Abstract
Caveolin 1 (Cav-1) is a major component of the caveolae structure and is expressed in a variety of cell types including macrophages, which are susceptible to human immunodeficiency virus (HIV) infection. Caveolae structures are present in abundance in mechanically stressed cells such as endothelial cells and adipocytes. HIV infection induces dysfunction of these cells and promotes pathogenesis. Cav-1 and the caveolae structure are believed to be involved in multiple cellular processes that include signal transduction, lipid regulation, endocytosis, transcytosis, and mechanoprotection. Such a broad biological role of Cav-1/caveolae is bound to have functional cross relationships with several molecular pathways including HIV replication and viral-induced pathogenesis. The current review covers the relationship of Cav-1 and HIV in respect to viral replication, persistence, and the potential role in pathogenesis.
Highlights
Human immunodeficiency virus (HIV) has an extraordinary survival advantage in the host, confounding existing therapies
These are further complicated by the findings and emerging evidence that caveolae serve as mechanosensing organelles and may play a role in the protection of cells from mechanical stress by stretching or internalizing the caveolae structure [122,123,124,125]
Comparative investigations between wild type and negative factor (Nef) defective HIV reveal no significant differences in the reduction of high-density lipoprotein (HDL) mediated cholesterol efflux from endothelial cells, suggesting that multiple factors are involved that include Nef to alter cholesterol efflux
Summary
Human immunodeficiency virus (HIV) has an extraordinary survival advantage in the host, confounding existing therapies. It has been confirmed that monocytes, dendritic cells, and macrophages can be infected latently or with a low-level replication and can contribute to viral persistence [29,30,31,32,33,34]. In this viral reservoir, HIV infection appears to not be associated with apoptosis but with a chronic productive infection [69,70]. The persistent infection and survival of macrophages is potentially regulated by the contest between viral and cellular factors at different steps in virus replication, implying that there may be several mechanisms for HIV longevity in macrophages. This review will cover the functional importance of Cav-1 in HIV replication and its potential contribution to HIV persistence and pathogenesis
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