Immune activation, viral gene product expression and neurotoxicity in the HIV-1 transgenic rat

Cigarette smoke and nicotine effects on brain proinflammatory responses and behavioral and motor function in HIV-1 transgenic rats

“…The model mimics a number of abnormalities that have been demonstrated in humans with HIV infection. As we and others have previously demonstrated, these animals show evidence of (1) an increased proinflammatory state in brain and in peripheral immune cells (Cho et al 2017; Gorantla et al 2012; Royal et al 2012); (2) expression of HIV proteins in macrophage/microglial cells and astrocytes in the brain with envelope glycoprotein and tat expressed in the macrophage/microglial cells (Royal et al 2012), a pattern that is observed with HIV-1 infection in humans (Brack-Werner 1999; Glass et al 1995); (3) neurodegenerative effects characterized by decreased numbers of frontal cortex parvalbumin + neurons (Sultana et al 2010); and (4) the development of behavioral and motor abnormalities (June et al 2009; Moran et al 2013), all which are also observed in human HIV infection (Chana et al 2006). …”

“…Total RNA was purified from lysates produced from frontal cortex and analyzed by reverse-transcriptase polymerase chain reaction, as previously described (Royal et al 2012). The PCR primers that were used are as follows: (1) TNF-α: forward = 5′-TCT TCT CGA ACC CCG AGT GA-3′, reverse = 5′-CGG TTC AGC CAC T-3′; (2) IL-1β: forward = 5′-TGT GAT GAA AGA CGG CAC AC-3′; reverse = 5′-CTT CTT CTT TGG GTATTG TTT GG-3′ (3) IL-6: forward = 5′-TCA AGG GAA AAG AAC CAG ACA-3′; reverse = 5′-GGT TTC AAA TCA CTC ACC CAT AC-3′; (4) GAPDH (internal control): forward = 5′-CGA CCA CTT TGT CAA GCT CA-3′; reverse = 5′-AGG GGA GAT TCA GTG TGG TG-3′.…”

Time and time again: Temporal processing demands implicate perceptual and gating deficits in the HIV-1 transgenic rat

“…The purpose of the present study was to characterize PPI of the ASR in the HIV-1 Tg rat, which expresses 7 of the 9 HIV-1 genes and displays brain proinflammatory immune responses (Royal et al 2012). The assessments were planned to be conducted from 2 to 8 months of age, antecedent to the documented neurological symptoms or clinical signs of wasting (Peng et al 2010).…”

NeuroHIV and Use of Addictive Substances

“…It is an ideal model for investigating the efficacy of therapeutic treatments which reduce neurological dysfunction in HIV-infected individuals in the post-HAART era. The use of this rodent model for investigating neurologically related issues has been well established Moran, Aksenov, Booze, Webb, & Mactutus, 2012;Moran, Booze, Webb, & Mactutus, 2013;Royal, Wang, Jones, Tran, & Bryant, 2007;Royal et al, 2012). For example, Moran et al (2012Moran et al ( , 2013 used this model to test alterations in sensorimotor gating and behavior resulting from HIV-1 infection, including changes in dopamine (DA) function.…”

“…For example, Moran et al (2012Moran et al ( , 2013 used this model to test alterations in sensorimotor gating and behavior resulting from HIV-1 infection, including changes in dopamine (DA) function. Royal et al (2007Royal et al ( , 2012 used the HIV-1Tg rat to test the effects of vitamin A deficiency on HIV-1-associated neuroinflammation and mu opioid receptor (MOR) expression as well as peripheral and CNS immune responses in HIV infection. Also, Rao et al (2011) found that HIV1Tg rats exhibit neurological markers for neuroinflammation which are associated with cognitive impairment and identified neuroinflammation as a target for improving such impairments in HIV-positive populations (Rao et al, 2011).…”