scholarly journals Plasminogen Binding Proteins and Plasmin Generation on the Surface ofLeptospiraspp.: The Contribution to the Bacteria-Host Interactions

2012 ◽  
Vol 2012 ◽  
pp. 1-17 ◽  
Author(s):  
Monica L. Vieira ◽  
Marina V. Atzingen ◽  
Rosane Oliveira ◽  
Renata S. Mendes ◽  
Renan F. Domingos ◽  
...  
Keyword(s):  
Infectious Disease ◽  
Immune Evasion ◽  
Host Tissue ◽  
Research Groups ◽  
Tissue Penetration ◽  
Bacterial Surface ◽  
Host Interactions ◽  
Evasion Strategy ◽  
Immune Attack ◽  
Human Plasminogen

Leptospirosis is considered a neglected infectious disease of human and veterinary concern. Although extensive investigations on host-pathogen interactions have been pursued by several research groups, mechanisms of infection, invasion and persistence of pathogenicLeptospiraspp. remain to be elucidated. We have reported the ability of leptospires to bind human plasminogen (PLG) and to generate enzimatically active plasmin (PLA) on the bacteria surface. PLA-coatedLeptospiracan degrade immobilized ECM molecules, an activity with implications in host tissue penetration. Moreover, we have identified and characterized several proteins that may act as PLG-binding receptors, each of them competent to generate active plasmin. The PLA activity associated to the outer surface ofLeptospiracould hamper the host immune attack by conferring the bacteria some benefit during infection. The PLA-coated leptospires obstruct complement C3b and IgG depositions on the bacterial surface, most probably through degradation. The decrease of leptospiral opsonization might be an important aspect of the immune evasion strategy. We believe that the presence of PLA on the leptospiral surface may (i) facilitate host tissue penetration, (ii) help the bacteria to evade the immune system and, as a consequence, (iii) permitLeptospirato reach secondary sites of infection.

scholarly journals Plasticity in early immune evasion strategies of a bacterial pathogen

2018 ◽  
Vol 115 (16) ◽  
pp. E3788-E3797 ◽  
Author(s):  
Quentin Bernard ◽  
Alexis A. Smith ◽  
Xiuli Yang ◽  
Juraj Koci ◽  
Shelby D. Foor ◽  
...  
Keyword(s):  
Immune Evasion ◽  
Bacterial Pathogen ◽  
Surface Protein ◽  
Innate Immune ◽  
Serum Complement ◽  
Term Survival ◽  
Evasion Strategy ◽  
Innate Immune Evasion ◽  
Novel Therapeutic

Borrelia burgdorferiis one of the few extracellular pathogens capable of establishing persistent infection in mammals. The mechanisms that sustain long-term survival of this bacterium are largely unknown. Here we report a unique innate immune evasion strategy ofB. burgdorferi, orchestrated by a surface protein annotated as BBA57, through its modulation of multiple spirochete virulent determinants. BBA57 function is critical for early infection but largely redundant for later stages of spirochetal persistence, either in mammals or in ticks. The protein influences host IFN responses as well as suppresses multiple host microbicidal activities involving serum complement, neutrophils, and antimicrobial peptides. We also discovered a remarkable plasticity in BBA57-mediated spirochete immune evasion strategy because its loss, although resulting in near clearance of pathogens at the inoculum site, triggers nonheritable adaptive changes that exclude detectable nucleotide alterations in the genome but incorporate transcriptional reprograming events. Understanding the malleability in spirochetal immune evasion mechanisms that ensures their host persistence is critical for the development of novel therapeutic and preventive approaches to combat long-term infections like Lyme borreliosis.

scholarly journals Fitness costs limit influenza A virus hemagglutinin glycosylation as an immune evasion strategy

2011 ◽  
Vol 108 (51) ◽  
pp. E1417-E1422 ◽  
Author(s):  
S. R. Das ◽  
S. E. Hensley ◽  
A. David ◽  
L. Schmidt ◽  
J. S. Gibbs ◽  
...  
Keyword(s):  
Influenza A Virus ◽  
Immune Evasion ◽  
Influenza A ◽  
Fitness Costs ◽  
Evasion Strategy

scholarly journals Trichinella spiralis Calreticulin Binds Human Complement C1q As an Immune Evasion Strategy

2017 ◽  
Vol 8 ◽  
Author(s):  
Limei Zhao ◽  
Shuai Shao ◽  
Yi Chen ◽  
Ximeng Sun ◽  
Ran Sun ◽  
...  
Keyword(s):  
Immune Evasion ◽  
Trichinella Spiralis ◽  
Human Complement ◽  
Evasion Strategy ◽  
Complement C1q

scholarly journals Viruses, cancer and non-self recognition

Open Biology ◽  
2021 ◽  
Vol 11 (3) ◽  
Author(s):  
Monikaben Padariya ◽  
Umesh Kalathiya ◽  
Sara Mikac ◽  
Katarzyna Dziubek ◽  
Maria C. Tovar Fernandez ◽  
...  
Keyword(s):  
Immune System ◽  
Mhc Class I ◽  
Immune Evasion ◽  
Genetic Material ◽  
Class I ◽  
Host Interactions ◽  
Host Interaction ◽  
Self Recognition ◽  
Cancer Mutations ◽  
Cellular Pathways

Virus–host interactions form an essential part of every aspect of life, and this review is aimed at looking at the balance between the host and persistent viruses with a focus on the immune system. The virus–host interaction is like a cat-and-mouse game and viruses have developed ingenious mechanisms to manipulate cellular pathways, most notably the major histocompatibility (MHC) class I pathway, to reside within infected cell while evading detection and destruction by the immune system. However, some of the signals sensing and responding to viral infection are derived from viruses and the fact that certain viruses can prevent the infection of others, highlights a more complex coexistence between the host and the viral microbiota. Viral immune evasion strategies also illustrate that processes whereby cells detect and present non-self genetic material to the immune system are interlinked with other cellular pathways. Immune evasion is a target also for cancer cells and a more detailed look at the interfaces between viral factors and components of the MHC class I peptide-loading complex indicates that these interfaces are also targets for cancer mutations. In terms of the immune checkpoint, however, viral and cancer strategies appear different.

scholarly journals INFEKTA: A General Agent-based Model for Transmission of Infectious Diseases: Studying the COVID-19 Propagation in Bogotá - Colombia

2020 ◽  
Author(s):  
Jonatan Gomez ◽  
Jeisson Prieto ◽  
Elizabeth Leon ◽  
Arles Rodríguez
Keyword(s):  
Infectious Disease ◽  
Euclidean Space ◽  
Infectious Diseases ◽  
Complex Network ◽  
Computational Models ◽  
Compartmental Model ◽  
Transmission Dynamics ◽  
Agent Based Model ◽  
Research Groups ◽  
Agent Based

AbstractThe transmission dynamics of the coronavirus - COVID-19-have challenged humankind at almost every level. Currently, research groups around the globe are trying to figure out such transmission dynamics using different scientific and technological approaches. One of those is by using mathematical and computational models like the compartmental model or the agent-based models. In this paper, a general agent-based model, called INFEKTA, that combines the transmission dynamics of an infectious disease with agents (individuals) that can move on a complex network of accessible places defined over a Euclidean space representing a real town or city is proposed. The applicability of INFEKTA is shown by modeling the transmission dynamics of the COVID-19 in Bogotá city, the capital of Colombia.

HCV:CD81 Interactions Inhibit Il-2 Production by T Cells: A Novel HCV Immune Evasion Strategy

Endoscopy ◽  
2004 ◽  
Vol 36 (10) ◽  
Author(s):  
L Golden-Mason ◽  
AM Kelly ◽  
HR Rosen ◽  
JE Hegarty ◽  
C O'Farrelly ◽  
...  
Keyword(s):  
T Cells ◽  
Immune Evasion ◽  
Evasion Strategy

scholarly journals Diversified local CRISPR-Cas immunity to viruses of Sulfolobus islandicus

2019 ◽  
Vol 374 (1772) ◽  
pp. 20180093 ◽  
Author(s):  
Matthew D. Pauly ◽  
Maria A. Bautista ◽  
Jesse A. Black ◽  
Rachel J. Whitaker
Keyword(s):  
Immune Evasion ◽  
National Park ◽  
Natural Populations ◽  
Population Diversity ◽  
Potential Mechanism ◽  
Host Interactions ◽  
Adaptive Immune ◽  
Sulfolobus Islandicus ◽  
Immune Diversity ◽  
Adaptive Immune Systems

The population diversity and structure of CRISPR-Cas immunity provides key insights into virus–host interactions. Here, we examined two geographically and genetically distinct natural populations of the thermophilic crenarchaeon Sulfolobus islandicus and their interactions with Sulfolobus spindle-shaped viruses (SSVs) and S. islandicus rod-shaped viruses (SIRVs). We found that both virus families can be targeted with high population distributed immunity, whereby most immune strains target a virus using unique unshared CRISPR spacers. In Kamchatka, Russia, we observed high immunity to chronic SSVs that increases over time. In this context, we found that some SSVs had shortened genomes lacking genes that are highly targeted by the S. islandicus population, indicating a potential mechanism of immune evasion. By contrast, in Yellowstone National Park, we found high inter- and intra-strain immune diversity targeting lytic SIRVs and low immunity to chronic SSVs. In this population, we observed evidence of SIRVs evolving immunity through mutations concentrated in the first five bases of protospacers. These results indicate that diversity and structure of antiviral CRISPR-Cas immunity for a single microbial species can differ by both the population and virus type, and suggest that different virus families use different mechanisms to evade CRISPR-Cas immunity. This article is part of a discussion meeting issue ‘The ecology and evolution of prokaryotic CRISPR-Cas adaptive immune systems’.

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