effect of altering supplementation frequency on host N balance and key N transactions in the ruminal ecosystem were monitored. Four ruminally fistulated beef steers (BW = 513 kg; SEM = 6.5) were used in a 2 x 2 crossover design with two periods and two supplementation frequency treatments. Supplementation frequencies were 2 and 7 d/wk. Steers were fed tallgrass prairie hay (73.1% NDF, 5.3% CP) ad libitum. Supplement (42% CP; DM basis) was fed at 0.36% BW/d to steers supplemented 7 d/wk. Steers supplemented 2 d/wk received the same amount of supplement per week, but it was equally split among the two supplementation events. Steers supplemented 7 d/wk had higher forage (P < 0.02) and total digestible OM intake (P < 0.06), total N intake, fecal N excretion, and N retention. Although both supplementation frequencies were characterized by positive N balance, the decrease in N retention in the steers supplemented 2 d/wk was due to higher (P < 0.01) urinary N loss. Ruminal fluid was sampled at 0, 2, 4, 6, 12, 24, 48, and 72 h after supplementation beginning on a day when both treatments were supplemented. Frequency x hour interactions (P < 0.02) were observed for ruminal N metabolism criteria. Counts of peptide- and AA-fermenting bacteria peaked at 2 h and returned to nadir by 12 h for steers supplemented 7 d/wk. Steers supplemented 2 d/wk peaked at 6 h with a greater population and returned to nadir at 48 h. Ruminal ammonia concentrations followed a similar trend. Specific activity of ammonia production was lower (P < or = 0.05) immediately after supplementation for steers supplemented 2 d/wk, but by 12 h was the same as for 7 d/wk steers. Ruminal peptides and free AA peaked at 2 h for steers supplemented 2 d/wk and were generally higher (P < or = 0.05) during the first 6 h compared with steers supplemented 7 d/wk. Total VFA concentration was not different (P = 0.35) due to supplementation frequency. Frequency x hour interactions (P < 0.01) were observed for all molar proportions of VFA. The molar proportion of acetate and acetate:propionate ratio were lower (P < 0.01) and the molar proportions of propionate and butyrate were higher for steers supplemented 2 d/wk from 4 h to 24 h. In conclusion, forage use and N balance improved with supplementation 7 d/wk, but supplementation 2 d/wk was associated with some desirable shifts in select ruminal events that may contribute to moderating potential negative impacts of supplementing infrequently.

Adaptation, Physiological↗