Displaying publications 1 - 20 of 124 in total

Abstract:
Sort:
  1. Fulltext 2BC Non-Structural Protein of Enterovirus A71 Interacts with SNARE Proteins to Trigger Autolysosome Formation
    Lai JKF, Sam IC, Verlhac P, Baguet J, Eskelinen EL, Faure M, et al.
    Viruses, 2017 07 04;9(7).
    PMID: 28677644 DOI: 10.3390/v9070169
    Viruses have evolved unique strategies to evade or subvert autophagy machinery. Enterovirus A71 (EV-A71) induces autophagy during infection in vitro and in vivo. In this study, we report that EV-A71 triggers autolysosome formation during infection in human rhabdomyosarcoma (RD) cells to facilitate its replication. Blocking autophagosome-lysosome fusion with chloroquine inhibited virus RNA replication, resulting in lower viral titres, viral RNA copies and viral proteins. Overexpression of the non-structural protein 2BC of EV-A71 induced autolysosome formation. Yeast 2-hybrid and co-affinity purification assays showed that 2BC physically and specifically interacted with aN-ethylmaleimide-sensitive factor attachment receptor (SNARE) protein, syntaxin-17 (STX17). Co-immunoprecipitation assay further showed that 2BC binds to SNARE proteins, STX17 and synaptosome associated protein 29 (SNAP29). Transient knockdown of STX17, SNAP29, and microtubule-associated protein 1 light chain 3B (LC3B), crucial proteins in the fusion between autophagosomes and lysosomes) as well as the lysosomal-associated membrane protein 1 (LAMP1) impaired production of infectious EV-A71 in RD cells. Collectively, these results demonstrate that the generation of autolysosomes triggered by the 2BC non-structural protein is important for EV-A71 replication, revealing a potential molecular pathway targeted by the virus to exploit autophagy. This study opens the possibility for the development of novel antivirals that specifically target 2BC to inhibit formation of autolysosomes during EV-A71 infection.
    Matched MeSH terms: Host-Pathogen Interactions
  2. A Glance on the Role of Bacterial Siderophore from the Perspectives of Medical and Biotechnological Approaches
    AlMatar M, Albarri O, Makky EA, Var I, Köksal F
    Curr Drug Targets, 2020;21(13):1326-1343.
    PMID: 32564749 DOI: 10.2174/1389450121666200621193018
    Iron, which is described as the most basic component found in nature, is hard to be assimilated by microorganisms. It has become increasingly complicated to obtain iron from nature as iron (II) in the presence of oxygen oxidized to press (III) oxide and hydroxide, becoming unsolvable at neutral pH. Microorganisms appeared to produce organic molecules known as siderophores in order to overcome this condition. Siderophore's essential function is to connect with iron (II) and make it dissolvable and enable cell absorption. These siderophores, apart from iron particles, have the ability to chelate various other metal particles that have collocated away to focus the use of siderophores on wound care items. There is a severe clash between the host and the bacterial pathogens during infection. By producing siderophores, small ferric iron-binding molecules, microorganisms obtain iron. In response, host immune cells produce lipocalin 2 to prevent bacterial reuptake of siderophores loaded with iron. Some bacteria are thought to produce lipocalin 2-resistant siderophores to counter this risk. The aim of this article is to discuss the recently described roles and applications of bacterial siderophore.
    Matched MeSH terms: Host-Pathogen Interactions
  3. Adaptation of the metabolomics profile of rice after Pyricularia oryzae infection
    Azizi P, Osman M, Hanafi MM, Sahebi M, Yusop MR, Taheri S
    Plant Physiol Biochem, 2019 Nov;144:466-479.
    PMID: 31655345 DOI: 10.1016/j.plaphy.2019.10.014
    Pyricularia oryzae (P. oryzae), one of the most devastating fungal pathogens, is the cause of blast disease in rice. Infection with a blast fungus induces biological responses in the host plant that lead to its survival through the termination or suppression of pathogen growth, and metabolite compounds play vital roles in plant interactions with a wide variety of other organisms. Numerous studies have indicated that rice has a multi-layered plant immune system that includes pre-developed (e.g., cell wall and phytoanticipins), constitutive and inducible (phytoalexins) defence barriers against stresses. Significant progress towards understanding the basis of the molecular mechanisms underlying the defence responses of rice to P. oryzae has been achieved. Nonetheless, even though the important metabolites in the responses of rice to pathogens have been identified, their exact mechanisms and their contributions to plant immunity against blast fungi have not been elucidated. The purpose of this review is to summarize and discuss recent advances towards the understanding of the integrated metabolite variations in rice after P. oryzae invasion.
    Matched MeSH terms: Host-Pathogen Interactions
  4. Fulltext Agro-ecological variations of sheath rot disease of rice caused by Sarocladium oryzae and DNA fingerprinting of the pathogen's population structure
    Tajul Islam Chowdhury M, Salim Mian M, Taher Mia MA, Rafii MY, Latif MA
    Genet. Mol. Res., 2015 Dec 28;14(4):18140-52.
    PMID: 26782461 DOI: 10.4238/2015.December.23.1
    To examine the impact of regional and seasonal variations on the incidence and severity of sheath rot, a major seed-borne disease of rice caused by Sarocladium oryzae, data on incidence and severity were collected from 27 selected fields in the Gazipur, Rangpur, Bogra, Chittagong, Comilla, Gopalgonj, Jessore, Manikgonj, and Bhola districts of Bangladesh in rain-fed and irrigated conditions. Cultural variability of 29 pathogen isolates obtained from 8 different locations was studied on potato dextrose agar (PDA) and genetic variability was determined by DNA fingerprinting using variable number tandem repeat-polymerase chain reaction markers. Overall, disease incidence and severity were higher in irrigated rice. Disease incidence and severity were highest in the Bhola district in rain-fed rice and lowest in irrigated rice. Mycelial growth of 29 representative isolates was found to vary on PDA and the isolates were divided into 6 groups. The range of the overall size of conidia of the selected isolates was 2.40-7.20 x 1.20-2.40 μm. Analysis of the DNA fingerprint types of the 29 isolates of S. oryzae, obtained from the amplification reactions, revealed 10 fingerprinting types (FPTs) that were 80% similar. FPT-1 was the largest group and included 13 isolates (44.8%), while FPT-2 was the third largest group and included 3 isolates. Each of FPT-3, 4, 5, and 6 included only 1 isolate. We observed no relationship between cultural and genetic groupings.
    Matched MeSH terms: Host-Pathogen Interactions/genetics
  5. Allele Mining Strategies: Principles and Utilisation for Blast Resistance Genes in Rice (Oryza sativa L.)
    Ashkani S, Yusop MR, Shabanimofrad M, Azady A, Ghasemzadeh A, Azizi P, et al.
    Curr Issues Mol Biol, 2015;17:57-73.
    PMID: 25706446
    Allele mining is a promising way to dissect naturally occurring allelic variants of candidate genes with essential agronomic qualities. With the identification, isolation and characterisation of blast resistance genes in rice, it is now possible to dissect the actual allelic variants of these genes within an array of rice cultivars via allele mining. Multiple alleles from the complex locus serve as a reservoir of variation to generate functional genes. The routine sequence exchange is one of the main mechanisms of R gene evolution and development. Allele mining for resistance genes can be an important method to identify additional resistance alleles and new haplotypes along with the development of allele-specific markers for use in marker-assisted selection. Allele mining can be visualised as a vital link between effective utilisation of genetic and genomic resources in genomics-driven modern plant breeding. This review studies the actual concepts and potential of mining approaches for the discovery of alleles and their utilisation for blast resistance genes in rice. The details provided here will be important to provide the rice breeder with a worthwhile introduction to allele mining and its methodology for breakthrough discovery of fresh alleles hidden in hereditary diversity, which is vital for crop improvement.
    Matched MeSH terms: Host-Pathogen Interactions
  6. An overview of Acinetobacter baumannii pathogenesis: Motility, adherence and biofilm formation
    Mea HJ, Yong PVC, Wong EH
    Microbiol Res, 2021 Jun;247:126722.
    PMID: 33618061 DOI: 10.1016/j.micres.2021.126722
    The Gram-negative opportunistic pathogen Acinetobacter baumannii has gain notoriety in recent decades, primarily due to its propensity to cause nosocomial infections in critically ill patients. Its global spread, multi-drug resistance features and plethora of virulence factors make it a serious threat to public health worldwide. Though much effort has been expended in uncovering its successes, it continues to confound researchers due to its highly adaptive nature, mutating to meet the needs of a given environment. Its persistence in the clinical setting allows it to be in close proximity to a potential host, where contact can be made facilitating infection and colonization. In this article, we aim to provide a current overview of the bacterial virulence factors, specifically focusing on factors involved in the initial stages of infection, highlighting the role of adaptation facilitated by two-component systems and biofilm formation. Finally, the study of host-pathogen interactions using available animal models, their suitability, notable findings and some perspectives moving forward are also discussed.
    Matched MeSH terms: Host-Pathogen Interactions
  7. Fulltext Analysis of nuclear and organellar genomes of Plasmodium knowlesi in humans reveals ancient population structure and recent recombination among host-specific subpopulations
    Diez Benavente E, Florez de Sessions P, Moon RW, Holder AA, Blackman MJ, Roper C, et al.
    PLoS Genet, 2017 Sep;13(9):e1007008.
    PMID: 28922357 DOI: 10.1371/journal.pgen.1007008
    The macaque parasite Plasmodium knowlesi is a significant concern in Malaysia where cases of human infection are increasing. Parasites infecting humans originate from genetically distinct subpopulations associated with the long-tailed (Macaca fascicularis (Mf)) or pig-tailed macaques (Macaca nemestrina (Mn)). We used a new high-quality reference genome to re-evaluate previously described subpopulations among human and macaque isolates from Malaysian-Borneo and Peninsular-Malaysia. Nuclear genomes were dimorphic, as expected, but new evidence of chromosomal-segment exchanges between subpopulations was found. A large segment on chromosome 8 originating from the Mn subpopulation and containing genes encoding proteins expressed in mosquito-borne parasite stages, was found in Mf genotypes. By contrast, non-recombining organelle genomes partitioned into 3 deeply branched lineages, unlinked with nuclear genomic dimorphism. Subpopulations which diverged in isolation have re-connected, possibly due to deforestation and disruption of wild macaque habitats. The resulting genomic mosaics reveal traits selected by host-vector-parasite interactions in a setting of ecological transition.
    Matched MeSH terms: Host-Pathogen Interactions/genetics*
  8. Annexin A2 extracellular translocation and virus interaction: A potential target for antivirus-drug discovery
    Aliyu IA, Ling KH, Md Hashim N, Chee HY
    Rev Med Virol, 2019 05;29(3):e2038.
    PMID: 30746844 DOI: 10.1002/rmv.2038
    Annexin A2 is a membrane scaffolding and binding protein, which mediated various cellular events. Its functions are generally affected by cellular localization. In the cytoplasm, they interacted with different phospholipid membranes in Ca2+ -dependent manner and play vital roles including actin binding, remodeling and dynamics, cytoskeletal rearrangement, and lipid-raft microdomain formation. However, upon cell exposure to certain stimuli, annexin A2 translocates to the external leaflets of the plasma membrane where annexin A2 was recently reported to serve as a virus receptor, play an important role in the formation of virus replication complex, or implicated in virus assembly and budding. Here, we review some of annexin A2 roles in virus infections and the potentiality of targeting annexin A2 in the design of novel and promising antivirus agent that may have a broader consequence in virus therapy.
    Matched MeSH terms: Host-Pathogen Interactions*
  9. Application of Spiroplasma melliferum proteogenomic profiling for the discovery of virulence factors and pathogenicity mechanisms in host-associated spiroplasmas
    Alexeev D, Kostrjukova E, Aliper A, Popenko A, Bazaleev N, Tyakht A, et al.
    J Proteome Res, 2012 Jan 1;11(1):224-36.
    PMID: 22129229 DOI: 10.1021/pr2008626
    To date, no genome of any of the species from the genus Spiroplasma has been completely sequenced. Long repetitive sequences similar to mobile units present a major obstacle for current genome sequencing technologies. Here, we report the assembly of the Spiroplasma melliferum KC3 genome into 4 contigs, followed by proteogenomic annotation and metabolic reconstruction based on the discovery of 521 expressed proteins and comprehensive metabolomic profiling. A systems approach allowed us to elucidate putative pathogenicity mechanisms and to discover major virulence factors, such as Chitinase utilization enzymes and toxins never before reported for insect pathogenic spiroplasmas.
    Matched MeSH terms: Host-Pathogen Interactions
  10. Bacterial regulatory RNAs: complexity, function, and putative drug targeting
    Cheah HL, Raabe CA, Lee LP, Rozhdestvensky TS, Citartan M, Ahmed SA, et al.
    Crit Rev Biochem Mol Biol, 2018 08;53(4):335-355.
    PMID: 29793351 DOI: 10.1080/10409238.2018.1473330
    Over the past decade, RNA-deep sequencing has uncovered copious non-protein coding RNAs (npcRNAs) in bacteria. Many of them are key players in the regulation of gene expression, taking part in various regulatory circuits, such as metabolic responses to different environmental stresses, virulence, antibiotic resistance, and host-pathogen interactions. This has contributed to the high adaptability of bacteria to changing or even hostile environments. Their mechanisms include the regulation of transcriptional termination, modulation of translation, and alteration of messenger RNA (mRNA) stability, as well as protein sequestration. Here, the mechanisms of gene expression by regulatory bacterial npcRNAs are comprehensively reviewed and supplemented with well-characterized examples. This class of molecules and their mechanisms of action might be useful targets for the development of novel antibiotics.
    Matched MeSH terms: Host-Pathogen Interactions
  11. Bactericidal and fungistatic activity of peptide derived from GH18 domain of prawn chitinase 3 and its immunological functions during biological stress
    Ravichandran G, Kumaresan V, Mahesh A, Dhayalan A, Arshad A, Arasu MV, et al.
    Int J Biol Macromol, 2018 Jan;106:1014-1022.
    PMID: 28837852 DOI: 10.1016/j.ijbiomac.2017.08.098
    Chitinases play a vital role during the pathogenic invasion and immunosuppression in various organisms including invertebrates and vertebrates. In this study, we have investigated the participation of MrChit-3 (Macrobrachium rosenbergii Chitinase-3) during host-pathogenic interaction in freshwater prawn, M. rosenbergii. Quantitative real-time PCR analysis showed that the expression of MrChit-3 was up-regulated during bacterial, viral and laminarin challenge. Moreover, to understand the antimicrobial role of the GH18 domain, a putative membrane-targeting antimicrobial peptide (MrVG) was identified from the GH18 domain region of the protein and it was chemically synthesized. Physico-chemical features of the GH18 derived antimicrobial peptide (AMP) was assessed by various in silico tools and the antimicrobial property of the peptide was confirmed from in vitro studies. The membrane targeting mechanism of the peptide was determined by flow cytometry (FACS) and scanning electron microscope (SEM) analysis. Interestingly, the peptide was able to inhibit the growth of a chitinolytic fungal pathogen, Aspergillus niger, which was isolated from the shells of M. rosenbergii. The toxicity studies such as hemolysis activity on human blood erythrocytes and cell viability assay with primary kidney cells, HEK293 of MrVG revealed that the peptide was not involved in inducing any toxicity.
    Matched MeSH terms: Host-Pathogen Interactions/genetics*
  12. Fulltext Blueberry red ringspot virus genomes from Florida inferred through analysis of blueberry root transcriptomes
    Saad N, Alcalá-Briseño RI, Polston JE, Olmstead JW, Varsani A, Harmon PF
    Sci Rep, 2020 Jul 21;10(1):12043.
    PMID: 32694553 DOI: 10.1038/s41598-020-68654-3
    A growing number of metagenomics-based approaches have been used for the discovery of viruses in insects, cultivated plants, and water in agricultural production systems. In this study, sixteen blueberry root transcriptomes from eight clonally propagated blueberry plants of cultivar 'Emerald' (interspecific hybrid of Vaccinium corymbosum and V. darrowi) generated as part of a separate study on varietal tolerance to soil salinity were analyzed for plant viral sequences. The objective was to determine if the asymptomatic plants harbored the latent blueberry red ringspot virus (BRRV) in their roots. The only currently known mechanism of transmission of BRRV is through vegetative propagation; however, the virus can remain latent for years with some plants of 'Emerald' never developing red ringspot symptoms. Bioinformatic analyses of 'Emerald' transcriptomes using de novo assembly and reference-based mapping approaches yielded eight complete viral genomes of BRRV (genus Soymovirus, family Caulimoviridae). Validation in vitro by PCR confirmed the presence of BRRV in 100% of the 'Emerald' root samples. Sequence and phylogenetic analyses showed 94% to 97% nucleotide identity between BRRV genomes from Florida and sequences from Czech Republic, Japan, Poland, Slovenia, and the United States. Taken together, this study documented the first detection of a complete BRRV genome from roots of asymptomatic blueberry plants and in Florida through in silico analysis of plant transcriptomes.
    Matched MeSH terms: Host-Pathogen Interactions
  13. Fulltext Breeding for Anthracnose Disease Resistance in Chili: Progress and Prospects
    Ridzuan R, Rafii MY, Ismail SI, Mohammad Yusoff M, Miah G, Usman M
    Int J Mol Sci, 2018 Oct 11;19(10).
    PMID: 30314374 DOI: 10.3390/ijms19103122
    Chili anthracnose is one of the most devastating fungal diseases affecting the quality and yield production of chili. The aim of this review is to summarize the current knowledge concerning the chili anthracnose disease, as well as to explore the use of marker-assisted breeding programs aimed at improving anthracnose disease resistance in this species. This disease is caused by the Colletotrichum species complex, and there have been ongoing screening methods of chili pepper genotypes with resistance to anthracnose in the field, as well as in laboratories. Conventional breeding involves phenotypic selection in the field, and it is more time-consuming compared to molecular breeding. The use of marker-assisted selection (MAS) on the basis of inheritance, the segregation ratio of resistance to susceptibility, and the gene-controlling resistance may contribute to the development of an improved chili variety and speed up the selection process, while also reducing genetic drag in the segregating population. More importantly, by using molecular markers, the linkage groups are determined dominantly and co-dominantly, meaning that the implementation of a reliable method to produce resistant varieties is crucial in future breeding programs. This updated information will offer a supportive direction for chili breeders to develop an anthracnose-resistant chili variety.
    Matched MeSH terms: Host-Pathogen Interactions
  14. Fulltext Burkholderia pseudomallei kills Caenorhabditis elegans through virulence mechanisms distinct from intestinal lumen colonization
    Ooi SK, Lim TY, Lee SH, Nathan S
    Virulence, 2012 Oct 01;3(6):485-96.
    PMID: 23076282 DOI: 10.4161/viru.21808
    The nematode Caenorhabditis elegans is hypersusceptible to Burkholderia pseudomallei infection. However, the virulence mechanisms underlying rapid lethality of C. elegans upon B. pseudomallei infection remain poorly defined. To probe the host-pathogen interaction, we constructed GFP-tagged B. pseudomallei and followed bacterial accumulation within the C. elegans intestinal lumen. Contrary to slow-killing by most bacterial pathogens, B. pseudomallei caused fairly limited intestinal lumen colonization throughout the period of observation. Using grinder-defective mutant worms that allow the entry of intact bacteria also did not result in full intestinal lumen colonization. In addition, we observed a significant decline in C. elegans defecation and pharyngeal pumping rates upon B. pseudomallei infection. The decline in defecation rates ruled out the contribution of defecation to the limited B. pseudomallei colonization. We also demonstrated that the limited intestinal lumen colonization was not attributed to slowed host feeding as bacterial loads did not change significantly when feeding was stimulated by exogenous serotonin. Both these observations confirm that B. pseudomallei is a poor colonizer of the C. elegans intestine. To explore the possibility of toxin-mediated killing, we examined the transcription of the C. elegans ABC transporter gene, pgp-5, upon B. pseudomallei infection of the ppgp-5::gfp reporter strain. Expression of pgp-5 was highly induced, notably in the pharynx and intestine, compared with Escherichia coli-fed worms, suggesting that the host actively thwarted the pathogenic assaults during infection. Collectively, our findings propose that B. pseudomallei specifically and continuously secretes toxins to overcome C. elegans immune responses.
    Matched MeSH terms: Host-Pathogen Interactions
  15. Fulltext Burkholderia pseudomallei suppresses Caenorhabditis elegans immunity by specific degradation of a GATA transcription factor
    Lee SH, Wong RR, Chin CY, Lim TY, Eng SA, Kong C, et al.
    Proc Natl Acad Sci U S A, 2013 Sep 10;110(37):15067-72.
    PMID: 23980181 DOI: 10.1073/pnas.1311725110
    Burkholderia pseudomallei is a Gram-negative soil bacterium that infects both humans and animals. Although cell culture studies have revealed significant insights into factors contributing to virulence and host defense, the interactions between this pathogen and its intact host remain to be elucidated. To gain insights into the host defense responses to B. pseudomallei infection within an intact host, we analyzed the genome-wide transcriptome of infected Caenorhabditis elegans and identified ∼6% of the nematode genes that were significantly altered over a 12-h course of infection. An unexpected feature of the transcriptional response to B. pseudomallei was a progressive increase in the proportion of down-regulated genes, of which ELT-2 transcriptional targets were significantly enriched. ELT-2 is an intestinal GATA transcription factor with a conserved role in immune responses. We demonstrate that B. pseudomallei down-regulation of ELT-2 targets is associated with degradation of ELT-2 protein by the host ubiquitin-proteasome system. Degradation of ELT-2 requires the B. pseudomallei type III secretion system. Together, our studies using an intact host provide evidence for pathogen-mediated host immune suppression through the destruction of a host transcription factor.
    Matched MeSH terms: Host-Pathogen Interactions/immunology
  16. Bursal transcriptome profiling of different inbred chicken lines reveals key differentially expressed genes at 3 days post-infection with very virulent infectious bursal disease virus
    Farhanah MI, Yasmin AR, Mat Isa N, Hair-Bejo M, Ideris A, Powers C, et al.
    J Gen Virol, 2018 Jan;99(1):21-35.
    PMID: 29058656 DOI: 10.1099/jgv.0.000956
    Infectious bursal disease is a highly contagious disease in the poultry industry and causes immunosuppression in chickens. Genome-wide regulations of immune response genes of inbred chickens with different genetic backgrounds, following very virulent infectious bursal disease virus (vvIBDV) infection are poorly characterized. Therefore, this study aims to analyse the bursal tissue transcriptome of six inbred chicken lines 6, 7, 15, N, O and P following infection with vvIBDV strain UK661 using strand-specific next-generation sequencing, by highlighting important genes and pathways involved in the infected chicken during peak infection at 3 days post-infection. All infected chickens succumbed to the infection without major variations among the different lines. However, based on the viral loads and bursal lesion scoring, lines P and 6 can be considered as the most susceptible lines, while lines 15 and N were regarded as the least affected lines. Transcriptome profiling of the bursa identified 4588 genes to be differentially expressed, with 2985 upregulated and 1642 downregulated genes, in which these genes were commonly or uniquely detected in all or several infected lines. Genes that were upregulated are primarily pro-inflammatory cytokines, chemokines and IFN-related. Various genes that are associated with B-cell functions and genes related to apoptosis were downregulated, together with the genes involved in p53 signalling. In conclusion, bursal transcriptome profiles of different inbred lines showed differential expressions of pro-inflammatory cytokines and chemokines, Th1 cytokines, JAK-STAT signalling genes, MAPK signalling genes, and their related pathways following vvIBDV infection.
    Matched MeSH terms: Host-Pathogen Interactions
  17. Fulltext Call to Action: SARS-CoV-2 and CerebrovAscular DisordErs (CASCADE)
    Abootalebi S, Aertker BM, Andalibi MS, Asdaghi N, Aykac O, Azarpazhooh MR, et al.
    J Stroke Cerebrovasc Dis, 2020 Sep;29(9):104938.
    PMID: 32807412 DOI: 10.1016/j.jstrokecerebrovasdis.2020.104938
    BACKGROUND AND PURPOSE: The novel severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2), now named coronavirus disease 2019 (COVID-19), may change the risk of stroke through an enhanced systemic inflammatory response, hypercoagulable state, and endothelial damage in the cerebrovascular system. Moreover, due to the current pandemic, some countries have prioritized health resources towards COVID-19 management, making it more challenging to appropriately care for other potentially disabling and fatal diseases such as stroke. The aim of this study is to identify and describe changes in stroke epidemiological trends before, during, and after the COVID-19 pandemic.

    METHODS: This is an international, multicenter, hospital-based study on stroke incidence and outcomes during the COVID-19 pandemic. We will describe patterns in stroke management, stroke hospitalization rate, and stroke severity, subtype (ischemic/hemorrhagic), and outcomes (including in-hospital mortality) in 2020 during COVID-19 pandemic, comparing them with the corresponding data from 2018 and 2019, and subsequently 2021. We will also use an interrupted time series (ITS) analysis to assess the change in stroke hospitalization rates before, during, and after COVID-19, in each participating center.

    CONCLUSION: The proposed study will potentially enable us to better understand the changes in stroke care protocols, differential hospitalization rate, and severity of stroke, as it pertains to the COVID-19 pandemic. Ultimately, this will help guide clinical-based policies surrounding COVID-19 and other similar global pandemics to ensure that management of cerebrovascular comorbidity is appropriately prioritized during the global crisis. It will also guide public health guidelines for at-risk populations to reduce risks of complications from such comorbidities.

    Matched MeSH terms: Host-Pathogen Interactions
  18. Fulltext Cell entry of a host-targeting protein of oomycetes requires gp96
    Trusch F, Loebach L, Wawra S, Durward E, Wuensch A, Iberahim NA, et al.
    Nat Commun, 2018 06 14;9(1):2347.
    PMID: 29904064 DOI: 10.1038/s41467-018-04796-3
    The animal-pathogenic oomycete Saprolegnia parasitica causes serious losses in aquaculture by infecting and killing freshwater fish. Like plant-pathogenic oomycetes, S. parasitica employs similar infection structures and secretes effector proteins that translocate into host cells to manipulate the host. Here, we show that the host-targeting protein SpHtp3 enters fish cells in a pathogen-independent manner. This uptake process is guided by a gp96-like receptor and can be inhibited by supramolecular tweezers. The C-terminus of SpHtp3 (containing the amino acid sequence YKARK), and not the N-terminal RxLR motif, is responsible for the uptake into host cells. Following translocation, SpHtp3 is released from vesicles into the cytoplasm by another host-targeting protein where it degrades nucleic acids. The effector translocation mechanism described here, is potentially also relevant for other pathogen-host interactions as gp96 is found in both animals and plants.
    Matched MeSH terms: Host-Pathogen Interactions
  19. Fulltext Cellular transcripts of chicken brain tissues in response to H5N1 and Newcastle disease virus infection
    Balasubramaniam VR, Wai TH, Omar AR, Othman I, Hassan SS
    Virol J, 2012;9:53.
    PMID: 22361110 DOI: 10.1186/1743-422X-9-53
    Highly-pathogenic avian influenza (HPAI) H5N1 and Newcastle disease (ND) viruses are the two most important poultry viruses in the world, with the ability to cause classic central nervous system dysfunction in poultry and migratory birds. To elucidate the mechanisms of neurovirulence caused by these viruses, a preliminary study was design to analyze host's cellular responses during infections of these viruses.
    Matched MeSH terms: Host-Pathogen Interactions*
  20. Fulltext Cellular transcripts regulated during infections with Highly Pathogenic H5N1 Avian Influenza virus in 3 host systems
    Balasubramaniam VR, Hassan SS, Omar AR, Mohamed M, Noor SM, Mohamed R, et al.
    Virol J, 2011;8:196.
    PMID: 21529348 DOI: 10.1186/1743-422X-8-196
    Highly pathogenic Avian Influenza (HPAI) virus is able to infect many hosts and the virus replicates in high levels in the respiratory tract inducing severe lung lesions. The pathogenesis of the disease is actually the outcome of the infection as determined by complex host-virus interactions involving the functional kinetics of large numbers of participating genes. Understanding the genes and proteins involved in host cellular responses are therefore, critical for the elucidation of the mechanisms of infection.
    Matched MeSH terms: Host-Pathogen Interactions*
Related Terms
Filters
Contact Us

Please provide feedback to Administrator (afdal@afpm.org.my)

External Links