Academic literature on the topic 'COMMENSAL VIRUS'

Abstract The diverse commensal ecosystem present in the mammalian intestine requires the host immune system to maintain a tolerogenic environment. The virome is an understudied component of the microbiota which promotes intestinal homeostasis and protection from injury, but the host mechanisms that regulate tolerance to viral commensals are poorly described. The antiviral signal transducer STAT1 has previously been shown to mediate tolerance to systemic viral pathogens by suppressing adaptive immune responses and protecting the host from immunopathology, but we sought to characterize its role in the context of a commensal intestinal viral infection. We used a persistent strain of murine norovirus (MNV CR6) to interrogate host mechanisms of viral tolerance and commensalism, as CR6 has previously been shown to promote intestinal homeostasis. While CR6 infections of wildtype mice were asymptomatic and limited to the colon, STAT1-deficient mice exhibited virus-induced weight loss and mortality accompanied by systemic viral spread, colonic bacterial dysbiosis, CD4+ T cell dysfunction and hyperaccumulation of CD8+ T cells. However, clinical manifestation of virus-induced disease in STAT1-deficient mice was independent of T cells and the bacterial microbiota. Instead, therapeutic control of viral replication was sufficient to prevent virus-induced disease despite ongoing T cell dysregulation. Collectively, our data indicate that STAT1 maintains tolerance to a viral component of the intestinal microbiota by control of viral replication rather than immunopathology, suggesting that STAT1 uses distinct strategies to tolerate pathogenic and commensal viruses.

Streptococcus pneumoniaecommonly inhabits the nasopharynx as a member of the commensal biofilm. Infection with respiratory viruses, such as influenza A virus, induces commensalS. pneumoniaeto disseminate beyond the nasopharynx and to elicit severe infections of the middle ears, lungs, and blood that are associated with high rates of morbidity and mortality. Current preventive strategies, including the polysaccharide conjugate vaccines, aim to eliminate asymptomatic carriage with vaccine-type pneumococci. However, this has resulted in serotype replacement with, so far, less fit pneumococcal strains, which has changed the nasopharyngeal flora, opening the niche for entry of other virulent pathogens (e.g.,Streptococcus pyogenes,Staphylococcus aureus, and potentiallyHaemophilus influenzae). The long-term effects of these changes are unknown. Here, we present an attractive, alternative preventive approach where we subvert virus-induced pneumococcal disease without interfering with commensal colonization, thus specifically targeting disease-causing organisms. In that regard, pneumococcal surface protein A (PspA), a major surface protein of pneumococci, is a promising vaccine target. Intradermal (i.d.) immunization of mice with recombinant PspA in combination with LT-IIb(T13I), a novel i.d. adjuvant of the type II heat-labile enterotoxin family, elicited strong systemic PspA-specific IgG responses without inducing mucosal anti-PspA IgA responses. This response protected mice from otitis media, pneumonia, and septicemia and averted the cytokine storm associated with septic infection but had no effect on asymptomatic colonization. Our results firmly demonstrated that this immunization strategy against virally induced pneumococcal disease can be conferred without disturbing the desirable preexisting commensal colonization of the nasopharynx.

Topicality: The chronic nasopharyngitis (CNP) morbidity rate tends to increase in childhood and adenoid removal is one of the most common of all surgeries in children. The state of the nasopharyngeal microbiome plays the significant role in the development of inflammatory processes of nasopharynx and adenoid hypertrophy and it is considered that the great progress can be made through its correction in conservative treatment and prevention of recurrence after surgery. Traditional cultural studies which reflect only a small proportion of bacteria present in the nasopharynx cannot describe the real state of microbiome. Therefore, the study of its quantitative and qualitative composit ion is essent ial for justified treatment. Aim: to examine the state of the nasopharyngeal microbiome in patients with CNP associated with EpsteinBarr virus and compare its characteristics with the severity of disease. Material and methods: 20 healthy persons and 32 patients diagnosed with CNP associated with EpsteinBarr virus have been included in the study. The qualitative composition of nasopharyngeal microflora and its quantitative characteristics have been studied by determining t itres of colony-forming units (CFU). The findings have been compared with the features of the clinical course of disease. Results: The healthy individuals of the control group have Lactobacillus spp. and Bifidobacterium spp., aerobic S. salivarius, which belong to commensal microorganisms, as the basis of the nasopharyngeal microbiome. There has been seen the preservation of the population level of commensal flora: lactobacilli, bifidobacteria, salivary streptococci and appearance of opportunistic flora (Staphylococcus aureus, Staphylococcus epidermidis, Streptococcus pyogenes, Escherichia coli) in small titres in the patients with mild CNP. During the moderate/severe course, there has been observed a sharp decline in the population level of commensal flora and an increase in the titer of opportunistic flora to the population level of commensals. In severe cases, the preservation of high titers of opportunistic flora, complete absence of commensal one and emergence of pathogenic microflora (Pneumococcus pneumoniae, Haemophilus influenzae, Pseudomonas aeruginosa and yeast-like fungi of the Candida type) can be seen. All patients have been observed the presence of microbiome disorders, regardless of its quantitative and qualitative changes, which are accompanied by hypertrophy of the pharyngeal tonsil. Conclusions: Dysfunction of the microbiome, i.e. changes in the quantitative and qualitative composition of microorganisms in patients with CNP, is important in the course of disease. Minor changes that are determined by a reduced level of commensal flora are associated with the mild disease course. If there is a significant reduction in the levels of commensals and emergence of opportunistic flora, the moderate/severe disease course can be observed. The complete absence of commensal flora, high titers of opportunistic pathogens and emergence of pathogenic flora including Candida albicans are characterized by a severe disease course.

Over the past two decades, there has been tremendous progress in understanding the impact of the intestinal microbiota on mammalian metabolism, physiology, and immune development and function. There has also been substantial advancement in elucidating the interplay between commensal and pathogenic bacteria. Relatively more recently, researchers have begun to investigate the effect of the intestinal microbiota on viral pathogenesis. Indeed, a growing body of literature has reported that commensal bacteria within the mammalian intestinal tract enhance enteric virus infections through a variety of mechanisms. Commensal bacteria or bacterial glycans can increase the stability of enteric viruses, enhance virus binding to host receptors, modulate host immune responses in a proviral manner, expand the numbers of host cell targets, and facilitate viral recombination. In this review, we will summarize the current literature exploring these effects of the intestinal microbiota on enteric virus infections.

Viral infections are influenced by various microorganisms in the environment surrounding the target tissue, and the correlation between the type and balance of commensal microbiota is the key to establishment of the infection and pathogenicity. Some commensal microorganisms are known to resist or promote viral infection, while others are involved in pathogenicity. It is also becoming evident that the profile of the commensal microbiota under normal conditions influences the progression of viral diseases. Thus, to understand the pathogenesis underlying viral infections, it is important to elucidate the interactions among viruses, target tissues, and the surrounding environment, including the commensal microbiota, which should have different relationships with each virus. In this review, we outline the role of microorganisms in viral infections. Particularly, we focus on gaining an in-depth understanding of the correlations among viral infections, target tissues, and the surrounding environment, including the commensal microbiota and the gut virome, and discussing the impact of changes in the microbiota (dysbiosis) on the pathological progression of viral infections.

The presence of commensal bacteria enhances both acute and persistent infection of murine noroviruses. For several enteric viral pathogens, mechanisms by which these bacteria enhance infection involve direct interactions between the virus and bacteria. While it has been demonstrated that human noroviruses bind to a variety of commensal bacteria, it is not known if this is also true for murine noroviruses. The goal of this study was to characterize interactions between murine noroviruses and commensal bacteria and determine the impact of bacterial growth conditions, incubation temperature and time, on murine norovirus attachment to microbes that comprise the mammalian microbiome. We show that murine noroviruses bind directly to commensal bacteria and show similar patterns of attachment as human norovirus VLPs examined under the same conditions. Furthermore, while binding levels are not impacted by the growth phase of the bacteria, they do change with time and incubation temperature. We also found that murine norovirus can bind to a commensal fungal species, Candida albicans.

Abstract Alterations in the composition of intestinal commensal bacteria in humans are associated with enhanced susceptibility to multiple inflammatory diseases suggesting that signals derived from commensal bacteria may influence the development and/or function of the immune system. Supporting this, germ-free or gnotobiotic mice exhibit reduced numbers of lymphocytes in the intestinal intraepithelial compartment. However, whether alterations in the acquisition or composition of commensal bacteria influence immunity to infection remains poorly defined. To test this, mice housed under conventional or gnotobiotic conditions were infected i.p. with Lymphocytic Choriomeningitis Virus (LCMV). At day 7 post-infection, gnotobiotic mice exhibited a significant reduction in the frequency and number of LCMV-specific CD8+ T cells in multiple tissues including the spleen and intraepithelial compartment. Furthermore, LCMV-specific CD8+ T cells from gnotobiotic mice were less capable of producing IFN-γ following LCMV peptide stimulation. In addition, at day 36 post-infection, when conventionally-housed mice have established a LCMV-specific CD8+ memory T cell population, gnotobiotic mice had a significantly impaired population of LCMV-specific CD8+ memory T cells. Diminished LCMV-specific CD8+ effector and memory T cell responses were not the result of inherent defects in gnotobiotic mice as oral administration of a cocktail of antibiotics to conventionally-housed mice also displayed a defective LCMV-specific CD8+ T cell response following infection. Collectively, these data suggest an integral role of commensal bacteria in influencing virus specific CD8+ T cell effector and memory responses.

The prevalence and epidemiology of autoimmune diseases in developed, as well as in developing countries have increased over the past decade. The human body consists of trillions of microorganisms and the composition is unique to each individual. It consists of commensal as well as pathogenic viruses. The interactions between host-microbiota helps to regulate immune system. However, there are many factors that can alter the interactions which ultimately leads to dysbiosis. Dysbiosis can lead to development of autoimmune diseases along with other complex diseases. Viruses are obligate intracellular parasites. Commensal viruses is a new concept because there can be some viruses which may not be detrimental to human body. However, sometimes autoimmune reactions are generated as a result of cross-reactivity of epitopes of virus with autoantigens of humans. This study aims, to find various commensal viruses found in human body, to predict potential epitopes in viruses, sequence homology with autoantigens of humans and to check binding energy of viral epitopes with MHC class I and T-cell receptor. This will help us to develop new preventive and therapeutic strategies.

Le tractus intestinal humain abrite un groupe très diversifié de microorganismes commensaux qui jouent un rôle important dans l’homéostasie et la santé de l’intestin. Ce microbiote intestinal est essentiel au bon développement du système immunitaire de l’hôte, au métabolisme normal de l’intestin, à l’absorption des nutriments, à la protection contre les espèces bactériennes envahissantes et au maintien d’une physiologie intestinale normale.