Abstract
Purpose :
HIV-1 infection can cause visual impairment in 73% of patients. The HIV viral load is often detected in ocular fluids and the retina. Therefore, understanding the effect of HIV on retinal inflammation and homeostasis is of great importance.
Methods :
We used a localized HIV eye model developed by injecting 2.5ng/uL of HIV-Tat protein into the eyes of female Sprague Dawley rats (21 days). After five days, rats were euthanized, and their retinas enucleated. Immunohistochemical analysis and confocal microscopy was used to semi-quantitatively evaluate physiological changes in the BRB components using glial fibrillary acidic protein (GFAP), Aquaporin 4 (AQP4) and potassium channel Kir 4.1 for glial cell markers; intercellular adhesion molecule 1 (ICAM-1) for BRB markers; and Interleukin 1 Beta (IL-1B) and Tumor Necrosis Factor Alpha (TNFa) for inflammation markers. In addition, Western Blot was performed to quantitatively assess differences in Kir 4.1, AQP4 and GFAP expression between sham and HIV-Tat treated eyes.
Results :
Immunofluorescence results showed an increased expression of Kir4.1 and AQP4 in Müller glial cells in the retinas treated with HIV-Tat. Additionally, there was also an upregulation of ICAM-1 observed in the outer-BRB/RPE cells. Western Blot analysis showed that Kir 4.1 and AQP4 protein level expression was increased in retinas treated with HIV-Tat compared to sham.
Conclusions :
In conclusion, we suggest that such upregulation of Kir 4.1 and AQP4 are rather compensating effects of glial cells to maintain normal potassium and water buffering than commonly expected degradative process. Additionally, results suggests that ICAM-1 could be a promoter of HIV adhesion to the RPE cells by facilitating viral load invasion into the ocular tissues during HIV. Still, further investigation is needed.
This abstract was presented at the 2022 ARVO Annual Meeting, held in Denver, CO, May 1-4, 2022, and virtually.