# Cardiovascular Risk in HIV Patients: Ageing Analysis of the Involved Genes
###### Abstract
The longer life expectancy associated with HIV has led to a heightened prevalence of age-related illnesses, including morbidity and mortality linked to cardiovascular diseases [9]. In this paper, we focus on the possible interactions between HIV and the development of cardiovascular diseases with advancing age, considering the increase in life expectancy of these patients thanks to modern therapies. We focus on genes of interest for cardiovascular pathology and their association with HIV, and we also study variations in gene expression during patient life. Indeed, we use a publicly available database, GTEx [10], containing information about gene expression variation during patient ageing in given tissues. The risk of cardiovascular disease (CVD) mortality is significantly elevated among HIV patients across age groups from 25 to 64 years compared to the general population [11]. It has been observed that the risk of CVD mortality is markedly reduced in individuals living with HIV who achieve viral suppression compared to those without complete suppression. The development of cardiovascular diseases is connected to gene dysregulation exacerbated by the infection and the associated inflammatory environment [12]. The upregulation or downregulation of some Rho-associated kinases and T-cell components is common in People Living With HIV (PLWHs), with their expression patterns varying based on the specific tissue, while also being influenced by factors like sex, race, and age. Their involvement is at the basis of inflammatory and fibrosis processes in cardiovascular diseases. The introduction of Highly Active Antiretroviral Therapy (HAART) has significantly reduced AIDS-related mortality, as demonstrated by [PERSON] et al. [13]. However, non-HIV-related mortality, such as that attributable to CVD, has become increasingly crucial for the estimated 33.3 million People Living With HIV (PLWHs) [14]. Data from the New York City HIV Surveillance Registry for 2001 to 2012 showed that the proportion of CVD deaths among all deaths increased in the HIV population from 6 per cent to 15 per cent and decreased in the general population [15]. Thus, a growing number of subjects living with chronic HIV infection are experiencing early cardiovascular disease. Our goal is to offer a comprehensive quantitative synthesis of the genetic pathways implicated in HIV and their association with CVD, taking into account age- and sex-related disparities as well [16]. Figure 1 reports the workflow representing the performed analysis to gather genes involved in HIV infection and to study their role with respect to CVD. Despite evidence of the earlier onset of CVD in the population living with HIV, it is not well known how HIV infection increases the risk of cardiovascular diseases. Smoking remains one of the most significant contributors to the development of CVD among PLWHs [17]. At the same time, HIV infection has been recognized as a prothrombotic condition in which a hypercoagulable state places patients at increased risk for deep vein thrombosis and other ischemic CVD events. Activated platelets favour proinflammatory and thrombogenic effects. However, no genes have been identified as the cause of the increased risk of developing CVD in PLWHs. This paper aims to study gene expression variation during age in patients with HIV, focusing on genes associated with cardiovascular diseases. We use the GTEx database to identify genes of interest, and we review the genes associated with CVD, whose expression varies with age in HIV-infected subjects. We also performed a bioinformatic analysis to explore the biological impact of ageing-related genes.