Repository logo
 

Pathogenesis of oral FIV infection

Simple item page
dc.contributor.authorMiller, Craig, author
dc.contributor.authorBoegler, Karen, author
dc.contributor.authorCarver, Scott, author
dc.contributor.authorMacMillan, Martha, author
dc.contributor.authorBielefeldt-Ohmann, Helle, author
dc.contributor.authorVandeWoude, Susan, author
dc.date.accessioned2017-09-18T17:53:45Z
dc.date.available2017-09-18T17:53:45Z
dc.date.issued2017
dc.descriptionIncludes bibliographical references.
dc.description.abstractFeline 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.
dc.format.mediumborn digital
dc.format.mediumarticles
dc.identifier.bibliographicCitationMiller C, Boegler K, Carver S, MacMillan, M, Bielefeldt-Ohmann H, VandeWoude S (2017). Pathogenesis of oral FIV infection. PLoS ONE 12 (9): e0185138. https://doi.org/10.1371/journal.pone.0185138
dc.identifier.doihttps://doi.org/10.1371/journal.pone.0185138
dc.identifier.urihttps://hdl.handle.net/10217/184061
dc.languageEnglish
dc.language.isoeng
dc.publisherColorado State University. Libraries
dc.relation.ispartofFaculty Publications
dc.relation.referencesMiller, Craig A., Pathogenesis of Oral FIV Infection, 2017. https://hdl.handle.net/10217/183821
dc.rights.licenseThis article is open access and distributed under the terms and conditions of the Creative Commons Attribution 4.0 International (CC BY 4.0).
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subjectfeline immunodeficiency virus
dc.subjectFIV
dc.subjectHIV
dc.titlePathogenesis of oral FIV infection
dc.typeText

Files

Original bundle
Now showing 1 - 1 of 1
Thumbnail Image
Name:
FACF_MIPA_Miller-2017.pdf
Size:
16.43 MB
Format:
Adobe Portable Document Format
Description:
Download

Collections

Faculty Publications