Abstract
Autophagy is a lysosomal-dependent degradative process essential for maintaining cellular homeostasis, and is a key player in innate and adaptive immune responses to intracellular pathogens such as human immunodeficiency virus type 1 (HIV-1). In HIV-1 target cells, autophagy mechanisms can (i) selectively direct viral proteins and viruses for degradation; (ii) participate in the processing and presentation of viral-derived antigens through major histocompatibility complexes; and (iii) contribute to interferon production in response to HIV-1 infection. As a consequence, HIV-1 has evolved different strategies to finely regulate the autophagy pathway to favor its replication and dissemination. HIV-1 notably encodes accessory genes encoding Tat, Nef and Vpu proteins, which are able to perturb and hijack canonical and non-canonical autophagy mechanisms. This review outlines the current knowledge on the complex interplay between autophagy and HIV-1 replication cycle, providing an overview of the autophagy-mediated molecular processes deployed both by infected cells to combat the virus and by HIV-1 to evade antiviral response.
Highlights
Macroautophagy is a lysosomal degradation pathway-dependent mechanism, initially described as being involved in the turnover of cellular components, either to maintain cell homeostasis or as a source of energy in response of metabolic stress
These findings suggest that human immunodeficiency virus type 1 (HIV-1)-mediated inhibition of autophagy in dendritic cells (DCs) might be a mechanism for evading adaptive immune response
We demonstrated that the Human immunodeficiency virus (HIV)-1 Vpu activity to counteract the cellular restriction factor bone marrow stromal cell antigen 2 (BST2) requires, in part, the LC3-Associated Phagocytosis (LAP) mechanism (Figure 3B) [112]
Summary
Macroautophagy ( called autophagy) is a lysosomal degradation pathway-dependent mechanism, initially described as being involved in the turnover of cellular components (proteins, lipids and organelles), either to maintain cell homeostasis or as a source of energy in response of metabolic stress. In the early 2000s, it became obvious that autophagy is involved in immune response as a key element of innate defense against bacterial infection [1,2,3] or adaptive immunity by participating in major histocompatibility complex class II (MHC-II) processing of viral antigens [4]. Numerous studies have provided evidence that autophagy plays a crucial role in host response, especially by selectively degrading intracellular pathogens or targeting cytosolic exogenous antigens to MHC-II containing compartment. CD4+ T cells, macrophages and DCs form viral reservoirs, despite the fact that these cellular populations are among the most specialized host cells to detect and mount an immune response to eliminate pathogens. This review discusses the intricate interplay between HIV and autophagy, highlighting how HIV exercises fine control over the autophagy pathway in its target cells
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