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Journal of Virology, June 2002, p. 6311-6322, Vol. 76, No. 12
0022-538X/02/$04.00+0 DOI: 10.1128/JVI.76.12.6311-6322.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.
Early Pathogenesis of Transmucosal Feline Immunodeficiency Virus Infection
Leslie A. Obert and Edward A. Hoover*
Department of Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, Colorado 80523
Received 17 October 2001/
Accepted 19 February 2002
To identify the early target cells and tissues in transmucosal feline immunodeficiency virus (FIV) infection, cats were exposed to a clade C FIV isolate via the oral-nasal or vaginal mucosa and multiple tissues were examined by virus isolation coculture (VI), DNA PCR, catalyzed tyramide signal-amplified in situ hybridization (TSA-ISH), and immunohistochemistry between days 1 and 12 postinoculation (p.i.). FIV RNA was detected in tonsil and oral or vaginal mucosa as early as 1 day p.i. by TSA-ISH and in retropharyngeal, tracheobronchial, or external iliac lymph nodes and sometimes in spleen or blood mononuclear cells by day 2, indicating that regional and distant spread of virus-infected cells occurred rapidly after mucosal exposure. By day 8, viral RNA, DNA, and culturable virus were uniformly detected in regional and distant tissues, connoting systemic infection. TSA-ISH proved more sensitive than DNA PCR in detecting early FIV-infected cells. In mucosal tissues, the earliest demonstrable FIV-bearing cells were either within or subjacent to the mucosal epithelium or were in germinal centers of regional lymph nodes. The FIV+ cells were of either of two morphological types, large stellate or small round. Those FIV RNA+ cells which could be colabeled for a phenotype marker, were labeled for either dendritic-cell-associated protein p55 or T-lymphocyte receptor antigen CD3. These studies indicate that FIV crosses mucous membranes within hours after exposure and rapidly traffics via dendritic and T cells to systemic lymphoid tissues, a pathway similar to that thought to occur in the initial phase of infection by the human and simian immunodeficiency viruses.
* Corresponding author. Mailing address: Department of Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, 300 W. Lake St., Fort Collins, CO 80523. Phone: (970) 491-7587. Fax: (970) 491-0523. E-mail:
ehoover{at}lamar.colostate.edu.
Journal of Virology, June 2002, p. 6311-6322, Vol. 76, No. 12
0022-538X/02/$04.00+0 DOI: 10.1128/JVI.76.12.6311-6322.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.
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