scholarly journals The role of side tail fibers during the infection cycle of phage lambda

Virology ◽  
2019 ◽  
Vol 527 ◽  
pp. 57-63 ◽  
Author(s):  
Jingwen Guan ◽  
David Ibarra ◽  
Lanying Zeng
Keyword(s):  
Infection Cycle ◽  
Phage Lambda ◽  
Tail Fibers

scholarly journals The Dual Role of the Potyvirus P3 Protein of Turnip mosaic virus as a Symptom and Avirulence Determinant in Brassicas

2003 ◽  
Vol 16 (9) ◽  
pp. 777-784 ◽  
Author(s):  
Carol E. Jenner ◽  
Xiaowu Wang ◽  
Kenta Tomimura ◽  
Kazusato Ohshima ◽  
Fernando Ponz ◽  
...  
Keyword(s):  
Mosaic Virus ◽  
Resistance Genes ◽  
Plant Virus ◽  
Turnip Mosaic Virus ◽  
Single Amino Acid ◽  
Infection Cycle ◽  
In Planta ◽  
Napus Line ◽  
The Uk

Two isolates of the potyvirus Turnip mosaic virus (TuMV), UK 1 and CDN 1, differ both in their general symptoms on the susceptible propagation host Brassica juncea and in their ability to infect B. napus lines possessing a variety of dominant resistance genes. The isolate CDN 1 produces a more extreme mosaic in infected brassica leaves than UK 1 and is able to overcome the resistance genes TuRB01, TuRB04, and TuRB05. The resistance gene TuRB03, in the B. napus line 22S, is effective against CDN 1 but not UK 1. The nucleic acid sequences of the UK 1 and CDN 1 isolates were 90% identical. The C-terminal half of the P3 protein was identified as being responsible for the differences in symptoms in B. juncea. A single amino acid in the P3 protein was found to be the avirulence determinant for TuRB03. Previous work already has identified the P3 as an avirulence determinant for TuRB04. Our results increase the understanding of the basis of plant-virus recognition, show the importance of the potyviral P3 gene as a symptom determinant, and provide a role in planta for the poorly understood P3 protein in a normal infection cycle.

Role of the Gene N Product in Phage Lambda

1970 ◽  
Vol 35 (0) ◽  
pp. 315-318 ◽  
Author(s):  
S. F. Heinemann ◽  
W. G. Spiegelman
Keyword(s):  
Phage Lambda

Abstract P407: Role Of Cyclic AMP During The Intracellular Infection Cycle Of Trypanosoma Cruzi

2021 ◽  
Vol 129 (Suppl_1) ◽  
Author(s):  
Daniel E Velez-Ramirez ◽  
Michelle Shimogawa ◽  
Kent Hill
Keyword(s):  
Trypanosoma Cruzi ◽  
Chagas Disease ◽  
Host Cells ◽  
Camp Signaling ◽  
Host Immune System ◽  
Infection Cycle ◽  
Tropical Regions ◽  
Host Environment ◽  
Intracellular Infection

Trypanosoma cruzi is the causative agent of Chagas disease, a vector-borne disease. In the 1990s the distribution of the vector, a hematophagous triatomine, and consequently the parasite, was from the southeast tropical regions of Mexico to South America. Now, global warming is causing this distribution to expand to northern territories in Mexico, reaching southern parts of US, in which up to 300,000 people are affected. Furthermore, an increase in chronically-infected immigrants to the US makes Chagas disease a matter of Pan-American public health that it should be addressed by all the America countries. Chagas disease manifests clinically as cardiovascular disease, characterized by hypertrophy of heart, esophagus and colon. Congestive heart failure is the main cause of death (58%) in Chagas patients, whereas cardiac arrhythmias and unexpected deaths add another 36%. A major cause of heart pathology in Chagas disease damage is caused by the host immune system, as it attacks chronically infected tissue. Therefore, pathology of the disease is a direct consequence of the ability of the parasite to invade host cells, so it can establish chronic infection. To achieve this, T. cruzi must sense and adapt to the host environment, but the underlying mechanisms are poorly understood. In particular, parasite signaling pathways used to sense and transduce signals from the host environment are most completely unknown. Our lab studies cAMP signaling in trypanosome parasites and several lines of evidence suggest T. cruzi cAMP signaling is important for host cell invasion, differentiation and persistent infection, which in turn underlies heart tissue pathology of Chagas disease. A transcriptome analysis revealed that mRNA of proteins involved in cAMP metabolism, i.e. adenylate cyclases and phosphodiesterases, are either upregulated or downregulated during the intracellular infection cycle. In fact, the phosphodiesterases have flagellar homologs with known cAMP signaling functions in a related parasite. This suggests that cAMP might fluctuate during as T. cruzi invades, differentiates, and multiplies inside the host cells. We have implemented a cAMP FRET sensor to monitor cAMP levels in trypanosomes to understand the role of cAMP in T. cruzi pathogenesis.

Anti-idiotypic Antibody to the V3 Domain of gp120 Binds to Vimentin: A Possible Role of Intermediate Filaments in the Early Steps of HIV-1 Infection Cycle

1996 ◽  
Vol 9 (2) ◽  
pp. 73-87 ◽  
Author(s):  
ELAINE KINNEY THOMAS ◽  
ROBERTA J. CONNELLY ◽  
SRIDHAR PENNATHUR ◽  
LARISA DUBROVSKY ◽  
OMAR K. HAFFAR ◽  
...  
Keyword(s):  
Intermediate Filaments ◽  
Infection Cycle ◽  
Idiotypic Antibody ◽  
Hiv 1

scholarly journals Phages in Anaerobic Systems

Viruses ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 1091
Author(s):  
Santiago Hernández ◽  
Martha J. Vives
Keyword(s):  
Infection Process ◽  
Metabolic Changes ◽  
Phage Infection ◽  
Infection Cycle ◽  
Metabolic State ◽  
Great Abundance ◽  
Facultative Anaerobes ◽  
Available Information

Since the discovery of phages in 1915, these viruses have been studied mostly in aerobic systems, or without considering the availability of oxygen as a variable that may affect the interaction between the virus and its host. However, with such great abundance of anaerobic environments on the planet, the effect that a lack of oxygen can have on the phage-bacteria relationship is an important consideration. There are few studies on obligate anaerobes that investigate the role of anoxia in causing infection. In the case of facultative anaerobes, it is a well-known fact that their shifting from an aerobic environment to an anaerobic one involves metabolic changes in the bacteria. As the phage infection process depends on the metabolic state of the host bacteria, these changes are also expected to affect the phage infection cycle. This review summarizes the available information on phages active on facultative and obligate anaerobes and discusses how anaerobiosis can be an important parameter in phage infection, especially among facultative anaerobes.

scholarly journals Role of Borrelia burgdorferi Linear Plasmid 25 in Infection of Ixodes scapularis Ticks

2005 ◽  
Vol 187 (16) ◽  
pp. 5776-5781 ◽  
Author(s):  
Keith O. Strother ◽  
Aravinda de Silva
Keyword(s):  
Borrelia Burgdorferi ◽  
Genetic Manipulation ◽  
Natural Infection ◽  
Shuttle Vector ◽  
Linear Plasmid ◽  
Infection Prevalence ◽  
Infection Cycle ◽  
Tick Infection

ABSTRACT The tick-borne bacterium Borrelia burgdorferi has over 20 different circular and linear plasmids. Some B. burgdorferi plasmids are readily lost during in vitro culture or genetic manipulation. Linear plasmid 25, which is often lost in laboratory strains, is required for the infection of mice. Strains missing linear plasmid 25 (lp25−) are able to infect mice if the BBE22 gene on lp25 is provided on a shuttle vector. In this study, we examined the role of lp25 and BBE22 in tick infections. We tested the hypothesis that complementation with BBE22 in spirochetes lacking lp25 would restore the ability of spirochetes to infect ticks. A natural tick infection cycle was performed by feeding larvae on mice injected with the parental, lp25−, or lp25− BBE22-complemented spirochete strains. In addition, larvae and nymphs were artificially infected with different strains to study tick infections independent of mouse infections. B. burgdorferi missing lp25 was significantly impaired in its ability to infect larval and nymphal ticks. When an lp25− strain was complemented with BBE22, the ability to infect ticks was partially restored. Complementation with BBE22 allowed spirochetes lacking lp25 to establish short-term infections in ticks, but in most cases the infection prevalence was lower than that of the wild-type strain. In addition, the number of infected ticks decreased over time, suggesting that another gene(s) on lp25 is required for long-term persistence in ticks and completion of a natural infection cycle.

scholarly journals The Ubiquitin-Proteasome System Plays an Important Role during Various Stages of the Coronavirus Infection Cycle

2010 ◽  
Vol 84 (15) ◽  
pp. 7869-7879 ◽  
Author(s):  
Matthijs Raaben ◽  
Clara C. Posthuma ◽  
Monique H. Verheije ◽  
Eddie G. te Lintelo ◽  
Marjolein Kikkert ◽  
...  
Keyword(s):  
Protein Expression ◽  
Ubiquitin Proteasome System ◽  
Translation Initiation Factor ◽  
Initiation Factor ◽  
Infection Cycle ◽  
Protein Ubiquitination ◽  
Ubiquitin Proteasome ◽  
The Impact ◽  
In Cells

ABSTRACT The ubiquitin-proteasome system (UPS) is a key player in regulating the intracellular sorting and degradation of proteins. In this study we investigated the role of the UPS in different steps of the coronavirus (CoV) infection cycle. Inhibition of the proteasome by different chemical compounds (i.e., MG132, epoxomicin, and Velcade) appeared to not only impair entry but also RNA synthesis and subsequent protein expression of different CoVs (i.e., mouse hepatitis virus [MHV], feline infectious peritonitis virus, and severe acute respiratory syndrome CoV). MHV assembly and release were, however, not appreciably affected by these compounds. The inhibitory effect on CoV protein expression did not appear to result from a general inhibition of translation due to induction of a cellular stress response by the inhibitors. Stress-induced phosphorylation of eukaryotic translation initiation factor 2α (eIF2α) generally results in impaired initiation of protein synthesis, but the sensitivity of MHV infection to proteasome inhibitors was unchanged in cells lacking a phosphorylatable eIF2α. MHV infection was affected not only by inhibition of the proteasome but also by interfering with protein ubiquitination. Viral protein expression was reduced in cells expressing a temperature-sensitive ubiquitin-activating enzyme E1 at the restrictive temperature, as well as in cells in which ubiquitin was depleted by using small interfering RNAs. Under these conditions, the susceptibility of the cells to virus infection was, however, not affected, excluding an important role of ubiquitination in virus entry. Our observations reveal an important role of the UPS in multiple steps of the CoV infection cycle and identify the UPS as a potential drug target to modulate the impact of CoV infection.

scholarly journals MAPS integrates overlooked regulation of actin-targeting effector SteC into the virulence control network of Salmonella small RNA PinT

2020 ◽  
Author(s):  
Sara Correia Santos ◽  
Thorsten Bischler ◽  
Alexander J. Westermann ◽  
Jörg Vogel
Keyword(s):  
Small Rna ◽  
Small Rnas ◽  
Affinity Purification ◽  
Transcriptional Regulator ◽  
Bacterial Virulence ◽  
Host Cells ◽  
Integrative Approach ◽  
Infection Cycle

ABSTRACTA full understanding of the contribution of small RNAs (sRNAs) to bacterial virulence demands knowledge of their target suites under infection-relevant conditions. Here, we take an integrative approach to capturing targets of the Hfq-associated sRNA PinT, a known post-transcriptional timer of the two major virulence programs of Salmonella enterica. Using MS2 affinity purification and RNA-sequencing (MAPS), we identify PinT ligands in bacteria under in-vitro conditions mimicking specific stages of the infection cycle, and in bacteria growing inside macrophages. This reveals PinT-mediated translational inhibition of the secreted effector kinase SteC, which had gone unnoticed in previous target searches. Using genetic, biochemical, and microscopic assays, we provide evidence for PinT-mediated repression of steC mRNA, eventually preventing actin rearrangements in infected host cells. Our findings support the role of PinT as a central post-transcriptional regulator in Salmonella virulence and illustrate the need for complementary methods to reveal the full target suites of sRNAs.

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