@article {10.3844/ajidsp.2007.202.207,
article_type = {journal},
title = {Immunodeficient Parameters in the HIV-1 Transgenic Rat Model},
author = {Chang, Sulie L. and Ocasio, Frank and Beltran, Jose A.},
volume = {3},
number = {4},
year = {2007},
month = {Dec},
pages = {202-207},
doi = {10.3844/ajidsp.2007.202.207},
url = {https://thescipub.com/abstract/ajidsp.2007.202.207},
abstract = {Recently an HIV-1 transgenic (HIV-1Tg) rat model was created that carries a gag-pol-deleted HIV-1 genome under the control of the HIV-1 viral promoter. However, other viral proteins are expressed in most organs and tissues, and are found in the circulating blood. Since HIV-1 targets the immune system in humans, we examined two immunological parameters, leukocyte-endothelial adhesion (LEA) and inflammatory cytokine production, in 5 mo old HIV-1Tg rats to identify immune functions that may be impaired even before the onset of symptoms of HIV-1 infection. We administered a single injection (i.p.) of the bacterial endotoxin, lipopolysaccharide (LPS, 250 ug/kg), to 5 mo old HIV-1Tg rats, age-matched transgenic control (Tg) rats, and F344/NHsd (F344) control background strain rats. LPS induced an LEA response in both the Tg control and F344 control animals. However, in the HIV-1Tg rats, there was no LEA response to LPS. Following LPS administration, there was significantly greater serum levels of TNF-α and IL-1β, two pro-inflammatory cytokines, in the HIV-1Tg rats compared to the control animals. In contrast, the serum level of IL-10, an anti-inflammatory cytokine, was comparable in the HIV-1Tg, Tg control, and F344 control rats. Our data show that, in the HIV-1Tg rat, there is a negative correlation between the LEA response and the induction of pro-inflammatory cytokines in response to bacterial endotoxin. These findings suggest that the persistent presence of viral proteins may be, at least, partially responsible for the immunodeficiency that occurs with HIV-1 infection, and that the HIV-1Tg rat could be a valid rodent model in which to study various aspects of HIV-1 infection.},
journal = {American Journal of Infectious Diseases},
publisher = {Science Publications}
}