Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “host adaptation”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 181 records · Page 10Linked to original sources
PubMed2006

Natural selection and divergence in mate preference during speciation.

Sexual isolation can evolve due to natural selection against hybrids (reinforcement). However, many different forms of hybrid dysfunction, and selective processes that do not involve hybrids, can contribute to the evolution of sexual isolation. Here we review how different selective processes affect the evolution of sexual isolation, describe approaches for distinguishing among them, and assess how they contribute to variation in sexual isolation among populations of Timema cristinae stick-insects. Pairs of allopatric populations of T. cristinae living on different host-plant species exhibit greater sexual isolation than those on the same host, indicating that some sexual isolation has evolved due to host adaptation. Sexual isolation is strongest in regions where populations on different hosts are in geographic contact, a pattern of reproductive character displacement that is indicative of reinforcement. Ecological costs to hybridization do occur but traits under ecological selection (predation) do not co-vary strongly with the probability of between-population mating such that selection on ecological traits is not predicted to produce a strong correlated evolutionary response in mate preference. Moreover, F1 hybrid egg inviability is lacking and the factors contributing to reproductive character displacement require further study. Finally, we show that sexual isolation involves, at least in part, olfactory communication. Our results illustrate how understanding of the evolution of sexual isolation can be enhanced by isolating the roles of diverse ecological and evolutionary processes.

Adaptation, Biological↗
PubMed2006

Borrelia burgdorferi alters its gene expression and antigenic profile in response to CO2 levels.

The etiologic agent of Lyme disease, Borrelia burgdorferi, must adapt to the distinct environments of its arthropod vector and mammalian host during its complex life cycle. B. burgdorferi alters gene expression and protein synthesis in response to temperature, pH, and other uncharacterized environmental factors. The hypothesis tested in this study is that dissolved gases, including CO(2), serve as a signal for B. burgdorferi to alter protein production and gene expression. In this study we focused on characterization of in vitro anaerobic (5% CO(2), 3% H(2), 0.087 ppm O(2)) and microaerophilic (1% CO(2), 3.48 ppm O(2)) growth conditions and how they modulate protein synthesis and gene expression in B. burgdorferi. Higher levels of several immunoreactive proteins, including BosR, NapA, DbpA, OspC, BBK32, and RpoS, were synthesized under anaerobic conditions. Previous studies demonstrated that lower levels of NapA were produced when microaerophilic cultures were purged with nitrogen gas to displace oxygen and CO(2). In this study we identified CO(2) as a factor contributing to the observed change in NapA synthesis. Specifically, a reduction in the level of dissolved CO(2), independent of O(2) levels, resulted in reduced NapA synthesis. BosR, DbpA, OspC, and RpoS synthesis was also decreased with the displacement of CO(2). Quantitative reverse transcription-PCR indicated that the levels of the dbpA, ospC, and BBK32 transcripts are increased in the presence of CO(2), indicating that these putative borrelial virulence determinants are regulated at the transcriptional level. Thus, dissolved CO(2) may be an additional cue for borrelial host adaptation and gene regulation.

Anaerobiosis↗
PubMed1999

The virulence plasmids of Salmonella.

Certain Salmonella serovars belonging to subspecies I carry a large, low-copy-number plasmid that contains virulence genes. Virulence plasmids are required to trigger systemic disease; their involvement in the enteric stage of the infection is unclear. Salmonella virulence plasmids are heterogeneous in size (50-90 kb), but all share a 7.8 kb region, spv, required for bacterial multiplication in the reticuloendothelial system. Other loci of the plasmid, such as the fimbrial operon pef, the conjugal transfer gene traT and the enigmatic rck and rsk loci, may play a role in other stages of the infection process. The virulence plasmid of Salmonella typhimurium LT2 is self-transmissible; virulence plasmids from other serovars, such as Salmonella enteritidis and Salmonella choleraesuis, carry incomplete tra operons. The presence of virulence plasmids in host-adapted serovars suggests that virulence plasmid acquisition may have expanded the host range of Salmonella.

Bacterial Adhesion↗
PubMed2004

Brood parasitic cowbird nestlings use host young to procure resources.

Young brood parasites that tolerate the company of host offspring challenge the existing evolutionary view of family life. In theory, all parasitic nestlings should be ruthlessly self-interested and should kill host offspring soon after hatching. Yet many species allow host young to live, even though they are rivals for host resources. Here we show that the tolerance of host nestlings by the parasitic brown-headed cowbird Molothrus ater is adaptive. Host young procure the cowbird a higher provisioning rate, so it grows more rapidly. The cowbird's unexpected altruism toward host offspring simply promotes its selfish interests in exploiting host parents.

Animals↗
PubMed2004

Salmonella typhimurium persists within macrophages in the mesenteric lymph nodes of chronically infected Nramp1+/+ mice and can be reactivated by IFNgamma neutralization.

Host-adapted strains of Salmonella are capable of establishing a persistent infection in their host often in the absence of clinical disease. The mouse model of Salmonella infection has primarily been used as a model for the acute systemic disease. Therefore, the sites of long-term S. typhimurium persistence in the mouse are not known nor are the mechanisms of persistent infection clearly understood. Here, we show that S. typhimurium can persist for as long as 1 yr in the mesenteric lymph nodes (MLNs) of 129sv Nramp1(+)(/)(+) (Slc11a1(+)(/)(+)) mice despite the presence of high levels of anti-S. typhimurium antibody. Tissues from 129sv mice colonized for 60 d contain numerous inflammatory foci and lesions with features resembling S. typhi granulomas. Tissues from mice infected for 365 d have very few organized inflammatory lesions, but the bacteria continue to persist within macrophages in the MLN and the animals generally remain disease-free. Finally, chronically infected mice treated with an interferon-gamma neutralizing antibody exhibited symptoms of acute systemic infection, with evidence of high levels of bacterial replication in most tissues and high levels of fecal shedding. Thus, interferon-gamma, which may affect the level of macrophage activation, plays an essential role in the control of the persistent S. typhimurium infection in mice.

Animals↗
PubMed2006

Inhibition of the type I interferon response by the nucleoprotein of the prototypic arenavirus lymphocytic choriomeningitis virus.

The prototypic arenavirus lymphocytic choriomeningitis virus (LCMV) is a formidable battle horse for the study of viral immunology, as well as viral persistence and associated diseases. Investigations with LCMV have uncovered basic mechanisms by which viruses avoid elimination by the host adaptive immune response. In this study we show that LCMV also disables the host innate defense by interfering with beta interferon (IFN-beta) production in response to different stimuli, including infection with Sendai virus and liposome-mediated DNA transfection. Inhibition of IFN production in LCMV-infected cells was caused by an early block in the IFN regulatory factor 3 (IRF-3) activation pathway. This defect was restored in cells cured of LCMV, indicating that one or more LCMV products are responsible for the inhibition of IRF-3 activation. Using expression plasmids encoding individual LCMV proteins, we found that expression of the LCMV nucleoprotein (NP) was sufficient to inhibit both IFN production and nuclear translocation of IRF-3. To our knowledge, this is the first evidence of an IFN-counteracting viral protein in the Arenaviridae family. Inhibition of IFN production by the arenavirus NP is likely to be a determinant of virulence in vivo.

Active Transport, Cell Nucleus↗
PubMed2004

Variation in Giardia: implications for taxonomy and epidemiology.

The taxonomy, life cycle patterns and zoonotic potential of Giardia infecting mammals and birds have been poorly understood and controversial for many years. The development of molecular tools for characterising isolates of Giardia directly from faeces or environmental samples has made an enormous contribution to resolving these issues. It is now clear that the G. duodenalis morphological group is a species complex comprising a series of what appear to be largely host-adapted species, and at least two zoonotic species for which humans are the major host, but which are also capable of infecting other mammals. It is proposed that this new information be reflected in the redesignation of several species of Giardia described previously. The molecular epidemiological tools that are now available need to be applied in different endemic foci of Giardia transmission, as well as in outbreak situations, in order to understand better the frequency of zoonotic transmission as well as to develop more effective approaches to controlling giardiasis.

Animals↗
PubMed2006

Organization of chromosome ends in the rice blast fungus, Magnaporthe oryzae.

Eukaryotic pathogens of humans often evade the immune system by switching the expression of surface proteins encoded by subtelomeric gene families. To determine if plant pathogenic fungi use a similar mechanism to avoid host defenses, we sequenced the 14 chromosome ends of the rice blast pathogen, Magnaporthe oryzae. One telomere is directly joined to ribosomal RNA-encoding genes, at the end of the approximately 2 Mb rDNA array. Two are attached to chromosome-unique sequences, and the remainder adjoin a distinct subtelomere region, consisting of a telomere-linked RecQ-helicase (TLH) gene flanked by several blocks of tandem repeats. Unlike other microbes, M.oryzae exhibits very little gene amplification in the subtelomere regions-out of 261 predicted genes found within 100 kb of the telomeres, only four were present at more than one chromosome end. Therefore, it seems unlikely that M.oryzae uses switching mechanisms to evade host defenses. Instead, the M.oryzae telomeres have undergone frequent terminal truncation, and there is evidence of extensive ectopic recombination among transposons in these regions. We propose that the M.oryzae chromosome termini play more subtle roles in host adaptation by promoting the loss of terminally-positioned genes that tend to trigger host defenses.

Adenosine Triphosphatases↗
PubMed2004

Differences in susceptibility of the European eel (Anguilla anguilla) and the Japanese eel (Anguilla japonica) to the swim-bladder nematode Anguillicola crassus.

The swim-bladder nematode Anguillicola crassus originates from the Far East where it is a parasite of the Japanese eel (Anguilla japonica). After A. crassus was introduced to Europe, it became a predominant parasite of the European eel (Anguilla anguilla). A study performed with experimentally infected eels (98 days, 23 degrees C) revealed significant differences in the susceptibility of the two eel species to this parasite. The recovery rate of 30 administered infective A. crassus larvae (L3) from A. japonica was less than half of that from A. anguilla (33.2% and 13.8%, respectively). Almost 60% of the worms recovered from A. japonica were found as dead, encapsulated and necrotic larvae in the swimbladder wall. In contrast, no dead larvae were found in A. anguilla. Additionally, the development of the worms was shown to be significantly slower in A. japonica compared with A. anguilla. The lower survival rate of the worms, together with their slower development, resulted in a significantly lower adult worm burden (11 and 428 mg wet weight, respectively) and in a decreased reproductive success in A. japonica compared with A. anguilla. These results demonstrate that the original host, A. japonica, possesses more effective defence mechanisms against A. crassus than does the non-adapted host, A. anguilla.

Air Sacs↗
PubMed2006

Bizarre interactions and endgames: entomopathogenic fungi and their arthropod hosts.

Invertebrate pathogens and their hosts are taxonomically diverse. Despite this, there is one unifying concept relevant to all such parasitic associations: Both pathogen and host adapt to maximize their own reproductive output and ultimate fitness. The strategies adopted by pathogens and hosts to achieve this goal are almost as diverse as the organisms themselves, but studies examining such relationships have traditionally concentrated only on aspects of host physiology. Here we review examples of host-altered behavior and consider these within a broad ecological and evolutionary context. Research on pathogen-induced and host-mediated behavioral changes demonstrates the range of altered behaviors exhibited by invertebrates including behaviorally induced fever, elevation seeking, reduced or increased activity, reduced response to semiochemicals, and changes in reproductive behavior. These interactions are sometimes quite bizarre, intricate, and of great scientific interest.

Animals↗
PubMed2005

Analysis of porcine differential gene expression following challenge with Salmonella enterica serovar Choleraesuis using suppression subtractive hybridization.

Swine-adapted Salmonella enterica subsp. enterica serovar Choleraesuis (S. Choleraesuis) is the pathogen most frequently isolated from diseased pigs and may affect host gene expression in a species-specific manner. To characterize the porcine transcriptional response to S. Choleraesuis infection, the mRNA profiles from the mesenteric lymph nodes of three non-infected and three experimentally infected pigs at 24 h post-inoculation were analyzed by suppression subtractive hybridization (SSH). Forty-four up-regulated and 44 down-regulated genes were revealed by differential cDNA screening of 384 forward and 288 reverse subtracted cDNA clones. The DNA sequence of the cDNA clones identified genes with a role in a variety of cellular functions as well as gene products of unknown function. Seven up-regulated genes (CXCL10, CXCR4, SDCBP, DNAJA1, HSPH1, HSP90 and ANXA5) and two functionally related genes (HSP70 and DNAJA4:pDJA1) were selected for further analysis based on their predicted roles in infection and immunity. Real-time RT-PCR was performed using RNA collected from a time course of infection spanning from the acute phase (8 h) to the chronic phase (21 days) to confirm and quantitate the up-regulation of the SSH-enriched genes. Correlating with the clinical signs of infection (fever, diarrhea and lethargy), the most dramatic induction of gene expression for all nine genes occurred at 48 h post-inoculation. This investigation further defines the porcine response to a host-adapted strain of Salmonella by revealing the differential expression of genes with a role in a variety of host cellular functions including innate immunity and cytoskeleton regulation.

Animals↗
PubMed2005

Effect of alternating passage on adaptation of sindbis virus to vertebrate and invertebrate cells.

Mosquito-borne alphaviruses, which replicate alternately and obligately in mosquitoes and vertebrates, appear to experience lower rates of evolution than do many RNA viruses that replicate solely in vertebrates. This genetic stability is hypothesized to result from the alternating host cycle, which constrains evolution by imposing compromise fitness solutions in each host. To test this hypothesis, Sindbis virus was passaged serially, either in one cell type to eliminate host alteration or alternately between vertebrate (BHK) and mosquito (C6/36) cells. Following 20 to 50 serial passages, mutations were identified and changes in fitness were assessed using competition assays against genetically marked, surrogate parent viruses. Specialized viruses passaged in a single cell exhibited more mutations and amino acid changes per passage than those passaged alternately. Single host-adapted viruses exhibited fitness gains in the cells in which they specialized but fitness losses in the bypassed cell type. Most but not all viruses passaged alternately experienced lesser fitness gains than specialized viruses, with fewer mutations per passage. Clonal populations derived from alternately passaged viruses also exhibited adaptation to both cell lines, indicating that polymorphic populations are not required for simultaneous fitness gains in vertebrate and mosquito cells. Nearly all passaged viruses acquired Arg or Lys substitutions in the E2 envelope glycoprotein, but enhanced binding was only detected for BHK cells. These results support the hypothesis that arbovirus evolution may be constrained by alternating host transmission cycles, but they indicate a surprising ability for simultaneous adaptation to highly divergent cell types by combinations of mutations in single genomes.

Adaptation, Physiological↗
PubMed2004

Extracellular secretion of the Borrelia burgdorferi Oms28 porin and Bgp, a glycosaminoglycan binding protein.

Borrelia burgdorferi, the Lyme disease pathogen, cycles between its Ixodes tick vector and vertebrate hosts, adapting to vastly different biochemical environments. Spirochete gene expression as a function of temperature, pH, growth phase, and host milieu is well studied, and recent work suggests that regulatory networks are involved. Here, we examine the release of Borrelia burgdorferi strain B31 proteins into conditioned medium. Spirochetes intrinsically radiolabeled at concentrations ranging from 10(7) to 10(9) cells per ml secreted Oms28, a previously characterized outer membrane porin, into RPMI medium. As determined by immunoblotting, this secretion was not associated with outer membrane blebs or cytoplasmic contamination. A similar profile of secreted proteins was obtained for spirochetes radiolabeled in mixtures of RPMI medium and serum-free Barbour-Stoenner-Kelly (BSK II) medium. Proteomic liquid chromatography-tandem mass spectrometry analysis of tryptic fragments derived from strain B31 culture supernatants confirmed the identity of the 28-kDa species as Oms28 and revealed a 26-kDa protein as 5'-methylthioadenosine/S-adenosylhomocysteine nucleosidase (Pfs-2), previously described as Bgp, a glycosaminoglycan-binding protein. The release of Oms28 into the culture medium is more selective when the spirochetes are in logarithmic phase of growth compared to organisms obtained from stationary phase. As determined by immunoblotting, stationary-phase spirochetes released OspA, OspB, and flagellin. Oms28 secreted by strains B31, HB19, and N40 was also recovered by radioimmunoprecipitation. This is the first report of B. burgdorferi protein secretion into the extracellular environment. The possible roles of Oms28 and Bgp in the host-pathogen interaction are considered.

Bacterial Proteins↗
PubMed1984

[The nature of the so-called symptom-free periods of a disease].

The first structural changes in human diseases are the changes of cell membranes followed by their corresponding functional alterations (principle of the structure and function unity). In parallel with the destructive changes compensatory and adaptive processes (regenerative and hyperplastic) develop that level these changes and prevent homeostasis disorders. The higher is the host adaptive potential the longer clinical well-being can be retained in spite of the existing pathological process and the longer a patient with progressing morphological changes of a given organ is considered to be practically healthy. The first clinical symptoms of the disease appear when compensatory-adaptive reactions are not able to overmatch fully the organ destructive changes and resulting functional disorders. Therefore the preclinical period of the disease results in good compensation of morphological changes leading to the absence of the corresponding clinical symptoms.

Adaptation, Physiological↗
PubMed2005

Immunoglobulin-regulated expression of Borrelia burgdorferi outer surface protein A in vivo.

Borrelia burgdorferi, the agent of Lyme disease, down-regulates outer surface protein A (OspA), which is abundantly expressed in ticks, during infection of the mammalian host. In this study we examined the signals that may be responsible for maintaining the OspA-negative state of spirochetes during infection. Transcription of ospA mRNA was found in tissues of C3H-severe combined immunodeficient (C3H-scid) mice, but not immunocompetent C3H mice, inoculated with cultured B. burgdorferi, tick-borne spirochetes, and host-adapted spirochetes. Transcription was more frequent at 4 weeks than at 1 week. Transcription was present at the host-tick interface as early as 24 h after tick attachment but declined at 48 and 72 h. Thus, ospA mRNA transcription in distant tissues and at later times in C3H-scid mice is probably due to up-regulation during infection. Adoptive lymphocyte transfer from naive C3H mice to infected C3H-scid mice resulted in OspA seroconversion, confirming OspA expression in the host. Passive transfer of normal mouse serum, immunoglobulin M (IgM) from normal mouse serum, or IgG from normal mouse serum into infected C3H-scid mice resulted in down-regulation of ospA, but transfer of normal mouse serum depleted of immunoglobulin did not influence ospA mRNA transcription. Collectively, our results indicate that ospA mRNA transcription in the host is regulated by nonspecific immunoglobulin, which may be a natural antibody.

Animals↗
PubMed2004

Sequence diversity and molecular evolution of the heat-modifiable outer membrane protein gene (ompA) of Mannheimia(Pasteurella) haemolytica, Mannheimia glucosida, and Pasteurella trehalosi.

The OmpA (or heat-modifiable) protein is a major structural component of the outer membranes of gram-negative bacteria. The protein contains eight membrane-traversing beta-strands and four surface-exposed loops. The genetic diversity and molecular evolution of OmpA were investigated in 31 Mannheimia (Pasteurella) haemolytica, 6 Mannheimia glucosida, and 4 Pasteurella trehalosi strains by comparative nucleotide sequence analysis. The OmpA proteins of M. haemolytica and M. glucosida contain four hypervariable domains located at the distal ends of the surface-exposed loops. The hypervariable domains of OmpA proteins from bovine and ovine M. haemolytica isolates are very different but are highly conserved among strains from each of these two host species. Fourteen different alleles representing four distinct phylogenetic classes, classes I to IV, were identified in M. haemolytica and M. glucosida. Class I, II, and IV alleles were associated with bovine M. haemolytica, ovine M. haemolytica, and M. glucosida strains, respectively, whereas class III alleles were present in certain M. haemolytica and M. glucosida isolates. Class I and II alleles were associated with divergent lineages of bovine and ovine M. haemolytica strains, respectively, indicating a history of horizontal DNA transfer and assortative (entire gene) recombination. Class III alleles have mosaic structures and were derived by horizontal DNA transfer and intragenic recombination. Our findings suggest that OmpA is under strong selective pressure from the host species and that it plays an important role in host adaptation. It is proposed that the OmpA protein of M. haemolytica acts as a ligand and is involved in binding to specific host cell receptor molecules in cattle and sheep. P. trehalosi expresses two OmpA homologs that are encoded by different tandemly arranged ompA genes. The P. trehalosi ompA genes are highly diverged from those of M. haemolytica and M. glucosida, and evidence is presented to suggest that at least one of these genes was acquired by horizontal DNA transfer.

Adaptation, Biological↗
PubMed2005

Molecular and physiological insights into plague transmission, virulence and etiology.

Plague is caused by Yersinia pestis, which evolved from the enteric pathogen Y. pseudotuberculosis, which normally causes a chronic and relatively mild disease. Y. pestis is not only able to parasitize the flea but also highly virulent to rodents and humans, causing epidemics of a systemic and often fatal disease. Y. pestis could be used as a bio-weapon and for bio-terrorism. It uses a number of strategies that allow the pathogen to change its lifestyle rapidly to survive in fleas and to grow in the mammalian hosts. Extensive studies reviewed here give an overall picture of the determinants responsible for plague pathogenesis in mammalians and the transmission by fleas. The availability of multiple genomic sequences and more extensive use of genomics and proteomics technologies should allow a comprehensive dissection of the complex of host-adaptation and virulence in Y. pestis.

Animals↗
PubMed2006

Urbanization and the ecology of wildlife diseases.

Urbanization is intensifying worldwide, with two-thirds of the human population expected to reside in cities within 30 years. The role of cities in human infectious disease is well established, but less is known about how urban landscapes influence wildlife-pathogen interactions. Here, we draw on recent advances in wildlife epidemiology to consider how environmental changes linked with urbanization can alter the biology of hosts, pathogens and vectors. Although urbanization reduces the abundance of many wildlife parasites, transmission can, in some cases, increase among urban-adapted hosts, with effects on rarer wildlife or those living beyond city limits. Continued rapid urbanization, together with risks posed by multi-host pathogens for humans and vulnerable wildlife populations, emphasize the need for future research on wildlife diseases in urban landscapes.

Animals↗