Mathematical models of parasite responses to host immune defences

Parasitology ◽  
1997 ◽  
Vol 115 (7) ◽  
pp. 155-167 ◽  
Author(s):  
R. ANTIA ◽  
M. LIPSITCH
Keyword(s):  
Immune System ◽  
Simple Model ◽  
Acute Infection ◽  
Multiple Infections ◽  
Host Immune System ◽  
Host Genotype ◽  
Immune Mediated ◽  
Host Parasite ◽  
Immune Defences ◽  
Rates Of Growth

We examine the evolution of microparasites in response to the immune system of vertebrate hosts. We first describe a simple model for an acute infection. This model suggests that the within-host dynamics of the microparasite will be a ‘race’ between parasite multiplication and a clonally expanding response by the host immune system, resulting either in immune-mediated clearance or host death. In this very simple model, in which there is only a single parasite and host genotype, maximum transmission is obtained by parasites with intermediate rates of growth (and virulence). We examine how these predictions depend on key assumptions about the parasite and the host, and consider how this model may be expanded to incorporate the effect of additional complexities such as host–parasite co-evolution, host polymorphism, and multiple infections.

scholarly journals Chronic microbial infections: Manipulation of host immunity as interventional approach

1970 ◽  
Vol 1 (1) ◽  
pp. 13-19
Author(s):  
Sheikh Mohammad Fazle Akbar ◽  
Md Sakirul Islam Khan ◽  
Shunji Mishiro
Keyword(s):  
Immune System ◽  
Immune Responses ◽  
Viral Infections ◽  
Inflammatory Diseases ◽  
Acute Infection ◽  
Immune Surveillance ◽  
Host Immune System ◽  
Related Factors ◽  
Chronic Viral Infections ◽  
Microbial Infections

Chronic viral infections represent major challenges in contemporary medicine, virology and pharmacology. The virus-bearing hosts are commonly found in every parts of the world and it is extremely difficult to manage these patients. In addition, considerable numbers of these patients develop progressive diseases and severe complications. Finally, most of these patients act as permanent reservoirs of virus. Understandings of viral life cycle during the last decade of 20th century and the first decade of 21st century have allowed development of hundreds of antiviral agents for different diseases. But, the clinical efficacy of these drugs is not yet satisfactory. In addition, virologists have provided conclusive evidences suggesting that eradication of most chronic virus from infected hosts may an unachievable goal. In this context, it is essential to develop alternative, novel, and evidence-based therapeutic maneuver for these patients. Manipulation of host immune system may be one of these approaches. We would discuss about scopes, limitations, and strategies for manipulation for controlling of chronic viral infections. The primary function of the host's immune system is to mount responses that protect the individual from various microbial infections including viruses. Host's immune responses also control the spread and virulence of the viruses [1]. This is applicable to viruses that cause acute infection. After entering the hosts, these viruses are localized in host's tissues, proliferate and induce antiviral immunity. These cellular events may cause damage and destruction of tissues and the host exhibit features of acute inflammatory diseases. However, the viruses are either almost completely eliminated from the hosts or adequately controlled in situ by host's immune systems. However, chronic infection is established by many viruses because the hosts induce improper and uncoordinated immune responses against these viruses. Most viruses cause persistent infection by evading the host immune surveillance mechanism. Both virus-related factors and host-dependent factors are primarily responsible for viral persistency in subjects with chronic viral infections.    doi: 10.3329/blj.v1i1.2620 Bangladesh Liver Journal Vol.1(1) 2009 p.13-19 

scholarly journals Convergent Evolution by Cancer and Viruses in Evading the NKG2D Immune Response

Cancers ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3827
Author(s):  
Richard Baugh ◽  
Hena Khalique ◽  
Leonard W. Seymour
Keyword(s):  
Immune System ◽  
Immune Responses ◽  
Cancer Cells ◽  
Innate Immune System ◽  
Cell Transformation ◽  
Innate Immune ◽  
Immune Mediated ◽  
Pathogenic Viruses ◽  
Group 2 ◽  
Immune Defences

The natural killer group 2 member D (NKG2D) receptor and its family of NKG2D ligands (NKG2DLs) are key components in the innate immune system, triggering NK, γδ and CD8+ T cell-mediated immune responses. While surface NKG2DL are rarely found on healthy cells, expression is significantly increased in response to various types of cellular stress, viral infection, and tumour cell transformation. In order to evade immune-mediated cytotoxicity, both pathogenic viruses and cancer cells have evolved various mechanisms of subverting immune defences and preventing NKG2DL expression. Comparisons of the mechanisms employed following virus infection or malignant transformation reveal a pattern of converging evolution at many of the key regulatory steps involved in NKG2DL expression and subsequent immune responses. Exploring ways to target these shared steps in virus- and cancer-mediated immune evasion may provide new mechanistic insights and therapeutic opportunities, for example, using oncolytic virotherapy to re-engage the innate immune system towards cancer cells.

Role of the surface coat of Romanomermis culicivorax in immune evasion

Nematology ◽  
2007 ◽  
Vol 9 (1) ◽  
pp. 17-24 ◽  
Author(s):  
Edward Platzer ◽  
Randy Gaugler ◽  
Muhammad Shamseldean
Keyword(s):  
Immune System ◽  
Immune Evasion ◽  
Immune Reaction ◽  
Parasitic Nematodes ◽  
Broad Host Range ◽  
Host Immune System ◽  
Surface Coat ◽  
Mermithid Nematode ◽  
Host Parasite

AbstractInteractions of the mermithid nematode Romanomermis culicivorax with the immune system of mosquito larvae were examined by scanning electron microscopy. The host immune system rapidly recognised invading parasites, as granulocytes and discharged granules were observed attached to parasitic nematodes within 5 min. Melanin deposition was infrequently observed. As a counter measure, the parasites secreted and shed an extracellular surface coat which aided immune evasion. During the first 4 days of infection, when parasite growth was limited, the coat served as a disposable, renewable barrier between parasite and host that was intermittently shed to cleanse the nematode of adhering host immune products. In the later infection phase the parasite grew rapidly and was beyond the effect of the depleted host immune response. The broad host range of R. culcivorax within culicines may be partly a function of the nonspecific defence it mounts against the host immune system. In summary, shedding of the surface coat is an adaptive counter response by R. culicivorax to the mosquito immune reaction to infection and provides a classic example of host-parasite coevolution.

scholarly journals Role of Intestinal Microbiota on Gut Homeostasis and Rheumatoid Arthritis

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Mingxin Li ◽  
Fang Wang
Keyword(s):  
Rheumatoid Arthritis ◽  
Immune System ◽  
Gut Microbiota ◽  
Intestinal Microbiota ◽  
Chronic Inflammatory Disease ◽  
Host Immune System ◽  
Healthy Controls ◽  
Gastrointestinal Microbiota ◽  
Intestinal Dysbiosis ◽  
Immune Mediated

Rheumatoid arthritis (RA) is a chronic inflammatory disease that is immune mediated. Patients typically present with synovial inflammation, which gradually deteriorates to investigate severe cartilage and bone damage, affecting an individual’s ability to perform basic tasks and impairing the quality of life. When evaluated against healthy controls, patients with RA have notable variations within the constituents of the gut microbiota. The human gastrointestinal tract mucosa is colonized by trillions of commensal microbacteria, which are key actors in the initiation, upkeep, and operation of the host immune system. Gut microbiota dysbiosis can adversely influence the immune system both locally and throughout the host, thus predisposing the host to a number of pathologies, including RA. Proximal intestinal immunomodulatory cells, situated in specific locales within the intestine, are a promising intermediary through which the gastrointestinal microbiota can influence the pathogenesis and progression of RA. In the early stages of the disease, the microbiota appear to differ from those present in healthy controls. This difference may reflect potential autoimmune mechanisms. Research studies evaluating intestinal microbiota have demonstrated that RA is associated with a bacterial population growth or with a decline when judged against control groups. The aim of this review is to examine the studies that connect intestinal dysbiosis with the autoimmune pathways implicated in the pathogenesis of RA.

Multiple sclerosis and faecal microbiome transplantation: are you going to eat that?

2019 ◽  
Vol 10 (1) ◽  
pp. 27-32 ◽  
Author(s):  
A.C. Wing ◽  
M. Kremenchutzky
Keyword(s):  
Multiple Sclerosis ◽  
Immune System ◽  
Current Knowledge ◽  
Clinical Trial Design ◽  
Host Immune System ◽  
Immune Mediated ◽  
Clinical Benefits ◽  
Multiple Sclerosis Patients ◽  
Faecal Microbiome ◽  
Vitamin Production

Gut microbiome interaction goes beyond commensal function as vitamin production or support nutrients digestion. It also interplays with the host immune system and may be related to the development of immune-mediated diseases. Multiple sclerosis patients have dysbiosis compared to healthy individuals. But how this relates to disease development and severity is still uncertain. Dietary change including probiotic mixtures or ketogenic regimen has proven to change microbiome in multiple sclerosis (MS) subjects to one similar to healthy controls. However, proof of clinical benefits is lacking. We dissert on current knowledge about immune system and gut bacteria interactions. We discuss faecal microbial transplantation as a potential intervention to ameliorate gut dysbiosis in MS as well as the caveats of a clinical trial design.

scholarly journals Disentangling the influence of parasite genotype, host genotype and maternal environment on different stages of bacterial infection in Daphnia magna

2012 ◽  
Vol 279 (1741) ◽  
pp. 3176-3183 ◽  
Author(s):  
Matthew D. Hall ◽  
Dieter Ebert
Keyword(s):  
Infectious Disease ◽  
Daphnia Magna ◽  
Parasite Clearance ◽  
Infection Process ◽  
Host Immune System ◽  
Parasite Genotype ◽  
Host Genotype ◽  
Maternal Environment ◽  
Host Infection ◽  
Host Parasite

Individuals naturally vary in the severity of infectious disease when exposed to a parasite. Dissecting this variation into genetic and environmental components can reveal whether or not this variation depends on the host genotype, parasite genotype or a range of environmental conditions. Complicating this task, however, is that the symptoms of disease result from the combined effect of a series of events, from the initial encounter between a host and parasite, through to the activation of the host immune system and the exploitation of host resources. Here, we use the crustacean Daphnia magna and its parasite Pasteuria ramosa to show how disentangling genetic and environmental factors at different stages of infection improves our understanding of the processes shaping infectious disease. Using compatible host–parasite combinations, we experimentally exclude variation in the ability of a parasite to penetrate the host, from measures of parasite clearance, the reduction in host fecundity and the proliferation of the parasite. We show how parasite resistance consists of two components that vary in environmental sensitivity, how the maternal environment influences all measured aspects of the within-host infection process and how host–parasite interactions following the penetration of the parasite into the host have a distinct temporal component.

scholarly journals Activation of host constitutive immune defence by an intestinal trypanosome parasite of bumble bees

Parasitology ◽  
2003 ◽  
Vol 126 (3) ◽  
pp. 253-260 ◽  
Author(s):  
M. J. F. BROWN ◽  
Y. MORET ◽  
P. SCHMID-HEMPEL
Keyword(s):  
Immune System ◽  
Bombus Terrestris ◽  
Parasitic Infection ◽  
Bumble Bees ◽  
Host Immune System ◽  
Immune Defence ◽  
Important Species ◽  
Crithidia Bombi ◽  
Resource Stress ◽  
Host Parasite

Many parasites, including important species that affect humans and livestock, must survive the harsh environment of insect guts to complete their life-cycle. Hence, understanding how insects protect themselves against such parasites has immediate practical implications. Previously, such protection has been thought to consist mainly of mechanical structures and the action of lectins. However, recently it has become apparent that gut infections may interact with the host immune system in more complex ways. Here, using bumble bees, Bombus terrestris and their non-invasive gut trypanosome, Crithidia bombi, as a model system we investigated the effects of parasitic infection, host resources and the duration of infections on the host immune system. We found that infection doubled standing levels of immune defence in the haemolymph (the constitutive pro-phenoloxidase system), which is used as a first, general defence against parasites. However, physical separation of the parasite from the haemolymph suggests the presence of a messenger system between the gut and the genes that control the pro-phenoloxidase system. Surprisingly, we found no direct effect of host resource-stress or duration of the infection on the immune system. Our results suggest a novel and tactical response of insects to gut infections, demonstrating the complexity of such host–parasite systems.

scholarly journals Interplay Between Skin Microbiota Dysbiosis and the Host Immune System in Psoriasis: Potential Pathogenesis

2021 ◽  
Vol 12 ◽  
Author(s):  
Xiaoqian Liang ◽  
Caixin Ou ◽  
Jiayi Zhuang ◽  
Jinsheng Li ◽  
Fangfei Zhang ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Immune System ◽  
Skin Diseases ◽  
Cell Populations ◽  
Host Immune System ◽  
Skin Microbiota ◽  
Inflammatory Skin Diseases ◽  
Immune Mediated ◽  
Underlying Pathogenesis ◽  
Novel Therapeutic

Psoriasis is a multifactorial immune-mediated disease. The highly effective and eligible treatment for psoriasis is limited, for its specific pathogenesis is incompletely elucidated. Skin microbiota is a research hotspot in the pathogenesis of immune-mediated inflammatory skin diseases nowadays, and it may have significant involvement in the provocation or exacerbation of psoriasis with broadly applicable prospects. It is postulated that skin microbiota alternation may interplay with innate immunity such as antimicrobial peptides and Toll-like receptors to stimulate T-cell populations, resulting in immune cascade responses and ultimately psoriasis. Achieving a thorough understanding of its underlying pathogenesis is crucial. Herein, we discuss the potential immunopathogenesis of psoriasis from the aspect of skin microbiota in an attempt to yield insights for novel therapeutic and preventive modalities for psoriasis.

scholarly journals Helminth Glycans at the Host-Parasite Interface and Their Potential for Developing Novel Therapeutics

2022 ◽  
Vol 8 ◽  
Author(s):  
Myrna J. M. Bunte ◽  
Arjen Schots ◽  
Jan E. Kammenga ◽  
Ruud H. P. Wilbers
Keyword(s):  
Immune System ◽  
Immune Cells ◽  
Helminth Infection ◽  
Host Immune System ◽  
Lewis X ◽  
Novel Therapeutics ◽  
Antigenic Properties ◽  
Parasitic Worms ◽  
Host Parasite

Helminths are parasitic worms that have successfully co-evolved with their host immune system to sustain long-term infections. Their successful parasitism is mainly facilitated by modulation of the host immune system via the release of excretory-secretory (ES) products covered with glycan motifs such as Lewis X, fucosylated LDN, phosphorylcholine and tyvelose. Evidence is accumulating that these glycans play key roles in different aspects of helminth infection including interactions with immune cells for recognition and evasion of host defences. Moreover, antigenic properties of glycans can be exploited for improving the efficacy of anti-helminthic vaccines. Here, we illustrate that glycans have the potential to open new avenues for the development of novel biopharmaceuticals and effective vaccines based on helminth glycoproteins.

scholarly journals The Secretome of Filarial Nematodes and Its Role in Host-Parasite Interactions and Pathogenicity in Onchocerciasis-Associated Epilepsy

2021 ◽  
Vol 11 ◽  
Author(s):  
An Hotterbeekx ◽  
Jolien Perneel ◽  
Melissa Krizia Vieri ◽  
Robert Colebunders ◽  
Samir Kumar-Singh
Keyword(s):  
Immune System ◽  
Current Knowledge ◽  
Bioactive Molecules ◽  
Mammalian Host ◽  
Host Immune System ◽  
Pathogenic Potential ◽  
Host Parasite Interactions ◽  
Filarial Nematodes ◽  
Secretory Products ◽  
Host Parasite

Filarial nematodes secrete bioactive molecules which are of interest as potential mediators for manipulating host biology, as they are readily available at the host-parasite interface. The adult parasites can survive for years in the mammalian host, due to their successful modulation of the host immune system and most of these immunomodulatory strategies are based on soluble mediators excreted by the parasite. The secretome of filarial nematodes is a key player in both infection and pathology, making them an interesting target for further investigation. This review summarises the current knowledge regarding the components of the excretory-secretory products (ESPs) of filarial parasites and their bioactive functions in the human host. In addition, the pathogenic potential of the identified components, which are mostly proteins, in the pathophysiology of onchocerciasis-associated epilepsy is discussed.

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