Early Pathogenesis of Transmucosal Feline Immunodeficiency Virus Infection

Abstract

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.

AIDS Vaccination Studies Using an Ex Vivo Feline Immunodeficiency Virus Model: Protection from an Intraclade Challenge Administered Systemically or Mucosally by an Attenuated Vaccine

“…Furthermore, vaccination did not consistently confer sterilizing immunity against this type of challenge, since GL8 was readily detected in three of four vaccinees starting from the first sampling performed at 1 month p.c. This could reflect the different form of challenge, the unequal virus dosage inherent therein, or the fact that the challenge virus expanded locally before spreading systemically (14,57), thus possibly eluding vaccinal immunity more effectively than following intraperitoneal challenge. However, the vaccinees exerted substantial control of the challenge virus even when delivered intravaginally, as evidenced by much lower GL8 loads than in the unvaccinated controls and by substantially stable circulating CD4 ϩ -T-lymphocyte counts.…”

Feline Immunodeficiency Virus Orf-A Is Required for Virus Particle Formation and Virus Infectivity

“…Immunological dysfunctions associated with infection by either virus include decreased CD4 T-cell counts, decreased CD4/CD8 T-cell ratios, and increased susceptibility to infectious agents and opportunistic infections (1-3, 24, 49). FIV exhibits a cell tropism similar to, although broader than, that described for HIV and has been shown to infect CD4 T cells, macrophages, and dendritic cells in vivo (3,9,10,14,15,26). As an immunodeficiency-inducing lentivirus, FIV provides an animal model for the development of HIV vaccines and antiviral therapies (4).…”

Concentrações séricas de proteína total, albumina e gamaglobulinas em gatos infectados pelo vírus da imunodeficiência felina

“…A linfoadenomegalia persistente observada em todos os felinos infectados é consistente com a hiperplasia linfóide associada à presença do vírus, conforme é citado por YAMAMOTO et al (1988). Como conseqüência, o estímulo antigênico representado pelo VIF resulta na produção de anticorpos (OBERT & HOOVER, 2002), refletindo no aumento da fração gamaglobulínica observada nos felinos infectados ao quarto mês pós-infecção.…”