Prolonged Gut Dysbiosis and Fecal Excretion of Hepatitis A Virus in Patients Infected with Human Immunodeficiency Virus.
Adult
Dysbiosis
/ microbiology
Feces
/ virology
Gastrointestinal Microbiome
/ physiology
HIV Infections
/ physiopathology
HIV-1
/ pathogenicity
Hepatitis A
/ complications
Hepatitis A virus
/ pathogenicity
Humans
Japan
/ epidemiology
Male
Middle Aged
RNA, Ribosomal, 16S
/ genetics
Viral Load
Virus Shedding
HAV
HIV
microbiome
Journal
Viruses
ISSN: 1999-4915
Titre abrégé: Viruses
Pays: Switzerland
ID NLM: 101509722
Informations de publication
Date de publication:
18 10 2021
18 10 2021
Historique:
received:
17
09
2021
revised:
13
10
2021
accepted:
14
10
2021
entrez:
26
10
2021
pubmed:
27
10
2021
medline:
8
2
2022
Statut:
epublish
Résumé
Hepatitis A virus (HAV) causes transient acute infection, and little is known of viral shedding via the duodenum and into the intestinal environment, including the gut microbiome, from the period of infection until after the recovery of symptoms. Therefore, in this study, we aimed to comprehensively observe the amount of virus excreted into the intestinal tract, the changes in the intestinal microbiome, and the level of inflammation during the healing process. We used blood and stool specimens from patients with human immunodeficiency virus who were infected with HAV during the HAV outbreak in Japan in 2018. Moreover, we observed changes in fecal HAV RNA and quantified the plasma cytokine level and gut microbiome by 16S rRNA analysis from clinical onset to at least 6 months after healing. HAV was detected from clinical onset up to a period of more than 150 days. Immediately after infection, many pro-inflammatory cytokines were elicited, and some cytokines showed different behaviors. The intestinal microbiome changed significantly after infection (dysbiosis), and the dysbiosis continued for a long time after healing. These observations suggest that the immunocompromised state is associated with prolonged viral shedding into the intestinal tract and delayed recovery of the intestinal environment.
Identifiants
pubmed: 34696531
pii: v13102101
doi: 10.3390/v13102101
pmc: PMC8539651
pii:
doi:
Substances chimiques
RNA, Ribosomal, 16S
0
Types de publication
Journal Article
Observational Study
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
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