Complement-Opsonized HIV Modulates Pathways Involved in Infection of Cervical Mucosal Tissues: A Transcriptomic and Proteomic Study.
Cervix Uteri
/ immunology
Complement System Proteins
/ immunology
Dendritic Cells
/ immunology
Female
Gene Expression Profiling
Gene Expression Regulation
HIV Infections
/ genetics
HIV-1
/ growth & development
Host-Pathogen Interactions
Humans
Immunity, Innate
Mucous Membrane
/ immunology
Proteome
Proteomics
Signal Transduction
T-Lymphocytes
/ immunology
Time Factors
Tissue Culture Techniques
Transcriptome
Virus Internalization
Virus Replication
HIV - human immunodeficiency virus
cervical tissue
complement opsonized HIV-1
innate immunity
primary infection
proteomics
transcriptomics
Journal
Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960
Informations de publication
Date de publication:
2021
2021
Historique:
received:
03
11
2020
accepted:
29
04
2021
entrez:
7
6
2021
pubmed:
8
6
2021
medline:
15
9
2021
Statut:
epublish
Résumé
Genital mucosal transmission is the most common route of HIV spread. The initial responses triggered at the site of viral entry are reportedly affected by host factors, especially complement components present at the site, and this will have profound consequences on the outcome and pathogenesis of HIV infection. We studied the initial events associated with host-pathogen interactions by exposing cervical biopsies to free or complement-opsonized HIV. Opsonization resulted in higher rates of HIV acquisition/infection in mucosal tissues and emigrating dendritic cells. Transcriptomic and proteomic data showed a significantly more pathways and higher expression of genes and proteins associated with viral replication and pathways involved in different aspects of viral infection including interferon signaling, cytokine profile and dendritic cell maturation for the opsonized HIV. Moreover, the proteomics data indicate a general suppression by the HIV exposure. This clearly suggests that HIV opsonization alters the initial signaling pathways in the cervical mucosa in a manner that promotes viral establishment and infection. Our findings provide a foundation for further studies of the role these early HIV induced events play in HIV pathogenesis.
Identifiants
pubmed: 34093520
doi: 10.3389/fimmu.2021.625649
pmc: PMC8173031
doi:
Substances chimiques
Proteome
0
Complement System Proteins
9007-36-7
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
625649Subventions
Organisme : NCI NIH HHS
ID : HHSN261200800001E
Pays : United States
Commentaires et corrections
Type : ErratumIn
Informations de copyright
Copyright © 2021 Svanberg, Ellegård, Crisci, Khalid, Borendal Wodlin, Svenvik, Nyström, Birse, Burgener, Shankar and Larsson.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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