Abstract
Macrophages have been postulated to play an important role in the pathogenesis of HIV-1 infection. Their ability to cross the blood-brain barrier and their resistance to virus-induced cytopathic effects allows them to serve as reservoirs for long-term infection. Thus, exploring the mechanisms of virus transmission from macrophages to target cells such as other macrophages or T lymphocytes is central to our understanding of HIV-1 pathogenesis and progression to AIDS, and is vital to the development of vaccines and novel antiretroviral therapies. This review provides an overview of the current understanding of cell-cell transmission in macrophages.
Highlights
Infection by HIV-1, a member of the genus Lentiviridae, results in an acute period characterized by high viral loads and a transient drop in CD4+ T cell counts
This study suggests that ESCRT components are sufficiently abundant both at the plasma membrane and in multivesicular bodies (MVBs) to promote HIV-1 budding
The first HIV-1 cell-associated transfer across a synapse was demonstrated in the context of trans-infection from DCs to T lymphocytes [76], where viruses and their receptors were recruited to the contact sites
Summary
Infection by HIV-1, a member of the genus Lentiviridae, results in an acute period characterized by high viral loads and a transient drop in CD4+ T cell counts. Following a vigorous adaptive immune response, viral loads decline and CD4+ T-cell counts recover. CD4 counts decline progressively, eventually leading to immunodeficiency and death [1]. HIV-1 enters target cells in most cases by using CD4 (a major attachment receptor), and chemokine coreceptors (CCR5 or CXCR4) [2]. CD4+ T cells represent a major target cell population in vivo. Other cell populations, notably macrophages, are productively infected by HIV-1. Viruses 2010, 2 periods of time post-infection [3,4] and their ability to cross the blood-brain barrier suggests an important role in disseminating virus to the central nervous system [5]
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