Abstract
Oncogenic and latent-persistent viruses belonging to both DNA and RNA groups are known to cause serious metabolism alterations. Among these, the Human Herpesvirus 8 (HHV8) infection induces stable modifications in biochemistry and cellular metabolism, which in turn affect its own pathological properties. HHV8 enhances the expression of insulin receptors, supports the accumulation of neutral lipids in cytoplasmic lipid droplets and induces alterations in both triglycerides and cholesterol metabolism in endothelial cells. In addition, HHV8 is also known to modify immune response and cytokine production with implications for cell oxidative status (i.e., reactive oxygen species activation). This review underlines the recent findings regarding the role of latent and persistent HHV8 viral infection in host physiology and pathogenesis.
Highlights
The Human Herpesvirus 8 (HHV8), known as Kaposi’s sarcoma-associated Herpesvirus (KSHV), is the most recently identified Herpesvirus found in tissue samples from immunodeficiency syndrome-associated Kaposi’s Sarcoma (KS) lesions by Chang et al [1]
While chronic infection of B-cells can lead to an impairment of the immune response [66], despite favouring the persistence and spread of the virus, the infection of endothelial cells may have a profound effect on the host’s metabolism, since it is strictly involved in the first step of food processing and in lipid metabolism [90]
In HHV8-infected endothelial cells, ATP production is mainly accomplished by glycolysis as often happens in tumour cells; interestingly, anaerobic metabolism is accompanied by enhanced reactive oxygen species (ROS) production which has been found to be involved in atherosclerosis, insulin resistance and diabetes
Summary
The Human Herpesvirus 8 (HHV8), known as Kaposi’s sarcoma-associated Herpesvirus (KSHV), is the most recently identified Herpesvirus found in tissue samples from immunodeficiency syndrome-associated Kaposi’s Sarcoma (KS) lesions by Chang et al [1]. Just like other Herpesviruses, HHV8 is characterized by a biphasic life cycle consisting of an acute phase during primary infection and a subsequent latent phase that involves the expression of very few genes and which may persist throughout the life of the host [4]. The mechanisms that control virus latency may represent a crucial target for the eradication of the latent infection and for the design of specific drugs that could cure the typical chronic HHV8-related disorders. Molecular biology and pathogenicity of HHV8 have been properly dealt with by others [2,3,5,6,7], this review wishes to mainly focus on lesser known aspects of HHV8 infection by remarking on the recent findings related to host metabolic alterations associated with the latent infection that, in turn, confers the specific behaviour and viral properties at the base of the pathogenicity
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