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Low nadir CD4+ T-cell counts predict gut dysbiosis in HIV-1 infection. 2019
Yolanda Guillén, and
Marc Noguera-Julian, and
Javier Rivera, and
Maria Casadellà, and
Alexander S Zevin, and
Muntsa Rocafort, and
Mariona Parera, and
Cristina Rodríguez, and
Marçal Arumí, and
Jorge Carrillo, and
Beatriz Mothe, and
Carla Estany, and
Josep Coll, and
Isabel Bravo, and
Cristina Herrero, and
Jorge Saz, and
Guillem Sirera, and
Ariadna Torrella, and
Jordi Navarro, and
Manuel Crespo, and
Eugènia Negredo, and
Christian Brander, and
Julià Blanco, and
Maria Luz Calle, and
Nichole R Klatt, and
Bonaventura Clotet, and
Roger Paredes
irsiCaixa AIDS Research Institute, Ctra de Canyet s/n, Badalona, 08916, Catalonia, Spain.
Human immunodeficiency virus (HIV)-1 infection causes severe gut and systemic immune damage, but its effects on the gut microbiome remain unclear. Previous shotgun metagenomic studies in HIV-negative subjects linked low-microbial gene counts (LGC) to gut dysbiosis in diseases featuring intestinal inflammation. Using a similar approach in 156 subjects with different HIV-1 phenotypes, we found a strong, independent, dose-effect association between nadir CD4+ T-cell counts and LGC. As in other diseases involving intestinal inflammation, the gut microbiomes of subjects with LGC were enriched in gram-negative Bacteroides, acetogenic bacteria and Proteobacteria, which are able to metabolize reactive oxygen and nitrogen species; and were depleted in oxygen-sensitive methanogenic archaea and sulfate-reducing bacteria. Interestingly, subjects with LGC also showed increased butyrate levels in direct fecal measurements, consistent with enrichment in Roseburia intestinalis despite reductions in other butyrate producers. The microbiomes of subjects with LGC were also enriched in bacterial virulence factors, as well as in genes associated with beta-lactam, lincosamide, tetracycline, and macrolide resistance. Thus, low nadir CD4+ T-cell counts, rather than HIV-1 serostatus per se, predict the presence of gut dysbiosis in HIV-1 infected subjects. Such dysbiosis does not display obvious HIV-specific features; instead, it shares many similarities with other diseases featuring gut inflammation.
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