Pathogenesis of oral FIV infection

Miller, Craig, Boegler, Karen, Carver, Scott, MacMillan, Martha, Bielefeldt-Ohmann, Helle and VandeWoude, Sue (2017) Pathogenesis of oral FIV infection. PLoS One, 12 9: e0185138. doi:10.1371/journal.pone.0185138


Author Miller, Craig
Boegler, Karen
Carver, Scott
MacMillan, Martha
Bielefeldt-Ohmann, Helle
VandeWoude, Sue
Title Pathogenesis of oral FIV infection
Journal name PLoS One   Check publisher's open access policy
ISSN 1932-6203
Publication date 2017-09-21
Year available 2017
Sub-type Article (original research)
DOI 10.1371/journal.pone.0185138
Open Access Status DOI
Volume 12
Issue 9
Start page e0185138
Total pages 24
Place of publication San Francisco, CA United States
Publisher Public Library of Science
Language eng
Subject 1300 Biochemistry, Genetics and Molecular Biology
1100 Agricultural and Biological Sciences
Abstract Feline immunodeficiency virus (FIV) is the feline analogue of human immunodeficiency virus (HIV) and features many hallmarks of HIV infection and pathogenesis, including the development of concurrent oral lesions. While HIV is typically transmitted via parenteral transmucosal contact, recent studies prove that oral transmission can occur, and that saliva from infected individuals contains significant amounts of HIV RNA and DNA. While it is accepted that FIV is primarily transmitted by biting, few studies have evaluated FIV oral infection kinetics and transmission mechanisms over the last 20 years. Modern quantitative analyses applied to natural FIV oral infection could significantly further our understanding of lentiviral oral disease and transmission. We therefore characterized FIV salivary viral kinetics and antibody secretions to more fully document oral viral pathogenesis. Our results demonstrate that: (i) saliva of FIV-infected cats contains infectious virus particles, FIV viral RNA at levels equivalent to circulation, and lower but significant amounts of FIV proviral DNA; (ii) the ratio of FIV RNA to DNA is significantly higher in saliva than in circulation; (iii) FIV viral load in oral lymphoid tissues (tonsil, lymph nodes) is significantly higher than mucosal tissues (buccal mucosa, salivary gland, tongue); (iv) salivary IgG antibodies increase significantly over time in FIV-infected cats, while salivary IgA levels remain static; and, (v) saliva from naïve Specific Pathogen Free cats inhibits FIV growth in vitro. Collectively, these results suggest that oral lymphoid tissues serve as a site for enhanced FIV replication, resulting in accumulation of FIV particles and FIV-infected cells in saliva. Failure to induce a virus-specific oral mucosal antibody response, and/or viral capability to overcome inhibitory components in saliva may perpetuate chronic oral cavity infection. Based upon these findings, we propose a model of oral FIV pathogenesis and suggest alternative diagnostic modalities and translational approaches to study oral HIV infection.
Keyword Feline Immunodeficiency Virus
Systemic Immune Activation
Cell-Free Siv
Hiv-Infection
Lymph-Nodes
Microbial Translocation
Gastrointestinal-Tract
Vertical Transmission
Commensal Bacteria
Homosexual-Men
Q-Index Code C1
Q-Index Status Provisional Code
Grant ID R01AI025825
4T32OD010437-15
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: HERDC Pre-Audit
School of Veterinary Science Publications
 
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Created: Tue, 03 Oct 2017, 00:05:20 EST by Web Cron on behalf of Biological Sciences Library