Статті в журналах: "COMMENSAL VIRUS"

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Sharon, Andrew J., Heather A. Filyk, Nicolette M. Fonseca, Rachel L. Simister, Wallace Yuen, Blair K. Hardman, Hannah G. Robinson, et al. "STAT1-dependent tolerance of intestinal viral infection." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 249.11. http://dx.doi.org/10.4049/jimmunol.204.supp.249.11.

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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.

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Greene, Christopher J., Laura R. Marks, John C. Hu, Ryan Reddinger, Lorrie Mandell, Hazeline Roche-Hakansson, Natalie D. King-Lyons, Terry D. Connell, and Anders P. Hakansson. "Novel Strategy To Protect against Influenza Virus-Induced Pneumococcal Disease without Interfering with Commensal Colonization." Infection and Immunity 84, no. 6 (March 21, 2016): 1693–703. http://dx.doi.org/10.1128/iai.01478-15.

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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.

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Flotte, Terence R., and Kenneth I. Berns. "Adeno-Associated Virus: A Ubiquitous Commensal of Mammals." Human Gene Therapy 16, no. 4 (April 2005): 401–7. http://dx.doi.org/10.1089/hum.2005.16.401.

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Leta, Oleksii I., and Ivanna V. Koshel. "The state of the nasopharyngeal microbiome in healthy people and in patients with chronic nasopharyngitis." OTORHINOLARYNGOLOGY, No6(5) 2022 (January 30, 2023): 57–65. http://dx.doi.org/10.37219/2528-8253-2022-6-57.

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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.

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Roth, Alexa N., Katrina R. Grau, and Stephanie M. Karst. "Diverse Mechanisms Underlie Enhancement of Enteric Viruses by the Mammalian Intestinal Microbiota." Viruses 11, no. 8 (August 17, 2019): 760. http://dx.doi.org/10.3390/v11080760.

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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.

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Stefan, Kailyn L., Myoungjoo V. Kim, Akiko Iwasaki, and Dennis L. Kasper. "Commensal Microbiota Modulation of Natural Resistance to Virus Infection." Cell 183, no. 5 (November 2020): 1312–24. http://dx.doi.org/10.1016/j.cell.2020.10.047.

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Griffiths, Paul. "Time to consider the concept of a commensal virus?" Reviews in Medical Virology 9, no. 2 (April 1999): 73–74. http://dx.doi.org/10.1002/(sici)1099-1654(199904/06)9:2<73::aid-rmv254>3.0.co;2-5.

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Mizutani, Taketoshi, Aya Ishizaka, Michiko Koga, Takeya Tsutsumi, and Hiroshi Yotsuyanagi. "Role of Microbiota in Viral Infections and Pathological Progression." Viruses 14, no. 5 (May 1, 2022): 950. http://dx.doi.org/10.3390/v14050950.

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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.

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Madrigal, Jasmine L., Sutonuka Bhar, Samantha Hackett, Haley Engelken, Ross Joseph, Nemat O. Keyhani, and Melissa K. Jones. "Attach Me If You Can: Murine Norovirus Binds to Commensal Bacteria and Fungi." Viruses 12, no. 7 (July 14, 2020): 759. http://dx.doi.org/10.3390/v12070759.

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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.

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Abt, Michael C., Daniel Beiting, Dymtro Kobuley, Yimin Yu, Colby Zaph, John Wherry, and David Artis. "The influence of commensal bacteria on anti-viral immunity (39.26)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 39.26. http://dx.doi.org/10.4049/jimmunol.182.supp.39.26.

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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.

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Cadwell, Ken. "Expanding the Role of the Virome: Commensalism in the Gut." Journal of Virology 89, no. 4 (December 10, 2014): 1951–53. http://dx.doi.org/10.1128/jvi.02966-14.

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Viruses affect host physiology beyond causing acute disease, thereby giving rise to the concept that the virome is a component of the microbiome. However, the role of the enteric virome is understudied relative to the fast-paced research examining commensal bacteria in the intestine. In this article, I discuss our recent work on murine norovirus indicating that an animal virus in the intestine can provide many of the signals to the host that have been attributed to commensal bacteria. Our findings suggest that the surge in microbiome research should incorporate examination of the enteric virome.

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Ortiz Moyano, Ramiro, Fernanda Raya Tonetti, Mikado Tomokiyo, Paulraj Kanmani, María Guadalupe Vizoso-Pinto, Hojun Kim, Sandra Quilodrán-Vega, et al. "The Ability of Respiratory Commensal Bacteria to Beneficially Modulate the Lung Innate Immune Response Is a Strain Dependent Characteristic." Microorganisms 8, no. 5 (May 13, 2020): 727. http://dx.doi.org/10.3390/microorganisms8050727.

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We investigated whether the ability of commensal respiratory bacteria to modulate the innate immune response against bacterial and viral pathogens was a shared or strain-specific characteristic. Bacterial strains belonging to the Corynebacterium pseudodiphtheriticum and Dolosigranulum pigrum species were compared by studying their influence in the Toll-like receptor (TLR)-2- and TLR3-triggered immune responses in the respiratory tract, as well as in the resistance to Respiratory Syncytial Virus (RSV) and Streptococcus pneumoniae infections. We demonstrated that nasally administered C. pseudodiphteriticum 090104 or D. pigrum 040417 were able to modulate respiratory immunity and increase the resistance against pathogens, while other strains of the same species did not influence the respiratory immune responses, demonstrating a clear strain-dependent immunomodulatory effect of respiratory commensal bacteria. We also reported here that bacterium-like particles (BLP) and cell walls derived from immunomodulatory respiratory commensal bacteria are an interesting alternative for the modulation of the respiratory immune system. Our study is a step forward in the positioning of certain strains of respiratory commensal bacteria as next-generation probiotics for the respiratory tract.

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Kernbauer, Elisabeth, Yi Ding, and Ken Cadwell. "An enteric virus can replace the beneficial function of commensal bacteria." Nature 516, no. 7529 (November 19, 2014): 94–98. http://dx.doi.org/10.1038/nature13960.

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Popovych, Vasyl І., Oleksii І. Leta, and Ivanna V. Koshel. "The Rehabilitation of the Nasopharyngeal Microbiome in Patients with Chronic Nasopharyngitis." Acta Balneologica 64, no. 4 (2022): 337–41. http://dx.doi.org/10.36740/abal202204111.

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Aim: To evaluate the effect of immunorehabilitation therapy of CNP associated with Epstein-Barr virus on the nasopharyngeal microbiome changes and related to them indications for surgery. Materials and Methods: 20 healthy individuals and 32 patients diagnosed with CNP associated with Epstein-Barr virus were included in the study. The qualitative composition of microbiome and its quantitative characteristics were studied during the course of immunorehabilitation therapy with the phytoextract BNO 1030. The findings were compared with the features of the course of disease and existence of indications for surgical treatment. Results: In patients with indications for adenotomy, a nasopharyngeal dysbiosis was formed through elimination of commensal bacteria and contamination of nasopharynx with opportunistic and pathogenic bacteria, Candida fungi. The immunorehabilitation therapy helped 75% patients gain a pronounced clinical response and refuse operative treatment. The qualitative and quantitative composition of commensal flora, reduction in the rate of opportunistic flora and elimination of pathogenic and fungal flora were observed in such patients. In 25% patients with poor therapeutic efficacy and indications for adenotomy against the background of elimination of pathogenic and fungal flora, the level of commensal and opportunistic flora of nasopharynx remained unchanged. Conclusions: The immunorehabilitation helps 75% patients normalize the microbiome of nasopharynx, improve the clinical symptomatology and cancel the indications for surgical treatment.

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Oh, Ji Eun, Byoung-Chan Kim, Dong-Ho Chang, Meehyang Kwon, Sun Young Lee, Dukjin Kang, Jin Young Kim, et al. "Dysbiosis-induced IL-33 contributes to impaired antiviral immunity in the genital mucosa." Proceedings of the National Academy of Sciences 113, no. 6 (January 25, 2016): E762—E771. http://dx.doi.org/10.1073/pnas.1518589113.

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Commensal microbiota are well known to play an important role in antiviral immunity by providing immune inductive signals; however, the consequence of dysbiosis on antiviral immunity remains unclear. We demonstrate that dysbiosis caused by oral antibiotic treatment directly impairs antiviral immunity following viral infection of the vaginal mucosa. Antibiotic-treated mice succumbed to mucosal herpes simplex virus type 2 infection more rapidly than water-fed mice, and also showed delayed viral clearance at the site of infection. However, innate immune responses, including type I IFN and proinflammatory cytokine production at infection sites, as well as induction of virus-specific CD4 and CD8 T-cell responses in draining lymph nodes, were not impaired in antibiotic-treated mice. By screening the factors controlling antiviral immunity, we found that IL-33, an alarmin released in response to tissue damage, was secreted from vaginal epithelium after the depletion of commensal microbiota. This cytokine suppresses local antiviral immunity by blocking the migration of effector T cells to the vaginal tissue, thereby inhibiting the production of IFN-γ, a critical cytokine for antiviral defense, at local infection sites. These findings provide insight into the mechanisms of homeostasis maintained by commensal bacteria, and reveal a deleterious consequence of dysbiosis in antiviral immune defense.

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Lee, Heung Kyu, and Ji Eun Oh. "Dysbiosis-induced IL-33 contributes to impaired antiviral immunity in the genital mucosa." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 67.18. http://dx.doi.org/10.4049/jimmunol.196.supp.67.18.

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Abstract Commensal microbiota are considered to play an important role in antiviral immunity. However, the consequence of dysbiosis on antiviral immunity remains unclear. We demonstrate that dysbiosis caused by oral antibiotics directly impairs antiviral immunity following viral infection of the vaginal mucosa. Antibiotic-treated mice succumbed to mucosal herpes simplex virus type 2 infection more rapidly than water-fed mice. The susceptibility of antibiotic-treated mice was attributed to compromised effector T cell responses rather than defects in innate immunity. By screening the factors controlling antiviral immunity, we found that interleukin-33 was secreted from vaginal epithelium after the depletion of commensal microbiota. This cytokine suppresses local antiviral immunity by blocking the migration of effector T cells to the vaginal tissue, thereby inhibiting the production of interferon-γ at local infection sites. These findings provide insight into the mechanisms of homeostasis maintained by commensal bacteria, and reveal a deleterious consequence of dysbiosis in antiviral immune defense.

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Sanchez, Luzmariel Medina, Yanlin Zeng, Magdalena Siller, Pamela H. Brigleb, Kishan A. Sangani, Terence S. Dermody, Bana Jabri, Elena F. Verdu, Marlies Meisel, and Reinhard Hinterleitner. "A gut commensal protist protects against virus-mediated loss of oral tolerance." Journal of Immunology 210, no. 1_Supplement (May 1, 2023): 82.22. http://dx.doi.org/10.4049/jimmunol.210.supp.82.22.

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Abstract Loss of oral tolerance (LOT) to gluten, characterized by a T helper 1 (Th1) gluten-specific immune response, is a hallmark of celiac disease (CeD) and can be triggered by enteric viral infections. We hypothesized that certain gut microbes have the capacity to protect against virus-mediated LOT. By using our previously defined reovirus-mediated LOT CeD model, we discovered that the gut colonizing protist Tritrichomonas promotes oral tolerance and protects against reovirus-mediated LOT by suppressing the reovirus-induced proinflammatory program of dietary-antigen-presenting CD103+ dendritic cells. Importantly, Tritrichomonas-mediated protection against T1L-induced LOT is not attributable to differences in antiviral host responses and is independent of the microbiota. Mechanistically, we show that Tritrichomonas colonization restrains reovirus-induced inflammatory responses in dendritic cells and thus limit their ability to promote Th1 immune responses. Finally, our studies using human stool samples support a role for Tritrichomonas sp. colonization in protecting against development of CeD. Supported by grants from NIH (T32 AI089443)

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Vargas, Kaaren, Shawn A. Messer, Michael Pfaller, Shawn R. Lockhart, Jack T. Stapleton, John Hellstein, and David R. Soll. "Elevated Phenotypic Switching and Drug Resistance ofCandida albicans from Human Immunodeficiency Virus-Positive Individuals prior to First Thrush Episode." Journal of Clinical Microbiology 38, no. 10 (2000): 3595–607. http://dx.doi.org/10.1128/jcm.38.10.3595-3607.2000.

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Strains of Candida albicans obtained from human immunodeficiency virus (HIV)-positive individuals prior to their first episode of oral thrush were already in a high-frequency mode of switching and were far more resistant to a number of antifungal drugs than commensal isolates from healthy individuals. Switching in these isolates also had profound effects both on susceptibility to antifungal drugs and on the levels of secreted proteinase activity. These results suggest that commensal strains colonizing HIV-positive individuals either undergo phenotypic alterations or are replaced prior to the first episode of oral thrush. They also support the suggestion that high-frequency phenotypic switching functions as a higher-order virulence trait, spontaneously generating in colonizing populations variants with alterations in a variety of specific virulence traits.

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Peterson, Anna C., Himanshu Sharma, Arvind Kumar, Bruno M. Ghersi, Scott J. Emrich, Kurt J. Vandegrift, Amit Kapoor, and Michael J. Blum. "Rodent Virus Diversity and Differentiation across Post-Katrina New Orleans." Sustainability 13, no. 14 (July 19, 2021): 8034. http://dx.doi.org/10.3390/su13148034.

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Concern about elevated disease risk following disasters has been growing with the progression of global trends in urbanization and climate, in part because shifts in socioecological conditions can promote greater human contact with pathogen reservoirs in cities. Remarkably little is known, however, about the diversity and distributions of pathogens carried by commensal reservoirs across disaster-affected urban landscapes. To address this deficit, we characterized the assemblage structure of viruses in the serum of three widespread commensal rodents (Rattus norvegicus, Rattus rattus, and Mus musculus) that were trapped in New Orleans (LA, USA) following Hurricane Katrina. We assessed virus diversity and differentiation according to host species identity, co-occurrence and abundance, as well as prevailing landscape features known to shape urban rodent assemblages. We detected ≥34 viruses in total, including several pathogens of concern, through metagenomic analysis of serum taken from ≥149 individuals of each host species. We found that virus richness as well as assemblage composition and spatial differentiation differed by host species. Notably, we detected associations with host species co-occurrence and abundance, and while we found that assemblage structure varied by study area, we did not detect strong associations with landscape features known to influence rodent hosts. Evidence that virus diversity and assemblage structure reflect host identity more so than other factors indicates that biotic benchmarks might serve as prognostic indicators of post-disaster pathogen exposure risk in cities worldwide.

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Spring, Jessica, Vera Beilinson, Brian C. DeFelice, Juan M. Sanchez, Michael Fischbach, Alexander Chervonsky, and Tatyana Golovkina. "Retroviral Infection and Commensal Bacteria Dependently Alter the Metabolomic Profile in a Sterile Organ." Viruses 15, no. 2 (January 29, 2023): 386. http://dx.doi.org/10.3390/v15020386.

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Both viruses and bacteria produce “pathogen associated molecular patterns” that may affect microbial pathogenesis and anti-microbial responses. Additionally, bacteria produce metabolites, while viruses could change the metabolic profiles of the infected cells. Here, we used an unbiased metabolomics approach to profile metabolites in spleens and blood of murine leukemia virus-infected mice monocolonized with Lactobacillus murinus to show that viral infection significantly changes the metabolite profile of monocolonized mice. We hypothesize that these changes could contribute to viral pathogenesis or to the host response against the virus and thus open a new avenue for future investigations.

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Kaczorowska, Joanna, and Lia van der Hoek. "Human anelloviruses: diverse, omnipresent and commensal members of the virome." FEMS Microbiology Reviews 44, no. 3 (March 19, 2020): 305–13. http://dx.doi.org/10.1093/femsre/fuaa007.

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ABSTRACT Anelloviruses are small, single stranded circular DNA viruses. They are extremely diverse and have not been associated with any disease so far. Strikingly, these small entities infect most probably the complete human population, and there are no convincing examples demonstrating viral clearance from infected individuals. The main transmission could be via fecal-oral or airway route, as infections occur at an early age. However, due to the lack of an appropriate culture system, the virus–host interactions remain enigmatic. Anelloviruses are obviously mysterious viruses, and their impact on human life is not yet known, but, with no evidence of a disease association, a potential beneficial effect on human health should also be investigated.

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Dupinay, Tatiana, Kieran C. Pounder, Florence Ayral, Maria-Halima Laaberki, Denise A. Marston, Sandra Lacôte, Catherine Rey, et al. "Detection and genetic characterization of Seoul Virus from commensal brown rats in France." Virology Journal 11, no. 1 (2014): 32. http://dx.doi.org/10.1186/1743-422x-11-32.

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Yitbarek, A., T. Alkie, K. Taha-Abdelaziz, J. Astill, J. C. Rodriguez-Lecompte, J. Parkinson, É. Nagy, and S. Sharif. "Gut microbiota modulates type I interferon and antibody-mediated immune responses in chickens infected with influenza virus subtype H9N2." Beneficial Microbes 9, no. 3 (April 25, 2018): 417–27. http://dx.doi.org/10.3920/bm2017.0088.

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Commensal gut microbes play a critical role in shaping host defences against pathogens, including influenza viruses. The current study was conducted to assess the role and mechanisms of action of commensal gut microbiota on the innate and antibody-mediated responses of layer chickens against influenza virus subtype H9N2. A total of 104 one-day-old specific pathogen free chickens were assigned to either of the four treatments, which included two levels of antibiotics treatment (ABX- and ABX+) and two levels of H9N2 virus infection (H9N2- and H9N2+). At day 17 of age, chickens in the H9N2+ group were infected via the oral-nasal route with 400 μl of 107 TCID50/ml (200 μl/each route). Oropharyngeal and cloacal swabs at days 1, 3, 5, 7 and 9 post-infection (p.i.) for virus shedding, tissue samples at 12 h, 24 h and 36 h p.i. for mRNA measurement, and serum samples at days 7 and 14 p.i. for hemagglutination inhibition (HI) assay and IgG antibodies were collected. Virus shedding analysis showed that antibiotic treated (depleted)-H9N2 virus infected chickens showed a significantly higher oropharyngeal virus shedding at all time points, and cloacal shedding at days 3 and 5 p.i. compared to control treated (undepleted)-H9N2 infected chickens. Analysis of mRNA expression showed that infection of depleted chickens with H9N2 virus resulted in significantly down-regulated type I interferon responses both in the respiratory and gastrointestinal tracts compared to undepleted-H9N2 infected chickens. However, antibody-mediated immune response analysis showed a significantly higher HI antibody titre and IgG levels in the serum of chickens depleted with antibiotics and infected with H9N2 virus compared to undepleted-H9N2 infected chickens. In conclusion, findings from the current study suggest that the gut microbiota of chickens plays an important role in the initiation of innate responses against influenza virus infection, while the antibody-mediated immune response remains unaffected.

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Maggi, Fabrizio, Massimo Pifferi, Elena Tempestini, Claudia Fornai, Letizia Lanini, Elisabetta Andreoli, Marialinda Vatteroni, et al. "TT Virus Loads and Lymphocyte Subpopulations in Children with Acute Respiratory Diseases." Journal of Virology 77, no. 16 (August 15, 2003): 9081–83. http://dx.doi.org/10.1128/jvi.77.16.9081-9083.2003.

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ABSTRACT TT virus (TTV) produces chronic plasma viremia in around 90% of healthy individuals of all ages and has, therefore, been proposed as a commensal human virus. We recently demonstrated that in children hospitalized for acute respiratory diseases high TTV loads were associated with severe forms of disease. Here, we report that in such children TTV loads showed an inverse correlation with the percentage of circulating total T and helper T cells and a direct correlation with the percentage of B cells. Thus, florid TTV replication might contribute to lymphocyte imbalances and, possibly, immunosuppressive effects, thus resembling related animal viruses.

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Seehusen, Frauke, Julia Lienhard, Sabrina Polster, Julia Lechmann, Deborah Peltzer, Barbara Prähauser, and Claudia Bachofen. "Torque teno sus virus 1 and association with porcine diseases – new pathogen or commensal?" Journal of Comparative Pathology 203 (May 2023): 60. http://dx.doi.org/10.1016/j.jcpa.2023.03.068.

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Goettsch, Winfried, Niko Beerenwinkel, Li Deng, Lars Dölken, Bas E. Dutilh, Florian Erhard, Lars Kaderali, et al. "ITN—VIROINF: Understanding (Harmful) Virus-Host Interactions by Linking Virology and Bioinformatics." Viruses 13, no. 5 (April 27, 2021): 766. http://dx.doi.org/10.3390/v13050766.

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Анотація:

Many recent studies highlight the fundamental importance of viruses. Besides their important role as human and animal pathogens, their beneficial, commensal or harmful functions are poorly understood. By developing and applying tailored bioinformatical tools in important virological models, the Marie Skłodowska-Curie Initiative International Training Network VIROINF will provide a better understanding of viruses and the interaction with their hosts. This will open the door to validate methods of improving viral growth, morphogenesis and development, as well as to control strategies against unwanted microorganisms. The key feature of VIROINF is its interdisciplinary nature, which brings together virologists and bioinformaticians to achieve common goals.

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Pusterla, Nicola, Molly Rice, Travis Henry, Samantha Barnum, and Kaitlyn James. "Investigation of the Shedding of Selected Respiratory Pathogens in Healthy Horses Presented for Routine Dental Care." Journal of Veterinary Dentistry 37, no. 2 (June 2020): 88–93. http://dx.doi.org/10.1177/0898756420949135.

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The main objective of the study was to determine the frequency of detection of selected infectious respiratory viruses and bacteria in healthy horses presented over a 12-month period for routine dental care at 2 veterinary hospitals. Nasal secretions were collected from 579 horses and tested for equine herpesviruses (EHV-1, EHV-2, EHV-4, EHV-5), equine influenza virus (EIV), equine rhinitis A and B viruses (ERAV, ERBV), Streptococcus equi subspecies equi ( S equi), S equi subspecies zooepidemicus ( S zooepidemicus), and methicillin-resistant Staphylococcus aureus (MRSA) using routine diagnostic quantitative polymerase chain reaction assays. True respiratory pathogens (EHV-1, EHV-4, EIV, ERBV, and MRSA) were detected in 129 (22%) of the horses. Commensal respiratory pathogens (EHV-2, EHV-5, and S zooepidemicus) were detected in 515 (89%) of the study horses. ERAV and S equi were not detected in any of the study horses. The horses showed statistical differences between the 2 veterinary hospitals in regard to breed, age, presence of nasal discharge, rectal temperature, and detection of true and commensal respiratory pathogens. The data generated from the present study supports the risk for the transmission of true and commensal respiratory pathogens from subclinical shedders to susceptible horses. Equine veterinarians performing routine dental care should engage in routine biosecurity practices, with the goal to reduce disease spread.

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Labarta-Bajo, Lara, Anna Gramalla-Schmitz, Romana R. Gerner, Katelynn R. Kazane, Gregory Humphrey, Tara Schwartz, Karenina Sanders, et al. "CD8 T cells drive anorexia, dysbiosis, and blooms of a commensal with immunosuppressive potential after viral infection." Proceedings of the National Academy of Sciences 117, no. 40 (September 21, 2020): 24998–5007. http://dx.doi.org/10.1073/pnas.2003656117.

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Infections elicit immune adaptations to enable pathogen resistance and/or tolerance and are associated with compositional shifts of the intestinal microbiome. However, a comprehensive understanding of how infections with pathogens that exhibit distinct capability to spread and/or persist differentially change the microbiome, the underlying mechanisms, and the relative contribution of individual commensal species to immune cell adaptations is still lacking. Here, we discovered that mouse infection with a fast-spreading and persistent (but not a slow-spreading acute) isolate of lymphocytic choriomeningitis virus induced large-scale microbiome shifts characterized by increased Verrucomicrobia and reduced Firmicute/Bacteroidetes ratio. Remarkably, the most profound microbiome changes occurred transiently after infection with the fast-spreading persistent isolate, were uncoupled from sustained viral loads, and were instead largely caused by CD8 T cell responses and/or CD8 T cell-induced anorexia. Among the taxa enriched by infection with the fast-spreading virus, Akkermansia muciniphila, broadly regarded as a beneficial commensal, bloomed upon starvation and in a CD8 T cell-dependent manner. Strikingly, oral administration of A. muciniphila suppressed selected effector features of CD8 T cells in the context of both infections. Our findings define unique microbiome differences after chronic versus acute viral infections and identify CD8 T cell responses and downstream anorexia as driver mechanisms of microbial dysbiosis after infection with a fast-spreading virus. Our data also highlight potential context-dependent effects of probiotics and suggest a model in which changes in host behavior and downstream microbiome dysbiosis may constitute a previously unrecognized negative feedback loop that contributes to CD8 T cell adaptations after infections with fast-spreading and/or persistent pathogens.

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Islam, Md Aminul, Leonardo Albarracin, Vyacheslav Melnikov, Bruno G. N. Andrade, Rafael R. C. Cuadrat, Haruki Kitazawa, and Julio Villena. "Dolosigranulum pigrum Modulates Immunity against SARS-CoV-2 in Respiratory Epithelial Cells." Pathogens 10, no. 6 (May 21, 2021): 634. http://dx.doi.org/10.3390/pathogens10060634.

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In a previous work, we demonstrated that nasally administered Dolosigranulum pigrum 040417 beneficially modulated the respiratory innate immune response triggered by the activation of Toll-like receptor 3 (TLR3) and improved protection against Respiratory Syncytial Virus (RSV) in mice. In this work, we aimed to evaluate the immunomodulatory effects of D. pigrum 040417 in human respiratory epithelial cells and the potential ability of this immunobiotic bacterium to increase the protection against Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). The respiratory commensal bacterium D. pigrum 040417 differentially modulated the production of IFN-β, IL-6, CXCL8, CCL5 and CXCL10 in the culture supernatants of Calu-3 cells stimulated with poly(I:C) or challenged with SARS-CoV-2. The differential cytokine profile induced by the 040417 strain was associated with a significant reduction in viral replication and cellular damage after coronavirus infection. Of note, D. pigrum 030918 was not able to modify the resistance of Calu-3 cells to SARS-CoV-2 infection, indicating a strain-specific immunomodulatory effect for respiratory commensal bacteria. The findings of this work improve our understanding of the immunological mechanisms involved in the modulation of respiratory immunity induced by respiratory commensal bacteria, by demonstrating their specific effect on respiratory epithelial cells. In addition, the results suggest that particular strains such as D. pigrum 040417 could be used as a promising alternative for combating SARS-CoV-2 and reducing the severity of COVID-19.

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Moriyama, Miyu, and Takeshi Ichinohe. "High ambient temperature dampens adaptive immune responses to influenza A virus infection." Proceedings of the National Academy of Sciences 116, no. 8 (February 4, 2019): 3118–25. http://dx.doi.org/10.1073/pnas.1815029116.

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Although climate change may expand the geographical distribution of several vector-borne diseases, the effects of environmental temperature in host defense to viral infection in vivo are unknown. Here, we demonstrate that exposure of mice to the high ambient temperature of 36 °C impaired adaptive immune responses against infection with viral pathogens, influenza, Zika, and severe fever with thrombocytopenia syndrome phlebovirus. Following influenza virus infection, the high heat-exposed mice failed to stimulate inflammasome-dependent cytokine secretion and respiratory dendritic cell migration to lymph nodes. Although commensal microbiota composition remained intact, the high heat-exposed mice decreased their food intake and increased autophagy in lung tissue. Induction of autophagy in room temperature-exposed mice severely impaired virus-specific CD8 T cells and antibody responses following respiratory influenza virus infection. In addition, we found that administration of glucose or dietary short-chain fatty acids restored influenza virus-specific adaptive immune responses in high heat-exposed mice. These findings uncover an unexpected mechanism by which ambient temperature and nutritional status control virus-specific adaptive immune responses.

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Moxon, E. Richard. "Bacterial variation, virulence and vaccines." Microbiology 155, no. 4 (April 1, 2009): 997–1003. http://dx.doi.org/10.1099/mic.0.024877-0.

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Research into Haemophilus influenzae, a commensal and pathogen of humans, has resulted in major scientific contributions to biology. The first endonucleases (restriction enzymes), which paved the way for the new genetics, and the DNA used to obtain the first complete genome sequence of a free-living organism were obtained from H. influenzae. Prevention of invasive bacterial infections of infants, such as meningitis, has been achieved using a novel class of vaccines, of which the glycoconjugates of H. influenzae were the first to be licensed. Originally fallaciously proposed to be the aetiological agent of epidemic influenza, now known to be caused by a virus, H. influenzae is a pathogen of global public health importance. Research into the pathogenesis of the infections it causes (for example, meningitis, septicaemia, pneumonia and otitis media) are case studies in understanding the molecular basis of the variation in gene expression and gene sequences that are critical to its commensal and virulence behaviour and for the strategies that can be pursued to prevent H. influenzae diseases through vaccines.

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Mirabelli, Carmen. "4412 Unraveling the role of the interaction between enteric virus and commensal bacteria in a physiological relevant model of human intestinal epithelium." Journal of Clinical and Translational Science 4, s1 (June 2020): 21. http://dx.doi.org/10.1017/cts.2020.103.

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OBJECTIVES/GOALS: In the crowded environment of the intestine, selected commensal bacteria and enteric viruses interact. The biological significance of this interaction, in either normal or pathological condition is not known. To study this interaction, we are developing a physiologically relevant model of an human intestinal epithelium. METHODS/STUDY POPULATION: Intestinal biopsies (ileum region) and fecal samples of 6 healthy and 6 active Crohn’s patients are being collected to derive human intestinal enteroid (HIE) lines. 2D-polarized HIE will be first characterized with studies of epithelial permeability, tight junctions and cell type composition, and co-cultured with matching fecal samples. The (co-)cultures will be then infected with human norovirus (HNoV), our model enteric virus, and infection will be quantified by RT-qPCR. In addition, the interaction of HNoV with bacteria derived from healthy or Crohn’s will be determined quantitatively by flow cytometry (viral tagging) and qualitatively by 16S sequencing of the total versus HNoV-bound bacterial species. RESULTS/ANTICIPATED RESULTS: Crohn’s patients are characterized by a microbiome dysbiosis and, in particular, by a high abundance of Enterobacteriacae. HNoV interacts with Enterobacter cloacae, and interestingly, HNoV infection is associated with exacerbation and reactivation of Crohn’s disease. By re-creating the intestinal milieu of healthy and Crohn’s patients, we expect that the kinetics of infection by HNoV will be higher in Crohn’s as compared to healthy volunteers. In addition, by studying the composition of the HNoV-bound bacterial component of Crohn’s versus heathy volunteers, we will be able to identify the contribution of selected bacteria to the expected increase of infection. DISCUSSION/SIGNIFICANCE OF IMPACT: With this study, we will fill the gap of knowledge on the importance of commensal bacteria and enteric virus interactions in healthy and diseased condition. This new knowledge will be paramount for the identification of novel strategies to combat highly prevalent virus infections.

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Lanahan, Matthew, Andrea Erickson, and Julie Pfeiffer. "2224 Determining if intestinal commensal bacteria enhance the frequency of reassortment of an enteric, segmented virus, reovirus." Journal of Clinical and Translational Science 2, S1 (June 2018): 9. http://dx.doi.org/10.1017/cts.2018.62.

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OBJECTIVES/SPECIFIC AIMS: The overall goal is to determine if intestinal commensal bacteria play a role in enteric virus evolution. We will use reovirus, an enteric segmented virus, to investigate specific goals. First, we will determine if specific bacterial species enhance the coinfection frequency of 2 separate strains of reovirus. Second, we will determine if the presence/absence of different bacterial species in the microbiota of mice results in different reovirus reassortment frequencies. Finally, we will discover if reassortant reovirus is present in human populations. METHODS/STUDY POPULATION: My first goal is to determine if specific bacterial species enhance the coinfection frequency of 2 strains of reovirus. In our lab, we have a panel of commensal intestinal bacterial strains, as well as a number of lab adapted bacterial strains. We will use this panel of bacteria to determine if reovirus binds to different species of bacteria using a binding assay involving radiolabeled virus. Additionally, we will determine if specific species of bacteria alter the coinfection frequency through a Flow cytometry based assay. This will involve mixing virus with bacteria, infecting cells in culture, and straining for reovirus proteins for flow cytometry. Our second goal is to determine if specific bacteria promote reassortment of reovirus in a mouse model of infection. To do this, we will use gnotobiotic techniques to create mice harboring different intestinal bacteria populations. Mice will be infected with 2 strains of reovirus, and then feces and organs will be collected. Progeny virus will be subjected to a plaque assay on 2 different types of cells. The first type of cells will be normal cells in culture in which all viable viruses will form plaques. The second will be a cell line that stably expresses siRNAs against specific reovirus segments in which only specific reassortants will form plaques. These 2 plaque assays will be used to quantify the total number of viruses present and the total number of reassortant viruses present. Additionally, SDS-PAGE and RT-PCR will be used to confirm reassortants. Our third goal is to determine if reassortant reovirus is present in infected humans. To do this, I will obtain feces from reovirus-infected children and isolate reovirus. One specific reovirus reassortant is known to propogate in dual-infected mice. I will use the plaque assay technique to determine if this reassortant is also present in humans. To determine if other reassortants are present, I will use RT-PCR and SDS-PAGE. RESULTS/ANTICIPATED RESULTS: Based on previous studies with other enteric viruses, we suspect that specific bacterial species bind reovirus strains with different efficiencies. It is likely that a number of bacterial species will promote coinfection. The bacterial strains that binds both reovirus strains at a high efficiency will likely enhance coinfection by the greatest amount. It is likely that mice harboring different bacterial populations will produce different reovirus reassortment frequencies. We predict that bacteria that enhance reovirus coinfection in vitro should also enhance reovirus reassortment in our mouse model. Therefore, mice specifically lacking bacteria that promote coinfection should have significantly lower amounts of reassortant reovirus. It will be important to control for the overall amount of replication within mice with different microbiotas, as this will affect the basal reassortment frequency. We suspect that reovirus reassortants are present in humans. Work done both in vitro and in mouse models indicates that reassortment happens at high frequencies. Additionally, one specific reassortant commonly propogates in mice due to an enhanced cellular attachment phenotype. Therefore, we predict that this reassortant also commonly emerges after coinfection and reassortment in humans. DISCUSSION/SIGNIFICANCE OF IMPACT: Segmented viruses, such as influenza and rotavirus, are important human pathogens. Viral reassortment poses a unique threat to humans, as it enables new viruses to emerge and cause pandemics or epidemics. However, little is known about what factors promote viral reassortment. This study will provide insight into a novel mechanism of segmented virus evolution.

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Chen, Shao-wei, Li-na Jiang, Xue-shan Zhong, Xue-yan Zheng, Shu-juan Ma, Yi-quan Xiong, Jun-hua Zhou, et al. "Serological Prevalence Against Japanese Encephalitis Virus-Serocomplex Flaviviruses in Commensal and Field Rodents in South China." Vector-Borne and Zoonotic Diseases 16, no. 12 (December 2016): 777–80. http://dx.doi.org/10.1089/vbz.2015.1934.

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35

Abaidullah, Muhammad, Shuwei Peng, Muhammad Kamran, Xu Song, and Zhongqiong Yin. "Current Findings on Gut Microbiota Mediated Immune Modulation against Viral Diseases in Chicken." Viruses 11, no. 8 (July 25, 2019): 681. http://dx.doi.org/10.3390/v11080681.

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Chicken gastrointestinal tract is an important site of immune cell development that not only regulates gut microbiota but also maintains extra-intestinal immunity. Recent studies have emphasized the important roles of gut microbiota in shaping immunity against viral diseases in chicken. Microbial diversity and its integrity are the key elements for deriving immunity against invading viral pathogens. Commensal bacteria provide protection against pathogens through direct competition and by the production of antibodies and activation of different cytokines to modulate innate and adaptive immune responses. There are few economically important viral diseases of chicken that perturb the intestinal microbiota diversity. Disruption of microbial homeostasis (dysbiosis) associates with a variety of pathological states, which facilitate the establishment of acute viral infections in chickens. In this review, we summarize the calibrated interactions among the microbiota mediated immune modulation through the production of different interferons (IFNs) ILs, and virus-specific IgA and IgG, and their impact on the severity of viral infections in chickens. Here, it also shows that acute viral infection diminishes commensal bacteria such as Lactobacillus, Bifidobacterium, Firmicutes, and Blautia spp. populations and enhances the colonization of pathobionts, including E. coli, Shigella, and Clostridial spp., in infected chickens.

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Chaudhary, Ansh, and Bhupendra Chaudhary. "Gut microbiota: changing the disease architecture." International Journal of Advances in Medicine 7, no. 6 (May 22, 2020): 1032. http://dx.doi.org/10.18203/2349-3933.ijam20202077.

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Gut microflora comprising of trillions of various bacteria, protozoan, virus and fungi who live as a super-complex ecosystem in human body mostly (around 70%) in gastrointestinal tract. In habitating skin, mouth, intestine and sexual organs they live as symbiotic, commensal or pathogenic organism in the human body. These gut microflora interplay with bodily metabolic, immune, endocrinal and nervous system which leads to various pathophysiological mechanism for the causation of related disorders. This altered ‘Brain gut axis’ is responsible for disorders like anxiety, depression, autism, schizoaffective or bipolar disorder and also diseases like Parkinson’s disease and multiple sclerosis.1

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Sciubba, J. J. "Opportunistic Oral Infections in the Immunosuppressed Patient: Oral Hairy Leukoplakia and Oral Candidiasis." Advances in Dental Research 10, no. 1 (April 1996): 69–72. http://dx.doi.org/10.1177/08959374960100011401.

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Several opportunistic infections associated with immunosuppression are noted to occur secondary to an altered relationship between host and organism. In relation to diminished host immunologic defenses, associated commensal organisms may evolve to a pathogen state. Candidiasis. a common oral marker disease reflective of immunosuppression, results from dysfunction of complex cellular interactions keyed by depressed T-cell activity or function. Certain viral infections may also serve as probable markers of immunosuppression. One such infection is typified by the development of oral hairy leukoplakia, a condition highly correlated to HIV infection in most, but not all, patients. Detection of Epstein-Barr virus particles and subsequent molecular analytic verification of such and the absence of other potential viral candidates, such as papilloma and human immunodeficiency viruses, have led to a general acceptance of this virus as the cause of this condition.

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Miesen, Pascal, and Ronald P. van Rij. "Crossing the Mucosal Barrier: A Commensal Bacterium Gives Dengue Virus a Leg-Up in the Mosquito Midgut." Cell Host & Microbe 25, no. 1 (January 2019): 1–2. http://dx.doi.org/10.1016/j.chom.2018.12.009.

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Matsuzawa, Yu, Luis E. Gomez, and Ken Cadwell. "Autophagy Protein ATG16L1 Confers Tolerance to a Commensal Virus by Preventing Cell Death in the Intestinal Epithelium." Gastroenterology 152, no. 5 (April 2017): S183. http://dx.doi.org/10.1016/s0016-5085(17)30923-x.

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40

Di Cristanziano, Veronica, Fedja Farowski, Federica Berrilli, Maristella Santoro, David Di Cave, Christophe Glé, Martin Daeumer, et al. "Analysis of Human Gut Microbiota Composition Associated to the Presence of Commensal and Pathogen Microorganisms in Côte d’Ivoire." Microorganisms 9, no. 8 (August 18, 2021): 1763. http://dx.doi.org/10.3390/microorganisms9081763.

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Background: The human gut microbiota is a microbial ecosystem contributing to the maintenance of host health with functions related to immune and metabolic aspects. Relations between microbiota and enteric pathogens in sub-Saharan Africa are scarcely investigated. The present study explored gut microbiota composition associated to the presence of common enteric pathogens and commensal microorganisms, e.g., Blastocystis and Entamoeba species, in children and adults from semi-urban and non-urban localities in Côte d’Ivoire. Methods: Seventy-six stool samples were analyzed for microbiota composition by 16S rRDNA sequencing. The presence of adeno-, entero-, parechoviruses, bacterial and protozoal pathogens, Blastocystis, and commensal Entamoeba species, was analyzed by different molecular assays. Results: Twelve individuals resulted negative for any tested microorganisms, 64 subjects were positive for one or more microorganisms. Adenovirus, enterovirus, enterotoxigenic Escherichia coli (ETEC), and Blastocystis were frequently detected. Conclusions: The bacterial composition driven by Prevotellaceae and Ruminococcaceae confirmed the biotype related to the traditional dietary and cooking practices in low-income countries. Clear separation in UniFrac distance in subjects co-harboring Entamoeba hartmanni and Blastocystis was evidenced. Alpha diversity variation in negative control group versus only Blastocystis positive suggested its possible regulatory contribution on intestinal microbiota. Pathogenic bacteria and virus did not affect the positive outcome of co-harbored Blastocystis.

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Dentice Maidana, Stefania, Ramiro Ortiz Moyano, Juan Martin Vargas, Kohtaro Fukuyama, Shoichiro Kurata, Vyacheslav Melnikov, María Ángela Jure, Haruki Kitazawa, and Julio Villena. "Respiratory Commensal Bacteria Increase Protection against Hypermucoviscous Carbapenem-Resistant Klebsiella pneumoniae ST25 Infection." Pathogens 11, no. 9 (September 19, 2022): 1063. http://dx.doi.org/10.3390/pathogens11091063.

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In a previous work, we demonstrated that nasally administered Corynebacterium pseudodiphtheriticum 090104 beneficially modulated the respiratory innate immune response and improved the protection against Respiratory Syncytial Virus and Streptococcus pneumoniae in mice. In this work, we aimed to evaluate whether the immunomodulatory 090104 strain was able to enhance the resistance against the respiratory infection induced by hypermucoviscous carbapenemase-producing (KPC-2) Klebsiella pneumoniae strains belonging to the sequence type (ST) 25. The nasal treatment of mice with C. pseudodiphtheriticum 090104 before the challenge with multiresistant K. pneumoniae ST25 strains significantly reduced lung bacterial cell counts and lung tissue damage. The protective effect of the 090104 strain was related to its ability to regulate the respiratory innate immune response triggered by K. pneumoniae challenge. C. pseudifteriticum 090104 differentially modulated the recruitment of leukocytes into the lung and the production of TNF-α, IFN-γ and IL-10 levels in the respiratory tract and serum. Our results make an advance in the positioning of C. pseudodiphtheriticum 090104 as a next-generation probiotic for the respiratory tract and encourage further research of this bacterium as a promising alternative to develop non-antibiotic therapeutical approaches to enhance the prevention of infections produced by microorganisms with multiple resistance to antimicrobials such as KPC-2-producing hypermucoviscous K. pneumoniae strains belonging to ST25.

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Scully, C., M. EI-Kabir, and Lakshman P. Samaranayake. "Candida and Oral Candidosis: A Review." Critical Reviews in Oral Biology & Medicine 5, no. 2 (May 1994): 125–57. http://dx.doi.org/10.1177/10454411940050020101.

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Candida species are the most common fungal pathogens isolated from the oral cavity. Their oral existence both as a commensal and an opportunist pathogen has intrigued clinicians and scientists for many decades, and recent investigations have revealed many attributes of this fungus contributing to its pathogenicity. In addition, the advent of the human immunodeficiency virus infection and AIDS has resulted in a resurgence of oral Candida infections. Clinicians are witnessing not only classic forms of the diseases but also newer clinical variants such as erythematous candidosis, rarely described hithertofore. Therefore, this review is an attempt at detailing the current knowledge on Candida and oral candidoses together with the newer therapeutic regimes employed in treating these mycoses.

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Seferovic, Maxim D., Gregory Valentine, Kristen Meyer, J. Michael Harnish, Melissa Suter, Amanda Prince, Rodion Gorchakov, et al. "270: Commensal microbes confer protection against Zika virus infection in a murine gnotobiotic model of congenital Zika syndrome." American Journal of Obstetrics and Gynecology 218, no. 1 (January 2018): S172—S173. http://dx.doi.org/10.1016/j.ajog.2017.10.199.

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Tarris, Georges, Alexis de Rougemont, Maëva Charkaoui, Christophe Michiels, Laurent Martin, and Gaël Belliot. "Enteric Viruses and Inflammatory Bowel Disease." Viruses 13, no. 1 (January 13, 2021): 104. http://dx.doi.org/10.3390/v13010104.

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Inflammatory bowel diseases (IBD), including ulcerative colitis (UC) and Crohn’s disease (CD), is a multifactorial disease in which dietary, genetic, immunological, and microbial factors are at play. The role of enteric viruses in IBD remains only partially explored. To date, epidemiological studies have not fully described the role of enteric viruses in inflammatory flare-ups, especially that of human noroviruses and rotaviruses, which are the main causative agents of viral gastroenteritis. Genome-wide association studies have demonstrated the association between IBD, polymorphisms of the FUT2 and FUT3 genes (which drive the synthesis of histo-blood group antigens), and ligands for norovirus and rotavirus in the intestine. The role of autophagy in defensin-deficient Paneth cells and the perturbations of cytokine secretion in T-helper 1 and T-helper 17 inflammatory pathways following enteric virus infections have been demonstrated as well. Enteric virus interactions with commensal bacteria could play a significant role in the modulation of enteric virus infections in IBD. Based on the currently incomplete knowledge of the complex phenomena underlying IBD pathogenesis, future studies using multi-sampling and data integration combined with new techniques such as human intestinal enteroids could help to decipher the role of enteric viruses in IBD.

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Ahmed, N., T. Hayashi, A. Hasegawa, H. Furukawa, N. Okamura, T. Chida, T. Masuda, and M. Kannagi. "Suppression of human immunodeficiency virus type 1 replication in macrophages by commensal bacteria preferentially stimulating Toll-like receptor 4." Journal of General Virology 91, no. 11 (August 18, 2010): 2804–13. http://dx.doi.org/10.1099/vir.0.022442-0.

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Yitbarek, Alexander, Jake Astill, Douglas C. Hodgins, John Parkinson, Éva Nagy, and Shayan Sharif. "Commensal gut microbiota can modulate adaptive immune responses in chickens vaccinated with whole inactivated avian influenza virus subtype H9N2." Vaccine 37, no. 44 (October 2019): 6640–47. http://dx.doi.org/10.1016/j.vaccine.2019.09.046.

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47

Cebra, John J., Sangeeta Bhargava Periwal, Gwen Lee, Fan Lee, and Khushroo E. Shroff. "Development and Maintenance of the Gut-Associated Lymphoid Tissue (Galt): the Roles of Enteric Bacteria and Viruses." Developmental Immunology 6, no. 1-2 (1998): 13–18. http://dx.doi.org/10.1155/1998/68382.

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GALT can be subdivided into several compartments: (a) Peyer's patches (PP); (b) lamina propria (LP); and (c) intraepithelial leukocyte (IEL) spaces. The B-cell follicles of PP are quiescent in neonatal and germ-free (GF) adult mice. Germinal centers (GC), including sIgA+blasts, appear in the B follicles of formerly GF adult mice about 10-14 days after monoassociation with various gut commensal bacteria. The GC wax and wane over about a 3-week period, although the bacterial colonizers remain in the gut at high density. Neonatal mice, born of conventionally reared (CV), immunocompetent mothers, display GC reactions in PP postweaning, although pups of SCID mothers display precocious GC reactions at about 14 days of life. Normally, gut colonization of neonates with segmented filamentous bacteria (SFB) leads to explosive development of IgA plasmablasts in LP shortly after weaning. Commensal gut bacteria and the immunocompetency of mothers also appears to control the rate of accumulation of primary B cells from “virgin” B cells in neonates.Enteric reovirus infection by the oral route can cause the activation of CD8+T cells in the interfollicular regions of PP and the appearance of virus-specific precursor cytotoxic T lymphocytes (pCTL) in the IEL spaces. Such oral stimulation can also lead to “activation” of both CTL and natural killer (NK) cells in the IEL spaces. More normally, colonization of the gut with SFB also leads to similar activations of NK cells and “constitutively” cytotoxic T cells.

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Huang, Zhenyu, Mengting Zhan, Gaofeng Cheng, Ruiqi Lin, Xue Zhai, Haiou Zheng, Qingchao Wang, Yongyao Yu, and Zhen Xu. "IHNV Infection Induces Strong Mucosal Immunity and Changes of Microbiota in Trout Intestine." Viruses 14, no. 8 (August 22, 2022): 1838. http://dx.doi.org/10.3390/v14081838.

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The fish intestinal mucosa is among the main sites through which environmental microorganisms interact with the host. Therefore, this tissue not only constitutes the first line of defense against pathogenic microorganisms but also plays a crucial role in commensal colonization. The interaction between the mucosal immune system, commensal microbiota, and viral pathogens has been extensively described in the mammalian intestine. However, very few studies have characterized these interactions in early vertebrates such as teleosts. In this study, rainbow trout (Oncorhynchus mykiss) was infected with infectious hematopoietic necrosis virus (IHNV) via a recently developed immersion method to explore the effects of viral infection on gut immunity and microbial community structure. IHNV successfully invaded the gut mucosa of trout, resulting in severe tissue damage, inflammation, and an increase in gut mucus. Moreover, viral infection triggered a strong innate and adaptive immune response in the gut, and RNA−seq analysis indicated that both antiviral and antibacterial immune pathways were induced, suggesting that the viral infection was accompanied by secondary bacterial infection. Furthermore, 16S rRNA sequencing also revealed that IHNV infection induced severe dysbiosis, which was characterized by large increases in the abundance of Bacteroidetes and pathobiont proliferation. Moreover, the fish that survived viral infection exhibited a reversal of tissue damage and inflammation, and their microbiome was restored to its pre−infection state. Our findings thus demonstrated that the relationships between the microbiota and gut immune system are highly sensitive to the physiological changes triggered by viral infection. Therefore, opportunistic bacterial infection must also be considered when developing strategies to control viral infection.

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Winkler, Emma S., Larissa B. Thackray, Barry L. Hykes, Scott A. Handley, Lindsay Droit, Prabhakar Andhey, Matthias Mack, et al. "A commensal Clostridium species restricts systemic alphavirus dissemination through a type I interferon signaling axis." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 171.5. http://dx.doi.org/10.4049/jimmunol.204.supp.171.5.

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Abstract The role of the gut microbiota in shaping antiviral immune responses at non-intestinal sites has been described in multiple models of viral pathogenesis. Although chikungunya virus (CHIKV), an emerging alphavirus, is a substantial global health threat, the impact of the microbiota in modulating immune responses to alphavirus infection is entirely unexplored. Here, we show that CHIKV infection of oral antibiotic-treated or germ-free mice resulted in increased viremia within one day of infection, and this enhanced viral dissemination. Microbiota depletion resulted in greater CHIKV infection of circulating monocytes, which was linked to dampened systemic type I interferon (IFN) responses. Differences in CHIKV tropism and replication following microbiota depletion depended on MyD88 signaling in plasmacytoid dendritic cells, which contributed to systemic type I IFN production within hours of infection. Colonization of antibiotic-treated mice with a single bacterial microbiota-derived Clostridium species resulted in MyD88-dependent type I IFN responses that restricted CHIKV infection in blood. We propose that select bacterial symbionts impact antiviral immunity to alphaviruses within hours of infection through a type I IFN signaling axis and by virtue of effects on viremia may determine disease severity and affect vector transmission and epidemic spread.

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50

Parry, Rhys, Fanny Naccache, El Hadji Ndiaye, Gamou Fall, Ilaria Castelli, Renke Lühken, Jolyon Medlock, et al. "Identification and RNAi Profile of a Novel Iflavirus Infecting Senegalese Aedes vexans arabiensis Mosquitoes." Viruses 12, no. 4 (April 14, 2020): 440. http://dx.doi.org/10.3390/v12040440.

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The inland floodwater mosquito Aedes vexans (Meigen, 1830) is a competent vector of numerous arthropod-borne viruses such as Rift Valley fever virus (Phenuiviridae) and Zika virus (Flaviviridae). Aedes vexans spp. have widespread Afrotropical distribution and are common European cosmopolitan mosquitoes. We examined the virome of Ae. vexans arabiensis samples from Barkédji village, Senegal, with small RNA sequencing, bioinformatic analysis, and RT-PCR screening. We identified a novel 9494 nt iflavirus (Picornaviridae) designated here as Aedes vexans iflavirus (AvIFV). Annotation of the AvIFV genome reveals a 2782 amino acid polyprotein with iflavirus protein domain architecture and typical iflavirus 5’ internal ribosomal entry site and 3’ poly-A tail. Aedes vexans iflavirus is most closely related to a partial virus sequence from Venturia canescens (a parasitoid wasp) with 56.77% pairwise amino acid identity. Analysis of AvIFV-derived small RNAs suggests that AvIFV is targeted by the exogenous RNA interference pathway but not the PIWI-interacting RNA response, as ~60% of AvIFV reads corresponded to 21 nt Dicer-2 virus-derived small RNAs and the 24–29 nt AvIFV read population did not exhibit a “ping-pong” signature. The RT-PCR screens of archival and current (circa 2011–2020) Ae. vexans arabiensis laboratory samples and wild-caught mosquitoes from Barkédji suggest that AvIFV is ubiquitous in these mosquitoes. Further, we screened wild-caught European Ae. vexans samples from Germany, the United Kingdom, Italy, and Sweden, all of which tested negative for AvIFV RNA. This report provides insight into the diversity of commensal Aedes viruses and the host RNAi response towards iflaviruses.

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