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PubMed2001

Parallel evolution of histophagy in ciliates of the genus Tetrahymena.

BACKGROUND: Species of Tetrahymena were grouped into three complexes based on morphological and life history traits: the pyriformis complex of microstomatous forms; the patula complex of microstome-macrostome transformers; and the rostrata complex of facultative and obligate histophages. We tested whether these three complexes are paraphyletic using the complete sequence of the small subunit rDNA (SSrDNA). RESULTS: In addition to the 16 species of Tetrahymena whose SSrDNA sequences are known, we sequenced the complete SSrDNA from the following histophagous Tetrahymena species; Tetrahymena bergeri, Tetrahymena mobilis, Tetrahymena rostrata, and Tetrahymena setosa as well as the macrostome species Tetrahymena vorax. We also included a ciliate tentatively identified as Lambornella sp., a parasite of the mosquito Aedes sp. We confirmed earlier results using SSrDNA, which showed two distinct clusters of Tetrahymena species: the australis group and borealis group. The genetic distances among Tetrahymena are in general very small. However, all nodes were supported by high bootstrap values. With the exception of T. bergeri and T. corlissi, which are both histophagous and group as sister species, all other histophagous Tetrahymena species are most closely related to a bacterivorous species. Furthermore, Lambornella sp. and T. empidokyrea, both mosquito parasites, are sister species, although there is a considerable genetic distance between them. CONCLUSIONS: There has been parallel evolution of histophagy in the genus Tetrahymena and the three classical species complexes are paraphyletic. As the genus Lambornella arises within the Tetrahymena clade, it is not likely a defensible one.

Animals↗
PubMed1991

Murine Taenia crassiceps cysticercosis: H-2 complex and sex influence on susceptibility.

Several inbred strains of mice were infected by intraperitoneal injection of ten Taenia crassiceps cysticerci per mouse. Genes linked with the major histocompatibility complex (H-2) were found to influence parasite growth greatly, as demonstrated by the different parasite loads of H-2 congenic mice with BALB background: BALB/c (H-2d) mice were the most susceptible, whereas BALB/k (H-2k) and BALB/b (H-2b) animals were comparatively resistant. Non-H-2 genes had no significant effect on susceptibility in H-2d strains, as reflected by the similar parasite loads in BALB/c, DBA/2, and (BALB/c x DBA/2)F1 mice. Using the H-2b (BALB/b, C57BL/6J) and H-2k (C3H/HeJ, BALB/k, and C3HeB/FeJ) strains, we found that non-H-2 background genes caused a small but significant influence on parasite load. A recombinant mouse strain alleles (Kk, Ik, Sd, Dd) was also susceptible, indicating that S and/or D regions of the H-2d complex are probably involved in the control of resistance to murine cysticercosis. Females of all mouse strains were more susceptible than males. The same effects were observed for H-2 genes and sex, with two strains of T. crassiceps differing in their rate of growth.

Animals↗
PubMed1991

Chronic infections and autoimmunity.

The studies summarized in this chapter indicate that chronic bacterial, viral, and parasitic infections can serve as a trigger factor of autoimmune reactivity according to various mechanisms. The relationship between microbes and autoimmunity could be manifested by the presence of autoantibodies, autoimmune complexes, or T cells with autoactivity. The presence of autoimmune phenomena in chronic infections could be related to polyclonal B-cell activation, molecular mimicry between microbial and host antigens, altered self, abnormal expression of immunoregulatory molecules, and the anti-idiotypic network. In most cases, the appearance of self-reactivity in the sera of patients with chronic infections is not associated with clinical manifestations. These findings suggest that autoimmune disease is the result of a combination of factors including immunologic, genetic, hormonal, and environmental. Infectious agents have a role in the breakdown of tolerance and the appearance of autoreactivity. However, only patients with the proper immunogenetic and hormonal background may develop clinical manifestations of autoimmune disease. In spite of the extensive knowledge that has accumulated, the specific relationship between infections and autoimmunity is still obscure. Clearly, additional studies are required to clarify the relevance of microbes to the pathogenesis of autoimmune diseases.

Acquired Immunodeficiency Syndrome↗
PubMed2001

Susceptibility to Leishmania mexicana infection is due to the inability to produce IL-12 rather than lack of IL-12 responsiveness.

Almost all inbred mice are highly susceptible to parasites of the Leishmania mexicana complex that includes L. amazonensis and L. mexicana. Recent studies have reported that T cells from L. amazonensis-infected mice fail to respond to IL-12 due to impaired IL-12R expression. Here, we demonstrate that lymph node cells from L. mexicana-infected C57BL/6 and 129Sv/Ev mice respond efficiently to exogenous IL-12 in vitro and produce IFN-gamma. Moreover, we also show that deletion of signal transducer and activator of transcription (STAT)4 gene in resistant STAT6-/- mice renders them susceptible to L. mexicana. These findings indicate that an inability to produce IL-12 rather than unresponsiveness to this cytokine is responsible for susceptibility to L. mexicana. Moreover, the data also demonstrate that the STAT4-mediated pathway is critical for the development of protective immunity against cutaneous leishmaniasis, regardless of the species of Leishmania and/or genetic background of the mice.

Animals↗
PubMed1988

The ecological context of child health in Saudi Arabia.

The general background to child health in Saudi Arabia is reviewed. Information is provided on the social and demographic characteristics of the population, on common health indicators, on the health care system and its utilization, and on the general pattern of childhood morbidity and mortality. The unprecendented socioeconomic development has transformed the health care system. In 15 years the number of nurses have increased from 3261 to 29896, physicians from 1172 to 14335, primary health care centers from 591 to 1821, and hospital beds from 9036 to 30707. In spite of this progress, the disease pattern seems to resemble that of some developing countries with more limited resources. Parasitic diseases are still widespread, and sample surveys have indicated suboptimal nutrition of rural preschool children. Recent estimates on the infant mortality rate have ranged from 65 to 120 per 1000 live births. The preferred marriage partner is a close relative, and genetic diseases, such as hemoglobin disorders, are common in certain areas. Thus, the prevalence of alpha thalassemia is reported at 50 percent, and the sickle cell trait at 4.4-20 percent in sample surveys from the Eastern Province. The modest educational attainment of the mother, the heavy reliance on foreign manpower in all sectors, including the health sector, and the further development of the primary health care system are key issues today. It is emphasized that demographic and epidemiological information from Saudi Arabia is scarce and frequently uncertain, and that further studies are needed to identify the health needs of Saudi children.

Breast Feeding↗
PubMed1999

Characterisation of a polymorphic Tc1-like transposable element of the parasitic nematode Haemonchus contortus.

Hctc1, a member of the Tc1-family of transposable elements was isolated from the parasitic nematode Haemonchus contortus. Hctc1 is 1590 bp long, is flanked by 55 bp inverted repeats and carries a single open reading frame of a 340 amino acid transposase-like protein. Hctc1 is similar to Tc1 of Caenorhabditis elegans and elements Tcb1 and Tcb2 of Caenorhabditis briggsae in the inverted terminal repeats, the open reading frame, as well as the target insertion sequence. Furthermore, the copy number of Hctc1 is comparable with the Tc1 copy number in low copy strains of C. elegans. The sequence of Hctc1 is highly variable in H. contortus due to deletions, insertions and point mutations, with at least five distinct length variants of Hctc1. Most of the Hctc1 variation was within rather than between H. contortus populations. The high level of sequence variation is probably due to variation generally found for members of the Tc1-family, as well as a high background level of genetic variation of H. contortus.

Amino Acid Sequence↗
PubMed1994

Transient transfection of the enteric parasite Entamoeba histolytica and expression of firefly luciferase.

Development of DNA-mediated transfection in Entamoeba histolytica will facilitate basic research toward the control of this protozoan parasite. A transient transfection system was established by using the firefly luciferase gene ligated to the 5' and 3' flanking regions of the amebic hgl1 gene. The optimal construct tested encoded an hgl1-luciferase fusion protein and contained 1 kb of 5' flanking sequence with 16 bases of coding sequence from the hgl1 gene ligated in-frame to the luciferase start codon and 2.3 kb of 3' flanking sequence from hgl1 ligated 3' to the luciferase stop codon. Optimal electroporation conditions in strain HM-1:IMSS trophozoites when using this construct were 500 microF and 500 V/cm, which resulted in luciferase activity up to 5000-fold above background 9-12 hr after electroporation. Constructs that contained the luciferase gene without amebic flanking sequences or that contained a simian virus 40 promoter, enhancer, and polyadenylylation signal produced only background levels of luciferase activity. The ability to introduce and express genes in amebae will now permit a genetic analysis of the virulence of this organism, which remains a serious threat to world health.

Animals↗
PubMed1983

Indochinese refugee health assessment and treatment.

Many Southeast Asian refugees have resettled in the United States. This report reviews data from 426 refugees who underwent comprehensive examination and treatment at the Mayo Clinic. Health problems identified were primarily selected contagious illnesses and stress syndromes with functional complaints. Counseling was necessary in 17 percent of adults for psychosomatic problems or psychiatric disorders. When family-planning issues were applicable and addressed, 80 percent of women chose some method of contraception. The prevalence rate of intestinal parasites was 82 percent, and pathogens necessitated persistent treatment and follow-up. Tuberculosis skin-sensitivity testing was positive in 54 percent; the risk of active disease warrants prophylactic treatment until age 35 years. Hepatitis antigen was positive in 13 percent; precautions should be taken for potentially exposed professionals. Hematologic genetic disorders were very common and accounted for most of the 25 percent incidence of microcytosis. Physicians should become aware of cultural attitudes and treatment acceptance among Indochinese patients and should carefully investigate for infectious diseases.

Adolescent↗
PubMed2003

Impaired expression of inflammatory cytokines and chemokines at early stages of infection with Leishmania amazonensis.

Infection of mice with Leishmania major results in disease progression or resolution, largely depending on the genetic backgrounds of the mouse strains. Infection with Leishmania amazonensis, on the other hand, causes progressive cutaneous lesions in most inbred strains of mice. We hypothesized that deficient activation of early immune responses contributes to the pathogenesis in L. amazonensis-infected mice. To distinguish early molecular events that determine the outcome of Leishmania infections, we examined cytokine gene expression in C57BL/6 mice infected with either L. amazonensis or L. major (a healing model). After 2 to 4 weeks, L. amazonensis-infected mice had significantly delayed and depressed expression of inflammatory cytokines (interleukin-12 [IL-12], gamma interferon, IL-1 alpha, IL-1 beta), CC chemokines (CC chemokine ligand 3 [CCL3]/macrophage inflammatory protein 1 alpha [MIP-1 alpha], CCL4/MIP-1 beta, CCL5/RANTES, MIP-2), and chemokine receptors (CCR1, CCR2, CCR5) in foot tissues and draining lymph nodes compared to the expression in L. major-infected controls. These findings correlated with defective T-cell responsiveness to parasite stimulation in vivo and in vitro. Adoptive transfer of L. amazonensis-specific Th1 cells prior to infection overcame the immune defects of the animals, leading to complete control of the disease. Studies with gene knockout mice suggested that IL-10, but not IL-4, contributed partially to compromised immunity in L. amazonensis-infected hosts. The data suggest that there is impairment in multiple immune functions at early stages of infection with L. amazonensis parasites and provide a compelling rationale to explore immune augmentation as an intervention in American cutaneous leishmaniasis.

Adoptive Transfer↗
PubMed1984

Immunoregulation of genetically controlled acquired responses to Leishmania donovani infection in mice: demonstration and characterization of suppressor T cells in noncure mice.

On a B10 genetic background, genes in the I region of H-2 influence the development of acquired T-cell mediated immunity to Leishmania donovani infection in mice. In previous studies, noncure in H-2d mice could be abrogated by pretreatments with cyclophosphamide or sublethal irradiation. The prophylactic effect of these pretreatments was consistent with deletion of the precursors of suppressor T cells suppressing T-cell-mediated immune responses. In this study, cell transfer experiments provide direct evidence for the role of suppressor T cells in the noncure response. T-cell-enriched populations isolated from the spleens of B10.D2/n mice infected 30, 61, or 85 days previously reversed the prophylactic effect of sublethal irradiation when injected before infection into B10.D2/n mice that had received 550 rads. B-cell-enriched populations failed to transfer suppression in this manner, and T-cell-enriched populations from the spleens of normal B10.D2/n mice had only a transient effect on liver parasite loads. Transfer of suppression with the T-cell-enriched populations from infected donors was abrogated by pretreatment with anti-Thy-1.2 and anti-Lyt-1.2 antisera plus complement but not by pretreatment with anti-Lyt-2.2 plus complement, indicating that the suppressor T cell involved has an Lyt-1+2- surface phenotype. Results are discussed in relation to the possible mechanism of H-2-linked control.

Animals↗
PubMed1999

Identification and characterization of a ran gene promoter in the protozoan pathogen Giardia lamblia.

The promoter elements that regulate transcription initiation in Giardia lamblia are poorly understood. In this report, the promoter of the Giardia ran gene was studied using a luciferase expression plasmid pRANluc+ to monitor transcription efficiency. An AT-rich sequence spanning -51/-20 relative to the translation start site of the ran gene was identified and was found to be required for efficient luciferase expression by deletion and mutation mapping of pRANluc+. The -51/-20 sequence was also sufficient for promoter activity as revealed from studies on a 32-base pair synthetic promoter derived from this region. Deletion mapping of the synthetic promoter revealed two minimal promoter elements, -51/-42 and -30/-20, sufficient for 6- and 30-fold luciferase expression above background, respectively. The transcription start sites on luc+ messenger RNA were determined by the position of the synthetic promoter in the luciferase expression plasmids as shown by primer extension experiments. Results from electrophoretic mobility shift assays revealed multiple DNA-protein complexes upon binding of nuclear proteins with either DNA strand but not the double-stranded DNA derived from the ran promoter. Our results delineate the first promoter sequence of the Giardia gene (ran), which provides an excellent model for future studies on transcription regulation in this protozoan parasite.

Animals↗
PubMed1997

Genetic control of antibody responses induced by recombinant Mycobacterium bovis BCG expressing a foreign antigen.

Recombinant Mycobacterium bovis BCG expressing foreign antigens represents a promising candidate for the development of future vaccines and was shown in several experimental models to induce protective immunity against bacterial or parasitic infections. Innate resistance to BCG infection is under genetic control and could modify the immune responses induced against an antigen delivered by such engineered microorganisms. To investigate this question, we analyzed the immune responses of various inbred strains of mice to recombinant BCG expressing beta-galactosidase. These experiments demonstrated that BALB/c mice developed strong antibody responses against BCG expressing beta-galactosidase under the control of two different promoters. In contrast, C57BL/6, C3H, and CBA mice produced high anti-beta-galactosidase antibody titers only when immunized with recombinant BCG expressing beta-galactosidase under the control of the pblaF* promoter, which induced the production of high levels of this antigen. This difference in mouse responsiveness to recombinant BCG was not due to innate resistance to BCG infection, since similar immune responses were induced in Ity(r) and Ity(s) congenic strains of mice. In contrast, the analysis of anti-beta-galactosidase antibody responses of H-2 congenic mice in two different genetic backgrounds demonstrated that H-2 genes are involved in the immune responsiveness to beta-galactosidase delivered by recombinant BCG. Together, these results demonstrate that immune responses to an antigen delivered by recombinant BCG are under complex genetic influences which could play a crucial role in the efficiency of future recombinant BCG vaccines.

Animals↗
PubMed2001

RuNAway Disease: A two cycle model for transmissible spongiform encephalopathies (TSEs) wherein SINE proliferation drives PrP overproduction.

BACKGROUND: Despite decades of research, the agent responsible for transmitting spongiform encephalopathies (TSEs) has not been identified. The Prion hypothesis, which dominates the field, supposes that modified host PrP protein, termed PrPSc, acts as the transmissible agent. This model fits the observation that TSE diseases elicit almost no immune reaction. Prion transmission has not been verified, however, as it has not been possible to produce pure PrPSc aggregates. One long-standing objection to the Prion model is the observation that TSE disease agents show classical genetic behaviours, such as reproducible strain variation, while also responding to selection for novel traits such as adaptation to new hosts. Moreover, evidence has been steadily accumulating that infectious titre is decoupled from the quantity (or even the presence) of PrPSc deposits. Rather awkwardly for the Prion hypothesis, PrP0/0 knockout mice have been found to incubate and transmit TSE agents (despite themselves being refractory to TSE disease). HYPOTHESIS: In this article, a new scheme, RuNAway, is proposed whereby uncontrolled proliferation of a type of parasitic gene, the small dispersed repeat sequences (SINEs), in somatic cells induces overproduction of PrP with pathogenic consequences. The RuNAway scheme involves twin tandem positive feedback loops: triggering the second loop leads to the pathogenic disease. This model is consistent with the long latency period and much shorter visible disease progression typical of TSEs.

Animals↗
PubMed2002

Trypanosoma cruzi: infection patterns in intact and athymic mice of susceptible and resistant genotypes.

Inbred strains of mice inoculated with the T cruzi Y strain behaved as susceptible (A/J, C3H/HeN), intermediate (BALB/c) or relatively resistant (C57BL/6) with respect to the magnitude of parasitaemia and mortality rate. C57BL/10 mice were susceptible in relation to parasitaemia but resistant when mortality was analyzed. Infection with T cruzi CL strain presented the same results, except for C57BL/6 which behaved as susceptible mice. Athymic mice of various backgrounds revealed no differences in susceptibility, presenting the same dramatic parasitaemia, tissue colonization pattern and no inflammatory reaction in any of the tissues studied. Infection of euthymic and athymic BALB/c mice elicited the production of parasite-specific antibodies, which reached similar levels on the first 9 days but differed after day 13. Serum transfer experiments in BALB/c mice did not show great differences in parasitaemia but altered T. cruzi polymorphism reducing the slender forms in athymic mice. Histopathology of athymic BALB/c mice showed the same tissue tropism when infected either with T cruzi Y or CL strain.

Animals↗
PubMed2025

Evolutionary Diversification and Functions of the Candidate Male Killing Gene wmk.

Symbiont-mediated male killing (MK) is a mechanism that selectively eliminates male offspring, often by disrupting sex-specific developmental processes. In Drosophila melanogaster, the WO-mediated killing gene wmk from Wolbachia prophage WO transgenically reproduces the MK phenotype, yet how the gene evolves and functions across diverse Wolbachia has not been systematically investigated. We analyzed 32 Wolbachia genomes available in the NCBI database to study wmk homologs across different arthropod hosts, reproductive parasitism functions, and Wolbachia supergroups. First, we report at least five distinct wmk phylogenetic clusters (Types I to V), often organized in multigenic dyads or triads. Second, among MK Wolbachia, there is a significantly higher number of wmk genes and diversity in Lepidoptera strains than in Drosophila strains, which exclusively harbor wmk Types I and III. Third, there are three patterns of wmk sequence and genomic organizational changes in Drosophila MK strains that associate with different evolutionary trajectories underpinning the MK phenotype. Fourth, single and combinatory transgenic expression of Types I and III in D. melanogaster uncovers male-biased lethality associated with Type I; however, dual expression of the Types together elicits a major reduction in offspring number. Fifth, wmk genes have low expression level across D. melanogaster developmental stages relative to the cifA and cifB genes, which could explain why cytoplasmic incompatibility is expressed in this system. These findings establish a complex and phylogenetically informed genetic basis of wmk-induced lethality, highlighting the role of gene copy number and expression, wmk Types, and host background in shaping the phenotype.

Animals↗
PubMed1980

Immunological regulation of experimental cutaneous leishmaniasis. 1. Immunogenetic aspects of susceptibility to Leishmania tropica in mice.

Models of the different disease patterns of cutaneous leishmaniasis can be induced by the same dose of L. tropica promastigotes in various inbred strains of mice. The susceptibility of BALB/c is exceptional, essentially dosage independent (being demonstratable with as few as 20 parasites) and leads to huge progressive lesions with fatal visceral and cutaneous metastasis. Lesions also extend progressively but more slowly in BDA/1 and BDA/2 mice. Strains A C57BL/6 and CBA are relatively resistant to even 2 X 10(7) promastigotes, with arrest of lesion growth within 3 weeks and subsequent gradual healing. Similar resistance of A.SW to 2 X 10(5) is overcome by a larger dose. The major inter-strain differences are H-2 independent, for C57BL/10 congenic mice possessing six different H-2 antigen complexes all show early arrest of lesion growth leading to healing (H-2s, H-2a, H-2k) or mild residual disease (H-2b, H-2d, H-2q). Inter-line differences within the latter group varied between experiments such that no clear rank order emerged. Inexorable disease progression was found in congenic BALB/B, BALB/c, and BALB/K alike, although it was significantly slower in the latter line when infected with smaller doses. Genetic control of BALB/c susceptibility is thus predominantly in the non-H-2 background with only a minor H-2 linked regulatory influence in the later stage. C57BL/6, BALB/c and their F1 hybrid characteristically display "healing", "fatal progressive" and "non-healing" lesions respectively over a wide dose range. "BALB/c-like" susceptibility segregates strictly in the F2 and backcross progeny according to a one predominant gene prediction. A comparison of the present data with those concerning genetic regulation of acute and chronic stages of systemic. L. donovani infection in mice (Bradley, 1977, Blackwell, Freeman & Bradley 1980) reveals differing control for the outcome of cutaneous L. tropica infection, in which other important genetic influences must be involved.

Animals↗
PubMed2003

Host background factors contributing to hepatitis C virus clearance.

This review is an attempt to characterize the host in the earliest events of hepatitis C virus (HCV) infection before the on-set of adaptive immune response. Host meets the replicating HCV with innate immune response in the form of proinflammatory cytokine production, activation of natural killer (NK), NKT and dendritic cells. The potency of innate response is shaped by a wide panel of genetically predetermined constants and acquired variables. Higher rates of HCV clearance associate with white ethnicity and certain HLA haplotypes. Lower clearance rates correlate with genetic immune deficiencies/disorders. Recent findings link infection outcome with variation in the genes for the low-density lipoprotein and complement type 1 receptors. Important though insufficiently characterized is the role of polymorphisms in the genes responsible for induction of antiviral immunity. The outcome of HCV entry and of subsequent acute infection (if that occurs) is pre-determined by the immune competence of the host at the moment of infection. Higher rate of HCV clearance is observed for pediatric patients and young adults. Bad prognostic markers would be post-transplantation immune suppression, transfusion-related immune modulation, alcohol-induced immune imbalance and intoxication. Among host variables is the immune modulation induced by parasitic and viral co-infections. Some of the variables are transient and hard to define in retrospective. These host characteristics set up the potency, kinetics, and profile (Th1/Th2) of subsequent adaptive immune response. Better understanding of the host correlates of viral clearance would be a step towards prophylaxis of infection and an efficient anti-HCV vaccine.

Age Factors↗
PubMed2026

The Source-Sink Dynamics of Plasmodium vivax May Undermine Malaria Elimination Efforts in the Amazon: An Epidemiological and Population Genomic Study.

BACKGROUND: Brazil's progress toward malaria elimination has stalled and 163 000 new cases (more than 80% caused by Plasmodium vivax) were recorded in the Brazilian Amazon in 2023. We hypothesize that human mobility continues to disperse parasites from hotspots to areas with decreasing endemicity. METHODS: We analyzed 5.5 million malaria case notifications between 2003 and 2023 to describe malaria case mobility and identify sources and sinks of P. vivax in the Brazilian Amazon. We leveraged whole-genome sequence data from 408 P. vivax isolates sampled from across South America to characterize parasite gene flow and infer likely regional routes of parasite dispersal. RESULTS: We found that nearly one-third of the P. vivax infections diagnosed in residents in the Brazilian Amazon over 21 years were acquired outside the locality or municipality of residence, but only 1.7% were imported from other countries in South America, mostly from the Guiana Shield. We show that large cities with residual malaria transmission-such as Manaus and Porto Velho-are receptive parasite sinks surrounded by high-risk source rural localities. Although the genetic relatedness of parasites tended to decrease with geographic distance, parasites from sites more than 1000 km apart often remained genetically connected. CONCLUSIONS: Understanding parasite source-sink dynamics on different geographic scales is crucial to target high-risk mobile populations and source localities along with receptive sinks within low-transmission municipalities, with the goal of eliminating malaria transmission and preventing its reintroduction into malaria-free areas.

Humans↗