Successful Transmission of a Retrovirus Depends on the Commensal Microbiota

Kane, Melissa; Case, Laure K.; Kopaskie, Karyl S.; Kozlova, Alena; MacDearmid, Cameron; Chervonsky, Alexander V.; Golovkina, Tatyana V.

doi:10.1126/science.1210718

Cited by 342 publications

(367 citation statements)

References 48 publications

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“…Recent data have documented that mechanisms of cooperation between viruses and microbiota in the intestine exist. Indeed, it has been shown that immunity against mouse mammary tumor virus (56) and systemic pathogenesis caused by enteric viruses (57) are dependent on interactions between the viruses and the microbiota.…”

Section: Foxp3mentioning

confidence: 99%

Prevention of Virus-Induced Type 1 Diabetes with Antibiotic Therapy

Hara

Alkanani

et al. 2012

The Journal of Immunology

111

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Microbes were hypothesized to play a key role in the progression of type 1 diabetes (T1D). We used the LEW1.WR1 rat model of Kilham rat virus (KRV)-induced T1D to test the hypothesis that the intestinal microbiota is involved in the mechanism leading to islet destruction. Treating LEW1.WR1 rats with KRV and a combination of trimethoprim and sulfamethoxazole (Sulfatrim) beginning on the day of infection protected the rats from insulitis and T1D. Pyrosequencing of bacterial 16S rRNA and quantitative RT-PCR indicated that KRV infection resulted in a transient increase in the abundance of Bifidobacterium spp. and Clostridium spp. in fecal samples from day 5- but not day 12-infected versus uninfected animals. Similar alterations in the gut microbiome were observed in the jejunum of infected animals on day 5. Treatment with Sulfatrim restored the level of intestinal Bifidobacterium spp. and Clostridium spp. We also observed that virus infection induced the expression of KRV transcripts and the rapid upregulation of innate immune responses in Peyer’s patches and pancreatic lymph nodes. However, antibiotic therapy reduced the virus-induced inflammation as reflected by the presence of lower amounts of proinflammatory molecules in both the Peyer’s patches and pancreatic lymph nodes. Finally, Sulfatrim treatment reduced the number of B cells in Peyer’s patches and downmodulated adaptive immune responses to KRV, but did not interfere with antiviral Ab responses or viral clearance from the spleen, pancreatic lymph nodes, and serum. The data suggest that gut microbiota may be involved in promoting virus-induced T1D in the LEW1.WR1 rat model.

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Section: Foxp3mentioning

confidence: 99%

Prevention of Virus-Induced Type 1 Diabetes with Antibiotic Therapy

Hara

Alkanani

et al. 2012

The Journal of Immunology

111

View full text Add to dashboard Cite

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“…Recent progress has been made to develop new culturing technologies so that we can grow previously ''unculturable'' organisms in the laboratory environment (Vartoukian et al 2010). We have expanded our view of the microbiome beyond bacteria and into the virome (viruses) (Minot et al 2011) and mycome (fungi) (Ghannoum et al 2010) and have begun to investigate the reciprocal interactions between these constituents (Kane et al 2011;Kuss et al 2011). The microbiome holds great potential for breakthroughs in translational medicine, including the promise of precision tools that will allow us to ''sculpt'' the microbiome with diet, prebiotics, probiotics, and targeted antibiotics to prevent and treat disease.…”

Section: Perspective and Future Directionsmentioning

confidence: 99%

Exploring host–microbiota interactions in animal models and humans

2013

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The animal and bacterial kingdoms have coevolved and coadapted in response to environmental selective pressures over hundreds of millions of years. The meta'omics revolution in both sequencing and its analytic pipelines is fostering an explosion of interest in how the gut microbiome impacts physiology and propensity to disease. Gut microbiome studies are inherently interdisciplinary, drawing on approaches and technical skill sets from the biomedical sciences, ecology, and computational biology. Central to unraveling the complex biology of environment, genetics, and microbiome interaction in human health and disease is a deeper understanding of the symbiosis between animals and bacteria. Experimental model systems, including mice, fish, insects, and the Hawaiian bobtail squid, continue to provide critical insight into how host-microbiota homeostasis is constructed and maintained. Here we consider how model systems are influencing current understanding of host-microbiota interactions and explore recent human microbiome studies.The distinctive body plans of animals offer many niches for members of the archaeal and bacterial kingdoms. While the lumen of the human distal gut is one of the most densely populated ecosystems on our planet, humans and other animals harbor several microbiomes on and within their body surfaces such as the respiratory and urogenital tracts and the skin. As the gut has evolved from the relatively simple tube of the ancient cyclostomatida to the more highly compartmentalized gastrointestinal tracts of mammalian species, the diversity and complexity of the microbial inhabitants of those spaces has increased as well (Fig.

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“…For example, commensal microbiota provide immune inductive signals for antiviral immunity against mucosal influenza virus or systemic lymphocytic choriomeningitis virus (LCMV) infections, whereas commensal microbiota promote viral infection by murine leukemia virus or poliovirus (3,4,6,7). To determine the importance of commensal bacteria in defense against mucosal infection by HSV-2, we examined the outcome of intravaginal infection with 10 4 pfu of WT HSV-2 after administration of a combination of five oral antibiotics for 4 wk.…”

Section: Significancementioning

confidence: 99%

Dysbiosis-induced IL-33 contributes to impaired antiviral immunity in the genital mucosa

Kim

Chang

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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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 virusspecific 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.commensal microbiota | dysbiosis | IL-33 | herpes simplex virus type 2 | genital tract

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Successful Transmission of a Retrovirus Depends on the Commensal Microbiota

Cited by 342 publications

References 48 publications

Prevention of Virus-Induced Type 1 Diabetes with Antibiotic Therapy

Prevention of Virus-Induced Type 1 Diabetes with Antibiotic Therapy

Exploring host–microbiota interactions in animal models and humans

Dysbiosis-induced IL-33 contributes to impaired antiviral immunity in the genital mucosa

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