title: HIV-associated changes in the enteric microbial community: potential role in loss of homeostasis and development of systemic inflammation.
abstract: Despite HIV therapy advances, average life expectancy in HIV-infected individuals on effective treatment is significantly decreased relative to uninfected persons, largely because of increased incidence of inflammation-related diseases, such as cardiovascular disease and renal dysfunction. The enteric microbial community could potentially cause this inflammation, as HIV-driven destruction of gastrointestinal CD4 T cells may disturb the microbiota-mucosal immune system balance, disrupting the stable gut microbiome and leading to further deleterious host outcomes.
  
  
  
  Varied enteric microbiome changes have been reported during HIV infection, but unifying patterns have emerged. Community diversity is decreased, similar to pathologies such as inflammatory bowel disease, obesity, and Clostridium difficile infection. Many taxa frequently enriched in HIV-infected individuals, such as Enterobacteriaceae and Erysipelotrichaceae, have pathogenic potential, whereas depleted taxa, such as Bacteroidaceae and Ruminococcaceae, are more linked with anti-inflammatory properties and maintenance of gut homeostasis. The gut viral community in HIV has been found to contain a greater abundance of pathogenesis-associated Adenoviridae and Anelloviridae. These bacterial and viral changes correlate with increased systemic inflammatory markers, such as serum sCD14, sCD163, and IL-6.
  
  
  
  Enteric microbial community changes may contribute to chronic HIV pathogenesis, but more investigation is necessary, especially in the developing world population with the greatest HIV burden (Video, Supplemental Digital Content 1, http://links.lww.com/COID/A15, which includes the authors' summary of the importance of the work).
authors.affiliation: aRagon Institute of MGH, MIT, and Harvard, Massachusetts General Hospital, Cambridge bHarvard Medical School, Boston cDivision of Infectious Diseases, Massachusetts General Hospital, Boston, Massachusetts, USA.
authors.forename: David B
authors.initials: DB
authors.lastname: Gootenberg
authors.forename: Jeffrey M
authors.initials: JM
authors.lastname: Paer
authors.forename: Jesus-Mario
authors.initials: JM
authors.lastname: Luevano
authors.forename: Douglas S
authors.initials: DS
authors.lastname: Kwon
mesh_terms: D002318:Cardiovascular Diseases / Q000209:etiology; D004755:Enterobacteriaceae; D000069196:Gastrointestinal Microbiome / Q000276:immunology; D015658:HIV Infections / Q000150:complications / Q000382:microbiology*; D006706:Homeostasis; D006801:Humans; D018928:Immunity, Mucosal; D007249:Inflammation / Q000382:microbiology*; D007413:Intestinal Mucosa / Q000276:immunology / Q000821:virology; D007674:Kidney Diseases / Q000209:etiology