A post-entry role for CD63 in early HIV-1 replication

Li, Guangyu; Dziuba, Natallia; Friedrich, Brian; Murray, James L.; Ferguson, Monique

doi:10.1016/j.virol.2011.01.017

Cited by 26 publications

(21 citation statements)

References 55 publications

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“…Tetraspanins incorporated into the membranes of virus particles may collaborate in fusion (93). In addition to its presence in transmission electron micrographs at the plasma membrane, CD63 also plays an early postentry role prior to or at the reverse transcription step of HIV (94). HIV fusion can also occur after endocytosis, as we describe below (2).…”

Section: Mechanism Of Viral Fusion With the Plasma Membrane Direct Fumentioning

confidence: 99%

Extracellular Vesicles Exploit Viral Entry Routes for Cargo Delivery

Dongen

Masoumi

Witwer

et al. 2016

Microbiol Mol Biol Rev

222

193

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SUMMARYExtracellular vesicles (EVs) have emerged as crucial mediators of intercellular communication, being involved in a wide array of key biological processes. Eukaryotic cells, and also bacteria, actively release heterogeneous subtypes of EVs into the extracellular space, where their contents reflect their (sub)cellular origin and the physiologic state of the parent cell. Within the past 20 years, presumed subtypes of EVs have been given a rather confusing diversity of names, including exosomes, microvesicles, ectosomes, microparticles, virosomes, virus-like particles, and oncosomes, and these names are variously defined by biogenesis, physical characteristics, or function. The latter category, functions, in particular the transmission of biological signals between cellsin vivoand how EVs control biological processes, has garnered much interest. EVs have pathophysiological properties in cancer, neurodegenerative disorders, infectious disease, and cardiovascular disease, highlighting possibilities not only for minimally invasive diagnostic applications but also for therapeutic interventions, like macromolecular drug delivery. Yet, in order to pursue therapies involving EVs and delivering their cargo, a better grasp of EV targeting is needed. Here, we review recent progress in understanding the molecular mechanisms underpinning EV uptake by receptor-ligand interactions with recipient cells, highlighting once again the overlap of EVs and viruses. Despite their highly heterogeneous nature, EVs require common viral entry pathways, and an unanticipated specificity for cargo delivery is being revealed. We discuss the challenges ahead in delineating specific roles for EV-associated ligands and cellular receptors.

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Section: Mechanism Of Viral Fusion With the Plasma Membrane Direct Fumentioning

confidence: 99%

Extracellular Vesicles Exploit Viral Entry Routes for Cargo Delivery

Dongen

Masoumi

Witwer

et al. 2016

Microbiol Mol Biol Rev

222

193

View full text Add to dashboard Cite

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“…The upregulation of various host molecules derived from exosomes (i.e., CD81, CD63, and CD9) by several viruses and incorporation into the viral membrane for various purposes have been previously described (Dongen et al, 2016). For example, CD63 upregulation during HIV-1 infection has been suggested to mediate CD63 integration into HIV-1 membranes to aid in both viral fusion and replication (Li et al, 2011(Li et al, , 2014Narayanan et al, 2013;Fu et al, 2015;Sampey et al, 2016). It is possible that EBOV VP40 may play a role in the upregulation of CD63 for a similar purpose.…”

Section: Introductionmentioning

confidence: 97%

The Role of Exosomal VP40 in Ebola Virus Disease

Pleet

DeMarino

Lepene

et al. 2017

DNA and Cell Biology

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Ebola virus (EBOV) can cause a devastating hemorrhagic disease, leading to death in a short period of time. After infection, the resulting EBOV disease results in high levels of circulating cytokines, endothelial dysfunction, coagulopathy, and bystander lymphocyte apoptosis in humans and nonhuman primates. The VP40 matrix protein of EBOV is essential for viral assembly and budding from the host cell. Recent data have shown that VP40 exists in the extracellular environment, including in exosomes, and exosomal VP40 can impact the viability of recipient immune cells, including myeloid and T cells, through the regulation of the RNAi and endosomal sorting complexes required for transport pathways. In this study, we discuss the latest findings of the impact of exosomal VP40 on immune cells in vitro and its potential implications for pathogenesis in vivo.

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“…Indeed, HIV-1 vpu protein downregulates CD81 in HIV-1 infected cells, promoting virion infectivity 18 . On the contrary, CD63 is important for viral RT 19 .…”

Section: Introductionmentioning

confidence: 99%

CD81 association with SAMHD1 enhances HIV-1 reverse transcription by increasing dNTP levels

et al. 2017

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In this study, we report that the tetraspanin CD81 enhances HIV-1 reverse transcription in HIV-1-infected cells. This is enabled by the direct interaction of CD81 with the deoxynucleoside triphosphate phosphohydrolase SAMHD1. This interaction prevents the endosomal accumulation and favours the proteasome-dependent degradation of SAMHD1. Consequently, CD81 depletion results in SAMHD1 increased expression, decreasing the availability of deoxynucleoside triphosphates (dNTP) and thus HIV-1 reverse transcription. Conversely, CD81 overexpression, but not the expression of a CD81 C-term deletion mutant, increases cellular dNTP content and HIV-1 reverse transcription. Our results demonstrate that the interaction of CD81 with SAMHD1 controls the metabolic rate of HIV-1 replication by tuning the availability of building blocks for reverse transcription, i.e. dNTPs. Together with its role in HIV-1 entry and budding into host cells, the data herein indicate that HIV-1 uses CD81 as a rheostat that controls different stages of the infection.

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A post-entry role for CD63 in early HIV-1 replication

Cited by 26 publications

References 55 publications

Extracellular Vesicles Exploit Viral Entry Routes for Cargo Delivery

Extracellular Vesicles Exploit Viral Entry Routes for Cargo Delivery

The Role of Exosomal VP40 in Ebola Virus Disease

CD81 association with SAMHD1 enhances HIV-1 reverse transcription by increasing dNTP levels

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