scholarly journals Mimicry between respiratory virus proteins and some human immune proteins

2020 ◽  
Vol 10 (2) ◽  
pp. 305-314
Author(s):  
I. N. Zhilinskaya

A comparative analysis on search for amino acid sequences in viral proteins causing respiratory infections (or respiratory infections syndrome) homologous to amino acid sequences from some human immune proteins was performed. The following viruses were used for comparative computer analysis: coronavirus (SARS-CoV), serotype C subgroup adenovirus C (adenoid 71 strain), measles virus (ICHINOSE-BA strain), rubella (Therien strain) and respiratory syncytial (B1 strain) virus. The search for homologous sequences in viral and human immune proteins was carried out by computer comparison of 12 amino acid fragments, which were assigned as homologous at identity in ≥ 8 positions. The data obtained showed that viral proteins contained homologous motifs in several host immune proteins involved in regulating both the inflammatory response and immune response. Mechanistically, all viruses studied were characterized by sequences homologous to host immune proteins such as complement system proteins, integrins, apoptosis inhibitory proteins, interleukins, and toll-like receptors. Such cellular proteins are actively involved in regulating host inflammatory process and immune response formation. Upon that, a set of host immune proteins, to which homologous fragments were found in viral proteins, was individual for each virus. Interestingly, the largest amount of homologous fragments (up to 20) was mainly concentrated in viral proteins with polymerase and protease activity suggesting that these proteins apart to their major role were involved in production of viral nucleic acids and might participate in regulating host immune system. Envelope, internal and non-structural viral proteins, homologous fragments were detected in much smaller quantities (from 1 to 4). In addition, two fragments homologous to various motifs of the same cellular protein were detected in some viral proteins. Thus, the data obtained further support our understanding that signs of immune system disorders in viral infections can result from multi-layered processes associated with modulation of host innate and adaptive immune system, and open up new approaches to study interaction of viruses with host immune system and identify new functions of viral proteins.

Author(s):  
Michael B. A. Oldstone

This chapter discusses how the human immune system combats viruses, either by spontaneously eliminating infections or by becoming stimulated via vaccination to prevent viral diseases. The proteins in viruses and bacteria that trigger an immune response are called antigens or immunogens, and the result of a satisfactory immune response to these antigens is immunity—long-term protection from repeated disease caused by a specific type of virus or bacteria. Similarly, a vaccine primes the immune response by programming it to anticipate and resist future pathogens like those in that particular vaccine. The immune system has evolved to deal with enormous numbers and varieties of every conceivable foreign antigen. However, the immune system must discriminate between foreign antigens, such as viral proteins, that are non-self and those antigens that are self, one’s own proteins (i.e., hormones such as insulin and cell proteins that make up muscle or nerve cells). Ultimately, the success of this system defines an organism’s capacity for survival.


2019 ◽  
Vol 26 (7) ◽  
pp. 542-549 ◽  
Author(s):  
Shan Shan Hao ◽  
Man Man Zong ◽  
Ze Zhang ◽  
Jia Xi Cai ◽  
Yang Zheng ◽  
...  

Background: Bursa of Fabricius is the acknowledged central humoral immune organ. The bursal-derived peptides play the important roles on the immature B cell development and antibody production. Objective: Here we explored the functions of the new isolated bursal hexapeptide and pentapeptide on the humoral, cellular immune response and antigen presentation to Avian Influenza Virus (AIV) vaccine in mice immunization. Methods: The bursa extract samples were purified following RP HPLC method, and were analyzed with MS/MS to identify the amino acid sequences. Mice were twice subcutaneously injected with AIV inactivated vaccine plus with two new isolated bursal peptides at three dosages, respectively. On two weeks after the second immunization, sera samples were collected from the immunized mice to measure AIV-specific IgG antibody levels and HI antibody titers. Also, on 7th day after the second immunization, lymphocytes were isolated from the immunized mice to detect T cell subtype and lymphocyte viabilities, and the expressions of co-stimulatory molecule on dendritic cells in the immunized mice. Results: Two new bursal hexapeptide and pentapeptide with amino acid sequences KGNRVY and MPPTH were isolated, respectively. Our investigation proved the strong regulatory roles of bursal hexapeptide on AIV-specific IgG levels and HI antibody titers, and lymphocyte viabilities, and the significant increased T cells subpopulation and expressions of MHCII molecule on dendritic cells in the immunized mice. Moreover, our findings verified the significantly enhanced AIV-specific IgG antibody and HI titers, and the strong increased T cell subpopulation and expressions of CD40 molecule on dendritic cells in the mice immunized with AIV vaccine and bursal pentapeptide. Conclusion: We isolated and identified two new hexapeptide and pentapeptide from bursa, and proved that these two bursal peptides effectively induced the AIV-specific antibody, T cell and antigen presentation immune responses, which provided an experimental basis for the further clinical application of the bursal derived active peptide on the vaccine improvement.


2020 ◽  
Vol 98 (Supplement_4) ◽  
pp. 181-181
Author(s):  
Martin Lessard ◽  
Mylène Blais ◽  
Guylaine Talbot ◽  
J Jacques Matte ◽  
Ann Letellier ◽  
...  

Abstract Lactation, feeding conditions, microbial interventions and piglet growth in the first few weeks of life have important impact on the intestinal microbiota establishment and immune system development of piglets. Indeed, colostrum and milk contain various bioactive components such as immune factors, antimicrobial peptides and oligosaccharides that contribute to maintain intestinal homeostasis and regulate interactions between microbiota and host immune system. Recent results revealed that low birth weight piglet (LBWP) with poor weight gain during the first two weeks of life develop different intestinal microbiota and immune response profiles compared to high BWP (HBWP) littermates. Consequently, piglets within litters may have different resilience to infections after weaning and benefit from feed additives in a specific manner. A study has been performed to evaluate the potential of bovine colostrum extract (BC) as replacement to plasma proteins for improving gut health and resilience to Salmonella infection in piglets. Results revealed that in weaned piglets fed BC, intestinal microbiota was differently modulated and bacterial dysbiosis induced by Salmonella was restored faster. Moreover, expression of genes involved in innate immunity such as β-defensin-2 and glutathione peroxidase-2 was respectively down- and up-regulated in BC fed piglets. A combination of dietary supplementation with BC, cupper and vitamins A and D has also been tested in LBWP and HBWP, and there is clear evidence that BC in combination with other feed additives promote growth and gut health in both LBWP and HBWP. The porcine intestinal epithelial cell line IPEC-J2 was used to better understand the functional properties of BC. Results indicated that BC improves wound healing, enhances barrier function and modulates the expression of several genes involved in innate immune response. Finally, as microbial intervention, the potential of fecal transplantation to modulate intestinal microbiota and immune system development of piglets is under investigation and will be discussed.


Author(s):  
Tanvir Bamra ◽  
Taj Shafi ◽  
Sushmita Das ◽  
Manjay Kumar ◽  
Manas Ranjan Dikhit ◽  
...  

Summary StatementLeishmania secretes over 151 proteins during in vitro cultivation. Cellular functions of one such novel protein: mevalonate kinase is discussed here; signifying its importance in Leishmania infection.Visceral Leishmaniasis is a persistent infection, caused by Leishmania donovani in Indian subcontinent. This persistence is partly due to phagocytosis and evasion of host immune response. The underlying mechanism involves secretory proteins of Leishmania parasite; however, related studies are meagre. We have identified a novel secretory Leishmania donovani glycoprotein, Mevalonate kinase (MVK), and shown its importance in parasite internalization and immuno-modulation. In our studies, MVK was found to be secreted maximum after 1 h temperature stress at 37°C. Its secretion was increased by 6.5-fold in phagolysosome-like condition (pH ~5.5, 37°C) than at pH ~7.4 and 25°C. Treatment with MVK modulated host immune system by inducing interleukin-10 and interleukin-4 secretion, suppressing host’s ability to kill the parasite. Peripheral blood mononuclear cell (PBMC)-derived macrophages infected with mevalonate kinase-overexpressing parasites showed an increase in intracellular parasite burden in comparison to infection with vector control parasites. Mechanism behind the increase in phagocytosis and immunosuppression was found to be phosphorylation of mitogen-activated protein (MAP) kinase pathway protein, Extracellular signal-regulated kinases-1/2, and actin scaffold protein, cortactin. Thus, we conclude that Leishmania donovani Mevalonate kinase aids in parasite engulfment and subvert the immune system by interfering with signal transduction pathways in host cells, which causes suppression of the protective response and facilitates their persistence in the host. Our work elucidates the involvement of Leishmania in the process of phagocytosis which is thought to be dependent largely on macrophages and contributes towards better understanding of host pathogen interactions.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Monica C. Gestal ◽  
Laura K. Howard ◽  
Kalyan Dewan ◽  
Hannah M. Johnson ◽  
Mariette Barbier ◽  
...  

AbstractWell-adapted pathogens must evade clearance by the host immune system and the study of how they do this has revealed myriad complex strategies and mechanisms. Classical bordetellae are very closely related subspecies that are known to modulate adaptive immunity in a variety of ways, permitting them to either persist for life or repeatedly infect the same host. Exploring the hypothesis that exposure to immune cells would cause bordetellae to induce expression of important immunomodulatory mechanisms, we identified a putative regulator of an immunomodulatory pathway. The deletion of btrS in B. bronchiseptica did not affect colonization or initial growth in the respiratory tract of mice, its natural host, but did increase activation of the inflammasome pathway, and recruitment of inflammatory cells. The mutant lacking btrS recruited many more B and T cells into the lungs, where they rapidly formed highly organized and distinctive Bronchial Associated Lymphoid Tissue (BALT) not induced by any wild type Bordetella species, and a much more rapid and strong antibody response than observed with any of these species. Immunity induced by the mutant was measurably more robust in all respiratory organs, providing completely sterilizing immunity that protected against challenge infections for many months. Moreover, the mutant induced sterilizing immunity against infection with other classical bordetellae, including B. pertussis and B. parapertussis, something the current vaccines do not provide. These findings reveal profound immunomodulation by bordetellae and demonstrate that by disrupting it much more robust protective immunity can be generated, providing a pathway to greatly improve vaccines and preventive treatments against these important pathogens.


2011 ◽  
Vol 73 (3) ◽  
pp. 171-175 ◽  
Author(s):  
Janet De Souza-Hart

Podcasts (digital audio files) can be utilized creatively to supplement classroom learning. They can be both easily created by instructors and conveniently accessed by students. Students are very receptive to the use of this type of technology as a way to reinforce conceptual understanding of course material. An activity combining a podcast with an active-learning worksheet references the literary classic "The Lord of the Rings" as an analogy to help students understand the many proteins, cells, and processes involved in the human immune response. This activity has helped a significant number of students improve their understanding of this subject.


2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Serena Delbue ◽  
Manola Comar ◽  
Pasquale Ferrante

The polyomaviruses are small DNA viruses that can establish latency in the human host. The name polyomavirus is derived from the Greek rootspoly-, which means “many,” and -oma, which means “tumours.” These viruses were originally isolated in mouse (mPyV) and in monkey (SV40). In 1971, the first human polyomaviruses BK and JC were isolated and subsequently demonstrated to be ubiquitous in the human population. To date, at least nine members of thePolyomaviridaefamily have been identified, some of them playing an etiological role in malignancies in immunosuppressed patients. Here, we describe the biology of human polyomaviruses, their nonmalignant and malignant potentials ability, and their relationship with the host immune response.


2016 ◽  
Vol 29 (8) ◽  
pp. 595-598 ◽  
Author(s):  
Yuri Miyashita ◽  
Go Atsumi ◽  
Kenji S. Nakahara

Plants recognize viral infection via an immune receptor, i.e., nucleotide-binding site (NB)-leucine-rich repeat (LRR) proteins. Another immune receptor, receptor-like kinase proteins, which share an LRR domain with NB-LRRs, perceive conserved molecules of pathogens called pathogen- or microbe-associated molecular patterns, but NB-LRRs generally perceive particular viral proteins. As viruses can evolve more rapidly than the host immune system, how do plant immune systems, which rely on the perception of proteins, remain effective? Viral adaptive evolution may be controlled by penalties that result from mutations in viral proteins that are perceived by NB-LRRs. Our recent studies in pea (Pisum sativum) suggest a penalty of increased susceptibility to another immune system. When a viral protein mutates to evade one immune system, the virus with the mutated protein becomes more susceptible to another. Such antagonistic pleiotropy of a viral protein by two independent plant immune systems may have precedents. Plants may rely on pairs of immune systems to constrain adaptive evolution by viruses and thereby maintain durable antiviral immunity.


mBio ◽  
2018 ◽  
Vol 9 (2) ◽  
Author(s):  
Boo Shan Tseng ◽  
Courtney Reichhardt ◽  
Gennifer E. Merrihew ◽  
Sophia A. Araujo-Hernandez ◽  
Joe J. Harrison ◽  
...  

ABSTRACTPseudomonas aeruginosaproduces an extracellular biofilm matrix that consists of nucleic acids, exopolysaccharides, lipid vesicles, and proteins. In general, the protein component of the biofilm matrix is poorly defined and understudied relative to the other major matrix constituents. While matrix proteins have been suggested to provide many functions to the biofilm, only proteins that play a structural role have been characterized thus far. Here we identify proteins enriched in the matrix ofP. aeruginosabiofilms. We then focused on a candidate matrix protein, the serine protease inhibitor ecotin (PA2755). This protein is able to inhibit neutrophil elastase, a bactericidal enzyme produced by the host immune system duringP. aeruginosabiofilm infections. We show that ecotin binds to the key biofilm matrix exopolysaccharide Psl and that it can inhibit neutrophil elastase when associated with Psl. Finally, we show that ecotin protects both planktonic and biofilmP. aeruginosacells from neutrophil elastase-mediated killing. This may represent a novel mechanism of protection for biofilms to increase their tolerance against the innate immune response.IMPORTANCEProteins associated with the extracellular matrix of bacterial aggregates called biofilms have long been suggested to provide many important functions to the community. To date, however, only proteins that provide structural roles have been described, and few matrix-associated proteins have been identified. We developed a method to identify matrix proteins and characterized one. We show that this protein, when associated with the biofilm matrix, can inhibit a bactericidal enzyme produced by the immune system during infection and protect biofilm cells from death induced by the enzyme. This may represent a novel mechanism of protection for biofilms, further increasing their tolerance against the immune response. Together, our results are the first to show a nonstructural function for a confirmed matrix-interacting protein.


mBio ◽  
2015 ◽  
Vol 6 (3) ◽  
Author(s):  
Philipp Engel ◽  
Kelsey D. Bartlett ◽  
Nancy A. Moran

ABSTRACT Honeybees harbor well-defined bacterial communities in their guts. The major members of these communities appear to benefit the host, but little is known about how they interact with the host and specifically how they interface with the host immune system. In the pylorus, a short region between the midgut and hindgut, honeybees frequently exhibit scab-like structures on the epithelial gut surface. These structures are reminiscent of a melanization response of the insect immune system. Despite the wide distribution of this phenotype in honeybee populations, its cause has remained elusive. Here, we show that the presence of a common member of the bee gut microbiota, the gammaproteobacterium Frischella perrara, correlates with the appearance of the scab phenotype. Bacterial colonization precedes scab formation, and F. perrara specifically localizes to the melanized regions of the host epithelium. Under controlled laboratory conditions, we demonstrate that exposure of microbiota-free bees to F. perrara but not to other bacteria results in scab formation. This shows that F. perrara can become established in a spatially restricted niche in the gut and triggers a morphological change of the epithelial surface, potentially due to a host immune response. As an intermittent colonizer, this bacterium holds promise for addressing questions of community invasion in a simple yet relevant model system. Moreover, our results show that gut symbionts of bees engage in differential host interactions that are likely to affect gut homeostasis. Future studies should focus on how these different gut bacteria impact honeybee health. IMPORTANCE As pollinators, honeybees are key species for agricultural and natural ecosystems. Their guts harbor simple communities composed of characteristic bacterial species. Because of these features, bees are ideal systems for studying fundamental aspects of gut microbiota-host interactions. However, little is known about how these bacteria interact with their host. Here, we show that a common member of the bee gut microbiota causes the formation of a scab-like structure on the gut epithelium of its host. This phenotype was first described in 1946, but since then it has not been much further characterized, despite being found in bee populations worldwide. The scab phenotype is reminiscent of melanization, a conserved innate immune response of insects. Our results show that high abundance of one member of the bee gut microbiota triggers this specific phenotype, suggesting that the gut microbiota composition can affect the immune status of this key pollinator species.


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