scholarly journals Theileria annulata Subtelomere-Encoded Variable Secreted Protein-TA05575 Binds to Bovine RBMX2

2021 ◽  
Vol 11 ◽  
Author(s):  
Zhi Li ◽  
Junlong Liu ◽  
Shuaiyang Zhao ◽  
Quanying Ma ◽  
Aihong Liu ◽  
...  
Keyword(s):  
Expression Profiles ◽  
Theileria Annulata ◽  
Host Cells ◽  
Transformed Cells ◽  
Tropical Theileriosis ◽  
Life Cycle Stages ◽  
New Information ◽  
Intracellular Compartments ◽  
Infected Cells

Tropical theileriosis is the disease caused by tick-transmitted apicomplexan parasite Theileria annulata, which has ability to transform bovine leukocytes, including B cells, macrophage cells, and dendritic cells. The T. annulata transformed cells are characterized as uncontrolled proliferation and shared some cancer-like phenotypes. The mechanism of the transformation by T. annulata is still not understood well. In previous reports, the subtelomere-encoded variable secreted proteins (SVSP) of T. parva were considered to contribute to phenotypic changes of the host cell, but the role of SVSP of T. annulata in host-pathogen relationship remains unknown. In the present study, a member of SVSP family, TA05575 of T. annulata was selected as the target molecule to analyze its expression profiles in different life cycle stages of T. annulata by qPCR and investigate its subcellular distribution of different passages of T. annulata transformed cells using confocal experiments. From the results, the transcription level of TA05575 at schizont stage was significantly higher than the other two life stages of T. annulata, and the protein of TA05575 was mainly distributed in nucleus of T. annulata infected cells. In addition, the potential proteins of host cells interacting with TA05575 were screened by Yeast-two hybrid system. The results of Co-IP experiment confirmed that TA05575 interacted with RBMX2-like protein that participated in transcription regulation of cells. In addition, a novel BiFC assay and flow cytometry were carried out, and the results further revealed that TA05575-RBMX2-like pair was directly interacted in cell context. Moreover, this interacting pair was found to distribute in intracellular compartments of HEK293T cells by using confocal microscopy. The results of the present study suggest that TA05575 may contribute for cells transformation due its distribution. According to the function of RBMX2, the interaction of TA05575 and RMMX2-like will provide a new information to further understand the mechanisms of cells transformation by T. annulata.

scholarly journals New Isolates of Pandoraviruses: Contribution to the Study of Replication Cycle Steps

2018 ◽  
Vol 93 (5) ◽  
Author(s):  
Ana Cláudia dos Santos Pereira Andrade ◽  
Paulo Victor de Miranda Boratto ◽  
Rodrigo Araújo Lima Rodrigues ◽  
Talita Machado Bastos ◽  
Bruna Luiza Azevedo ◽  
...  
Keyword(s):  
Time Course ◽  
Replication Cycle ◽  
Host Cells ◽  
Comprehensive Description ◽  
Genomic Features ◽  
New Information ◽  
Viral Particles ◽  
Infected Cells ◽  
Giant Viruses ◽  
Electron Lucent

ABSTRACT Giant viruses are complex members of the virosphere, exhibiting outstanding structural and genomic features. Among these viruses, the pandoraviruses are some of the most intriguing members, exhibiting giant particles and genomes presenting at up to 2.5 Mb, with many genes having no known function. In this work, we analyzed, by virological and microscopic methods, the replication cycle steps of three new pandoravirus isolates from samples collected in different regions of Brazil. Our data indicate that all analyzed pandoravirus isolates can deeply modify the Acanthamoeba cytoplasmic environment, recruiting mitochondria and membranes into and around the electron-lucent viral factories. We also observed that the viral factories start forming before the complete degradation of the cellular nucleus. Various patterns of pandoravirus particle morphogenesis were observed, and the assembly of the particles seemed to be started either by the apex or by the opposite side. On the basis of the counting of viral particles during the infection time course, we observed that pandoravirus particles could undergo exocytosis after their morphogenesis in a process that involved intense recruitment of membranes that wrapped the just-formed particles. The treatment of infected cells with brefeldin affected particle exocytosis in two of the three analyzed strains, indicating biological variability among isolates. Despite such particle exocytosis, the lysis of host cells also contributed to viral release. This work reinforces knowledge of and reveals important steps in the replication cycle of pandoraviruses. IMPORTANCE The emerging Pandoraviridae family is composed of some of the most complex viruses known to date. Only a few pandoravirus isolates have been described until now, and many aspects of their life cycle remain to be elucidated. A comprehensive description of the replication cycle is pivotal to a better understanding of the biology of the virus. For this report, we describe new pandoraviruses and used different methods to better characterize the steps of the replication cycle of this new group of viruses. Our results provide new information about the diversity and biology of these giant viruses.

scholarly journals Functional analysis of the putative antiapoptotic genes, p49 and iap4, of Spodoptera litura nucleopolyhedrovirus with RNAi

2008 ◽  
Vol 89 (8) ◽  
pp. 1873-1880 ◽  
Author(s):  
Qian Yu ◽  
Tiehao Lin ◽  
Guozhong Feng ◽  
Kai Yang ◽  
Yi Pang
Keyword(s):  
Spodoptera Litura ◽  
Virus Production ◽  
Host Cells ◽  
Homology Search ◽  
Pcr Analysis ◽  
Viability Analysis ◽  
Infected Cells ◽  
Budded Virus ◽  
Almost All

A homology search of a public database revealed that Spodoptera litura nucleopolyhedrovirus (SpltNPV) possesses two putative, antiapoptotic genes, p49 and inhibitor of apoptosis 4 (iap4), but their function has not been investigated in its native host cells. In the present study, we used RNA interference (RNAi) to silence the expression of Splt-iap4 and Splt-p49, independently or together, to determine their roles during the SpltNPV life cycle. RT-PCR analysis and Western blot analysis showed the target gene expression had been knocked out in the SpltNPV-infected SpLi-221 cells after treatment with Splt-p49 or Splt-iap4 double-stranded RNA (dsRNA), respectively, confirming that the two genes were effectively silenced. In SpltNPV-infected cells treated with Splt-p49 dsRNA, apoptosis was observed beginning at 14 h, and almost all cells had undergone apoptosis by 48 h. In contrast, budded virus production and polyhedra formation progressed normally in infected cells treated with Splt-iap4 dsRNA. Cell viability analysis showed that Splt-IAP4 had no synergistic effect on the inhibition of apoptosis of SpLi-221 cells induced by SpltNPV infection. Interestingly, after Splt-iap4 dsRNA treatment, cells did not congregate like those infected with SpltNPV in the early infection phase, implying an unknown role of baculovirus iap4. Our results determine that Splt-p49 is necessary to prevent apoptosis; however, Splt-iap4 has no antiapoptotic function during SpltNPV infection.

scholarly journals Role of Bcl-2 Family Members in Caspase-Independent Apoptosis during Chlamydia Infection

2002 ◽  
Vol 70 (1) ◽  
pp. 55-61 ◽  
Author(s):  
Jean-Luc Perfettini ◽  
John C. Reed ◽  
Nicole Israël ◽  
Jean-Claude Martinou ◽  
Alice Dautry-Varsat ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Chlamydia Psittaci ◽  
Host Cells ◽  
Chlamydia Infection ◽  
Caspase Inhibitor ◽  
Obligate Intracellular Bacterium ◽  
Obligate Intracellular ◽  
Infected Cells ◽  
Induced Apoptosis

ABSTRACT Infection with an obligate intracellular bacterium, the Chlamydia trachomatis lymphogranuloma venereum (LGV/L2) strain or the guinea pig inclusion conjunctivitis serovar of Chlamydia psittaci, leads to apoptosis of host cells. The apoptosis is not affected by a broad-spectrum caspase inhibitor, and caspase-3 is not activated in infected cells, suggesting that apoptosis mediated by these two strains of Chlamydia is independent of known caspases. Overexpression of the proapoptotic Bcl-2 family member, Bax, was previously shown to induce caspase-independent apoptosis, and we find that Bax is activated and translocates from the cytosol to the mitochondria in C. psittaci-infected cells. C. psittaci-induced apoptosis is inhibited in host cells overexpressing Bax inhibitor-1 and is inhibited through overexpression of Bcl-2, which blocks both caspase-dependent and -independent apoptosis. As Bax and mitochondria are ideally located to sense stress-related metabolic changes emanating from the interior of an infected cell, it is likely that Bax-dependent apoptosis may also be observed in cells infected with other intracellular pathogens.

The parasitophorous vacuole membrane surrounding Plasmodium and Toxoplasma: an unusual compartment in infected cells

1998 ◽  
Vol 111 (11) ◽  
pp. 1467-1475 ◽  
Author(s):  
K. Lingelbach ◽  
K.A. Joiner
Keyword(s):  
Cell Biology ◽  
Parasitophorous Vacuole ◽  
Vacuolar Membrane ◽  
Host Cells ◽  
Mammalian Host ◽  
Cellular Organization ◽  
Parasitophorous Vacuole Membrane ◽  
Endosomal Membranes ◽  
Infected Cells

Plasmodium and Toxoplasma belong to a group of unicellular parasites which actively penetrate their respective mammalian host cells. During the process of invasion, they initiate the formation of a membrane, the so-called parasitophorous vacuolar membrane, which surrounds the intracellular parasite and which differs substantially from endosomal membranes or the membrane of phagolysosomes. The biogenesis and the maintenance of the vacuolar membrane are closely related to the peculiar cellular organization of these parasites and are unique phenomena in cell biology. Here we compare biological similarities and differences between the two parasites, with respect to: (i) the formation, (ii) the maintenance, and (iii) the biological role of the vacuolar membrane. We conclude that most differences between the organisms primarily reflect the different biosynthetic capacities of the host cells they invade.

scholarly journals Destabilization of YopE by the Ubiquitin-Proteasome Pathway Fine-Tunes Yop Delivery into Host Cells and Facilitates Systemic Spread ofYersinia enterocoliticain Host Lymphoid Tissue

2010 ◽  
Vol 79 (3) ◽  
pp. 1166-1175 ◽  
Author(s):  
Kristin Gaus ◽  
Moritz Hentschke ◽  
Nicole Czymmeck ◽  
Lena Novikova ◽  
Konrad Trülzsch ◽  
...  
Keyword(s):  
Lymphoid Tissue ◽  
Defense Responses ◽  
Host Cells ◽  
Virulence Plasmid ◽  
Ubiquitin Proteasome Pathway ◽  
Systemic Spread ◽  
Ubiquitin Proteasome ◽  
Infected Cells ◽  
Proteasome Pathway

ABSTRACTPathogenicYersiniaspecies inject a panel of Yop virulence proteins by type III protein secretion into host cells to modulate cellular defense responses. This enables the survival and dissemination of the bacteria in the host lymphoid tissue. We have previously shown that YopE of theY. enterocoliticaserogroup O8 is degraded in the host cell through the ubiquitin-proteasome pathway. YopE normally manipulates rearrangements of the actin cytoskeleton and triggers phagocytosis resistance. To shed light into the physiological role of YopE inactivation, we mutagenized the lysine polyubiquitin acceptor sites of YopE in theY. enterocoliticaserogroup O8 virulence plasmid. The resulting mutant strain escaped polyubiquitination and degradation of YopE and displayed increased intracellular YopE levels, which was accompanied by a pronounced cytotoxic effect on infected cells. Despite its intensified activity on cultured cells, theYersiniamutant with stabilized YopE showed reduced dissemination into liver and spleen following enteral infection of mice. Furthermore, the accumulation of degradation-resistant YopE was accompanied by the diminished delivery of YopP and YopH into cultured,Yersinia-infected cells. A role of YopE in the regulation of Yop translocation has already been described. Our results imply that the inactivation of YopE by the proteasome could be a tool to ensure intermediate intracellular YopE levels, which may effectuate optimized Yop injection into host cells. In this regard,Y. enterocoliticaO8 appears to exploit the host ubiquitin proteasome system to destabilize YopE and to fine-tune the activities of the Yop virulence arsenal on the infected host organism.

scholarly journals Essential Role of CCL2 in Clustering of Splenic ERTR-9+ Macrophages during Infection of BALB/c Mice by Listeria monocytogenes

2006 ◽  
Vol 75 (1) ◽  
pp. 462-470 ◽  
Author(s):  
Jadwiga Jablonska ◽  
Kurt E. Dittmar ◽  
Tanja Kleinke ◽  
Jan Buer ◽  
Siegfried Weiss
Keyword(s):  
Listeria Monocytogenes ◽  
Marginal Zone ◽  
Early Time ◽  
Cell Types ◽  
Host Cells ◽  
Early Time Point ◽  
Infected Cells ◽  
Different Cell Types ◽  
Time Point

ABSTRACT Early interactions between pathogens and host cells are often decisive for the subsequent course of infection. Here we investigated early events during infection by Listeria monocytogenes, a ubiquitously occurring facultative intracellular microorganism that exhibits severe pathogenicity, mainly in immunocompromised individuals. We show that the inflammatory chemokine CCL2 is highly up-regulated early after Listeria infection in spleens of BALB/c mice. ERTR-9+ macrophages of the marginal zone were identified as the only infected cells and exclusive producers of CCL2 at the early time point. Consequently, clusters of different cell types were formed around infected ERTR-9+ cells. Metallophilic MOMA-1+ marginal zone macrophages were, however, excluded from the clusters and migrated into the B-cell follicles. Depletion of CCL2 during infection resulted in a different composition of cell clusters in the spleen and increased the mortality rate of treated mice. Interestingly, ERTR-9+ macrophages no longer were part of clusters in such mice but remained at their original location in the marginal zone.

scholarly journals The Role of Mcl-1 inS. aureus-Induced Cytoprotection of Infected Macrophages

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Joanna Koziel ◽  
Katarzyna Kmiecik ◽  
Daniela Chmiest ◽  
Katarzyna Maresz ◽  
Danuta Mizgalska ◽  
...  
Keyword(s):  
De Novo ◽  
Myeloid Cell ◽  
Underlying Mechanism ◽  
Host Cells ◽  
Intracellular Pathogen ◽  
Dependent Inhibition ◽  
Infected Cells ◽  
The Stability

As a facultative intracellular pathogen,Staphylococcus aureusinvades macrophages and then promotes the cytoprotection of infected cells thus stabilizing safe niche for silent persistence. This process occurs through the upregulation of crucial antiapoptotic genes, in particular,myeloid cell leukemia-1 (MCL-1). Here, we investigated the underlying mechanism and signal transduction pathways leading to increasedMCL-1expression in infected macrophages. LiveS. aureusnot only stimulatedde novosynthesis of Mcl-1, but also prolonged the stability of this antiapoptotic protein. Consistent with this, we proved a crucial role of Mcl-1 inS. aureus-induced cytoprotection, since silencing ofMCL1by siRNA profoundly reversed the cytoprotection of infected cells leading to apoptosis. IncreasedMCL1expression in infected cells was associated with enhanced NFκB activation and subsequent IL-6 secretion, since the inhibition of both NFκB and IL-6 signalling pathways abrogated Mcl-1 induction and cytoprotection. Finally, we confirmed our observationin vivoin murine model of septic arthritis showing the association between the severity of arthritis and Mcl-1 expression. Therefore, we propose thatS. aureusis hijacking the Mcl-1-dependent inhibition of apoptosis to prevent the elimination of infected host cells, thus allowing the intracellular persistence of the pathogen, its dissemination by infected macrophages, and the progression of staphylococci diseases.

scholarly journals Characterizing Cellular Responses During Oncolytic Maraba Virus Infection

2019 ◽  
Vol 20 (3) ◽  
pp. 580 ◽  
Author(s):  
Golnoush Hassanzadeh ◽  
Thet Naing ◽  
Tyson Graber ◽  
Seyed Jafarnejad ◽  
David Stojdl ◽  
...  
Keyword(s):  
High Selectivity ◽  
Cellular Responses ◽  
Oncolytic Viruses ◽  
Host Cells ◽  
End Joining ◽  
Viral Propagation ◽  
Infected Cells ◽  
Translational Arrest ◽  
Low Cytotoxicity

The rising demand for powerful oncolytic virotherapy agents has led to the identification of Maraba virus, one of the most potent oncolytic viruses from Rhabdoviridae family which displays high selectivity for killing malignant cells and low cytotoxicity in normal cells. Although the virus is readied to be used for clinical trials, the interactions between the virus and the host cells is still unclear. Using a newly developed interferon-sensitive mutant Maraba virus (MG1), we have identified two key regulators of global translation (4E-BP1 and eIF2α) as being involved in the regulation of protein synthesis in the infected cells. Despite the translational arrest upon viral stress, we showed an up-regulation of anti-apoptotic Bcl-xL protein that provides a survival benefit for the host cell, yet facilitates effective viral propagation. Given the fact that eIF5B canonically regulates 60S ribosome subunit end joining and is able to replace the role of eIF2 in delivering initiator tRNA to the 40S ribosome subunit upon the phosphorylation of eIF2α we have tested whether eIF5B mediates the translation of target mRNAs during MG1 infection. Our results show that the inhibition of eIF5B significantly down-regulates the level of Bcl-xL steady-state mRNA, thus indirectly attenuates viral propagation.

scholarly journals Contribution of the oxidative and nitrosative stresses to the development of placental malaria and the consequences for the fetus

2020 ◽  
Vol 12 (9) ◽  
pp. e3784
Author(s):  
Kassyo Lenno Sousa Dantas ◽  
Anna Beatriz da Silva Sousa Mota ◽  
Cristiane Santos Silva e Silva Figueiredo ◽  
Michael Ranniery Garcia Ribeiro ◽  
Adriana dos Santos Oliveira ◽  
...  
Keyword(s):  
Fetal Development ◽  
Cell Structure ◽  
Placental Malaria ◽  
Host Cells ◽  
Placental Barrier ◽  
Cytokines And Chemokines ◽  
Blood Microcirculation ◽  
Infected Cells ◽  
Placental Invasion

Objective: To describe the role of oxidative/nitrosative stresses in the pathogenesis of placental malaria and complications for the fetus. Bibliographic review: Placental malaria results from the sequestration of erythrocytes infected by Plasmodium falciparum in the blood microcirculation of the placental interventional spaces, leading to the infiltration of activated leukocytes in these sites, with subsequent production of cytokines and chemokines. These mediators, associated with phagocytosis of parasites and infected cells, activate the oxidative/nitrosative stresses pathways, producing free radicals and oxidation/nitration molecules, which act by attacking compounds of the cell structure of both the parasite and the host cells, causing damage to the integrity of the placental barrier and leading to insufficiency of the placenta to support fetal development. Final considerations: Therefore, we conclude that the immune response and oxidative/nitrosative stresses play an important role not only in the defense of the patient (reducing parasitaemia), but also in the progression of the disease and placental invasion, leading to serious changes and complications to the fetus.

scholarly journals Role of P Glycoprotein in the Course and Treatment of Encephalitozoon Microsporidiosis

2001 ◽  
Vol 45 (1) ◽  
pp. 73-78 ◽  
Author(s):  
Gordon J. Leitch ◽  
Mary Scanlon ◽  
Andrew Shaw ◽  
Govinda S. Visvesvara
Keyword(s):  
Multidrug Resistance ◽  
Cyclosporin A ◽  
Parasitophorous Vacuole ◽  
Host Cells ◽  
P Glycoprotein ◽  
Antiparasitic Drug ◽  
Infected Cells ◽  
Intracellular Fluorescence

ABSTRACT Encephalitozoon microsporidia are obligate intracellular protozoan parasites that proliferate and differentiate within a parasitophorous vacuole inside host cells that are usually epithelial in nature. Isolates of the three species of theEncephalitozoon microsporidia, E. cuniculi,E. hellem, and E. intestinalis, were obtained from AIDS patients and cultured in green monkey (E6) kidney cells. Anti-P-glycoprotein (anti-Pgp) and anti-multidrug resistance-associated protein (anti-MRP) monoclonal antibodies were used to probe for multidrug resistance (MDR) pump epitopes and verapamil- or cyclosporin A- and probenecid-modulated intracellular calcein fluorescence were used to assess the expression of Pgp and MRP respectively in uninfected and infected cells. Pgp, but not MRP, was detected immunocytochemically and by verapamil- and cyclosporin A-potentiated intracellular fluorescence in both host cells and parasite developing stages. When an in vitro infection assay was employed, verapamil and cyclosporin A acted as chemosensitizing agents for the antiparasitic drug albendazole. These observations suggest that inhibiting host cell and perhaps parasite MDR pumps may increase the efficacy of antiparasitic agents in these and other microsporidia species.

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