scholarly journals Limitation of Trypanosoma brucei parasitaemia results from density-dependent parasite differentiation and parasite killing by the host immune response

2001 ◽  
Vol 268 (1482) ◽  
pp. 2235-2243 ◽  
Author(s):  
Kevin M. Tyler ◽  
Paul G. Higgs ◽  
Keith R. Matthews ◽  
Keith Gull
Keyword(s):  
Immune Response ◽  
Trypanosoma Brucei ◽  
Host Immune Response ◽  
Density Dependent

Virulence and pathogenicity patterns of Trypanosoma brucei gambiense field isolates in experimentally infected mouse: differences in host immune response modulation by secretome and proteomics

2008 ◽  
Vol 10 (1) ◽  
pp. 79-86 ◽  
Author(s):  
Philippe Holzmuller ◽  
David G. Biron ◽  
Pierrette Courtois ◽  
Mathurin Koffi ◽  
Rachel Bras-Gonçalves ◽  
...  
Keyword(s):  
Immune Response ◽  
Trypanosoma Brucei ◽  
Infected Mouse ◽  
Host Immune Response ◽  
Response Modulation ◽  
Field Isolates ◽  
Trypanosoma Brucei Gambiense ◽  
Immune Response Modulation

scholarly journals Faster growth with shorter antigens explains a VSG hierarchy during African trypanosome infections: a feint attack by parasites

2017 ◽  
Author(s):  
Dianbo Liu ◽  
Luca Albergante ◽  
David Horn ◽  
Timothy Newman
Keyword(s):  
Immune Response ◽  
Trypanosoma Brucei ◽  
Temporal Distribution ◽  
Inverse Correlation ◽  
Host Immune Response ◽  
Surface Proteins ◽  
Host Immune System ◽  
Differential Growth ◽  
African Trypanosome

AbstractThe parasitic African trypanosome, Trypanosoma brucei, evades the adaptive host immune response by a process of antigenic variation that involves the clonal switching of variant surface glycoproteins (VSGs). The VSGs that periodically come to dominate in vivo display a hierarchy, but how this hierarchy arises is not well-understood. Combining publicly available genetic data with mathematical modelling, we report a VSG-length-dependent hierarchical timing of clonal VSG dominance in a mouse model, revealing an inverse correlation between VSG length and trypanosome growth-rate. Our analysis indicates that, among parasites switching to new VSGs, those expressing shorter VSGs preferentially accumulate to a detectable level that is sufficient to trigger an effective immune response. Subsequent elimination of faster-growing parasites then allows slower parasites with longer VSGs to accumulate. This interaction between the host and parasite is able by itself to explain the temporal distribution of VSGs observed in vivo. Thus, our findings reveal a length-dependent hierarchy that operates during T. brucei infection, representing a ‘feint attack’ diversion tactic utilised during infection by these persistent parasites to out-maneuver the host immune system.Significance StatementThe protozoan parasite Trypanosoma brucei causes devastating and lethal diseases in humans and livestock. This parasite continuously evades the host adaptive immune response by drawing on a library of variant surface proteins but the mechanisms determining the timing of surface protein – host interactions are not understood. We report a simple mechanism, based on differential growth of parasites with surface proteins of different lengths, which can explain the hierarchy of variants over time. This allows parasites to evade host immune responses for extended timeframes using limited cohorts of surface proteins. We liken this strategy to a military ‘feint attack’, that enhances the parasites ability to evade the host immune response. A similar mechanism may also operate in other important pathogens.

The Host Immune Response to Clostridium Difficile and the Immunomodulatory Effects of Probiotic Bacteria in Vitro

Endoscopy ◽  
2006 ◽  
Vol 38 (11) ◽  
Author(s):  
JA Ryan ◽  
A Fanning ◽  
B Sheil ◽  
L O'Mahony ◽  
F Shanahan
Keyword(s):  
Immune Response ◽  
Clostridium Difficile ◽  
Host Immune Response ◽  
Probiotic Bacteria ◽  
Immunomodulatory Effects

scholarly journals Human Norovirus Proteins: Implications in the Replicative Cycle, Pathogenesis, and the Host Immune Response

2020 ◽  
Vol 11 ◽  
Author(s):  
Claudia P. Campillay-Véliz ◽  
Jonatan J. Carvajal ◽  
Andrea M. Avellaneda ◽  
Darling Escobar ◽  
Camila Covián ◽  
...  
Keyword(s):  
Immune Response ◽  
Host Immune Response ◽  
Human Norovirus ◽  
Replicative Cycle

scholarly journals H-Ras gene takes part to the host immune response to COVID-19

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Salvatore Sciacchitano ◽  
Andrea Sacconi ◽  
Claudia De Vitis ◽  
Giovanni Blandino ◽  
Giulia Piaggio ◽  
...  
Keyword(s):  
Gene Expression ◽  
Immune Response ◽  
Expression Analysis ◽  
Gene Expression Analysis ◽  
Severe Disease ◽  
Host Immune Response ◽  
Severe Form ◽  
Ras Gene ◽  
Peripheral Blood Mononuclear ◽  
Ras Genes

AbstractRas gene family members play a relevant role in cancer, especially when they are mutated. However, they may play additional roles in other conditions beside cancer. We performed gene expression analysis using the NanoString PanCancer IO 360 panel in the peripheral blood mononuclear cell (PBMC) of six COVID-19 patients and we found that H-Ras gene was significantly upregulated, while both K-Ras and N-Ras genes were downregulated. In particular, H-Ras gene upregulation was more evident in COVID-19 patients with a more severe disease. We compared our results with those obtained by analyzing two different and independent datasets, including a total of 53 COVID-19 patients, in which the gene expression analysis was performed using the Immunology_V2 panel. Comparative analysis of the H-Ras gene expression in these patients confirmed our preliminary results. In both of them, in fact, we were able to confirm the upregulation of the expression of the H-Ras gene. The exact role of this specific upregulation of the H-Ras gene in response to SARS-CoV-2 infection and its possible role in cancer still remains to be elucidated. In conclusion, H-Ras gene participates to the host immune response to SARS-CoV-2 virus infection, especially in patients affected by the most severe form of the COVID-19.

Sign in / Sign up

Export Citation Format

Share Document