A bite so sweet: the glycobiology interface of tick-host-pathogen interactions

Existing Reviews

Please note, new claims can take a short while to show up.

No claims yet.

Annotation Summary

Term Occurence Count Dictionary
tick-borne encephalitis 1 infectiousdiseases
Lyme disease 11 infectiousdiseases
borreliosis 2 infectiousdiseases
human granulocytic anaplasmosis 2 infectiousdiseases
infectious disease 4 infectiousdiseases

There are not enough annotations found in this document to create the proximity graph.

Review

Having read the paper, please pick a pair of statements from the paper to indicate that a drug and disease are related.

Select Drug Character Offset Drug Term Instance
Select Disease Character Offset Disease Term Instance
Lyme disease 18658 integrins with high affinity to factor H and encoded by erp-loci localised on each of the cp32 plasmids. Lyme disease spirochetes control Erp synthesis throughout the bacterial infectious tabacycle, producing the proteins
Lyme disease 27761 cell surface signature of each cell type [[60]].BorreliaadhesinsVspsRelapsing fever Borrelia, unlike Lyme disease -causing Borrelia, are vectored by soft ticks of the genus Ornithodoros. They are present in the blood
Lyme disease 30159 Furthermore, Borrelia-infected patients produced anti-RevA antibodies throughout various stages of Lyme disease suggesting its involvement in Lyme disease establishment and persistence in the host. RevA appears to
Lyme disease 30202 produced anti-RevA antibodies throughout various stages of Lyme disease suggesting its involvement in Lyme disease establishment and persistence in the host. RevA appears to have multiple binding sites which Borrelia
Lyme disease 31719 cells in vitro and to colonize host target tissues leading to the reduced inflammatory manifestation of Lyme disease in the mouse model. The adherence was not fully disrupted due to the existence of other GAG-binding
Lyme disease 39495 antibody-mediated immune response [[116]], which makes this adhesin important for the diagnosis of Lyme disease infection. The triggered immune response does not, however, provide the host with protective immunity
Lyme disease 40495 [125]].Erps are not upregulated during Borrelia transmission but their expression gradually increases during Lyme disease progression, suggesting their role during mammalian infection [[125]]. Interestingly, Borrelia can regulate
Lyme disease 43687 carbohydrate-associated PAMPs, although only a few of them were directly observed to be involved in Lyme disease . NOD1 and NOD2 receptors are the most extensively investigated major PRRs [[138], [140]].Borrelia-infected
Lyme disease 44172 Their activities are assigned to a host proinflammatory response, although their particular role in Lyme disease establishment remains unknown [[142]]. NOD2 stimulation by Borrelia induces inflammation during the
Lyme disease 44301 remains unknown [[142]]. NOD2 stimulation by Borrelia induces inflammation during the early stages of Lyme disease but induces tolerance and suppresses B. burgdorferi-mediated Lyme arthritis and carditis in mice during
Lyme disease 46657 natural killer T cells (NKT) [[150]]. This then promotes their activation as well as the proliferation of Lyme disease -directed antibodies [[151]–[153]] which recognize glycolipids in the cell membrane of Borrelia but
borreliosis 11744 as the recognized molecules depending on the available information. Majority of proteins from Lyme borreliosis spirochetes are listed; in the case of relapsing fever Borrelia, the bacterial species is definedBorrelia
borreliosis 46932 against the glycolipid fraction cross-react with gangliosides, which explains the phenomenon of neuro borreliosis [[155]].The glycolipid recognition by invariant NKT cells seems to be an alternative system for innate
human granulocytic anaplasmosis 4116 significantly increased tick colonization by the bacterium Anaplasma phagocytophilum, the causative agent of human granulocytic anaplasmosis [[6]].Over the last decade, there has been a slow increase in the knowledge of vector-host-pathogen
human granulocytic anaplasmosis 52389 death [[173]–[175]]. In humans, A. phagocytophilum is the only confirmed pathogenic species causing human granulocytic anaplasmosis . Patients suffer from fever, headache, myalgias, chills, leukopenia, thrombocytopenia and liver damage
infectious disease 411 (pmc-release): 11/2018Publication date (collection): /2018AbstractVector-borne diseases constitute 17% of all infectious disease s in the world; among the blood-feeding arthropods, ticks transmit the highest number of pathogens. Understanding
infectious disease 1706 various bacteria and tick-borne encephalitis virus.BackgroundVector-borne diseases constitute 17% of all infectious disease s in the world [[1]]. Pathogenic viruses, bacteria, and protozoa are carried by blood-feeding arthropods
infectious disease 2968 socio-economics [[4]]. Research efforts to combat tick-borne diseases have usually centred, as with most other infectious disease s, on determining the Achilles’ heel of the pathogen. Most endeavours have focussed on understanding
infectious disease 91473 finish their life-cycles. Ultimately, the common goal of scientists working in any field dealing with infectious disease s is to find an effective countermeasure against the particular threat. Ticks transmit a great variety
tick-borne encephalitis 1622 on the interactions allowing the infection of both the ticks and the hosts by various bacteria and tick-borne encephalitis virus.BackgroundVector-borne diseases constitute 17% of all infectious diseases in the world [[1]].

You must be authorized to submit a review.