Related Experiment Video
Updated: Aug 17, 2026
A High-throughput Cre-Lox Activated Viral Membrane Fusion Assay to Identify Inhibitors of HIV-1 Viral Membrane Fusion
Published on: August 14, 2018
IgG from acutely infected cats blocks mucosal feline immunodeficiency virus infection
Mary Jo Burkhard1, Edward A Hoover
1Department of Veterinary Biosciences, College of Veterinary Medicine, The Ohio State University, Columbus, OH 43210, USA. burkhard.19@osu.edu
Insights
Antibodies in feline immunodeficiency virus (FIV) infected cat plasma block FIV infection of cells and reduce transmission. This finding may explain the inefficient mucosal transmission of human immunodeficiency virus-1 (HIV).
Area of Science:
- Virology
- Immunology
- Infectious Diseases
Background:
- Feline immunodeficiency virus (FIV) transmission via mucosa is less efficient than parenteral routes.
- Previous studies showed absence of infection in cats exposed to FIV plasma inoculum via rectal or vaginal mucosa, contrasting parenteral inoculation.
- Cell-free FIV inoculum, however, infected cats efficiently via mucosal routes.
Purpose of the Study:
- To identify a heat-stable factor in FIV-infected cat plasma that inhibits FIV infection in vitro.
- To evaluate the role of this factor in blocking FIV transmission via mucosal routes in vivo.
Main Methods:
- A tissue culture system was used to test plasma from acutely FIV-infected cats for inhibitory effects on naive peripheral blood mononuclear cells (PBMC).
- FIV p26 production was measured in co-culture experiments over 21 days.
- Antibody depletion using a protein A column was performed to assess the role of antibodies.
- In vivo experiments involved co-inoculation of heat-inactivated plasma with FIV onto the vaginal mucosa of cats.
Main Results:
- Plasma from acutely FIV-infected cats contained a heat-stable factor that blocked both cell-free and cell-associated FIV infection of PBMC in vitro.
- A 1:200 dilution of plasma effectively inhibited FIV p26 production over 21 days.
- The inhibitory effect was abrogated by antibody depletion.
- In vivo, co-inoculation of heat-inactivated plasma with FIV significantly inhibited or delayed vaginal mucosal transmission.
Conclusions:
- Antibodies in the plasma of acutely FIV-infected cats play a crucial role in inhibiting FIV infection.
- These antibodies block FIV transmission by cell-associated and cell-free virus, inhibit virus production in infected cells, and reduce mucosal transmission efficiency.
- These findings may offer insights into the relatively inefficient mucosal transmission of human immunodeficiency virus-1 (HIV) and other lentiviruses.
Abstract:
We have previously shown an absence of detectable systemic or local infection in cats exposed to an infectious (100 TCID(50)) feline immunodeficiency virus (FIV) plasma inoculum via either the rectal or vaginal mucosa. In contrast, this same plasma inoculum was infectious via parenteral inoculation. Moreover an equivalent dose of cell-free tissue culture-origin virus inoculum infected 100% of cats by either the rectal or vaginal exposure route. To evaluate this phenomena, we used a tissue culture system to identify a heat-stable factor in the plasma of cats acutely (3 weeks) infected with FIV that blocked infection of naive peripheral blood mononuclear cells (PBMC) by either cell-free or cell-associated FIV in vitro. A single application of as little as a 1:200 dilution of either heparinized or Alsevier's anticoagulated plasma effectively inhibited production of FIV p26 in culture over a 21-day co-culture period. Depletion of antibody using a protein A column abrogated the inhibitory effect of FIV plasma against in vitro FIV infection. Co-inoculation of heat-inactivated plasma with 400 TCID(50) FIV-B-2542 cell-free supernatant virus onto the vaginal mucosa of two cats resulted in complete inhibition of infection in one cat and increased time to infection in the second. Thus, antibody found in the plasma of cats acutely infected with FIV blocks cell-associated and cell-free infection, inhibits virus production in previously infected cells, and reduces mucosal transmission efficiency in vivo. Extrapolation may help explain the relatively inefficient mucosal transmission of human immunodeficiency virus-1 (HIV) and other lentiviruses.
