PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 12222963

Assembling the human immunodeficiency virus type 1.

A Cimarelli·J L Darlix
View original source ↗Export metadata ↓

Abstract

Retroviral assembly proceeds through a series of concerted events that lead to the formation and release of infectious virion particles from the infected cell. Upon translation, structural proteins are targeted to the plasma membrane where they accumulate. There, the nascent particle forces the plasma membrane to form a bud, which pinches off releasing the virion particle from the cell. In this review we describe the molecular mechanisms now known to be behind the process of virion assembly. In particular, we focus on the human immunodeficiency virus type 1, the prototype member of the lentivirus subfamily of the Retroviridae.

Explore related subjects

Cell MembraneGene Products, envGene Products, gagGene Products, vifGenes, ViralHIV-1Human Immunodeficiency Virus ProteinsModels, BiologicalProtein Structure, TertiaryRNA, ViralViral Regulatory and Accessory ProteinsVirionvif Gene Products, Human Immunodeficiency VirusViroporin ProteinsJournal ArticleResearch Support, Non-U.S. Gov'tReview

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

A Cimarelli, J L Darlix. 2002. Assembling the human immunodeficiency virus type 1.. https://doi.org/10.1007/s00018-002-8495-6

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2025

Time-resolved transcriptomics of S. cerevisiae and S. pastorianus in response to plasma membrane stresses.

Yeasts are beneficial microorganisms for human society and are utilized for academic and industrial purposes. For academic purposes, S. cerevisiae is a well-investigated model for studying eukaryotic cellular processes. For industrial purposes, S. pastorianus, which has a hybrid genome of S. cerevisiae and S. eubayanus, has been served for lager beer production. During fermentation, S. pastorianus produces ~7% of EtOH, which induces plasma membrane (PM)/cell wall stress in yeast. Therefore, S. pastorianus may experience PM stress and adapt to the self-forming environment during fermentation. However, how yeast adapts to PM stress remains unclear. Here, we investigated the temporal cellular responses of S. cerevisiae and S. pastorianus during adaptation to PM stresses by time-resolved mRNA-seq analysis. Our data showed different transcriptional phenotypes between S. cerevisiae and S. pastorianus during adaptation. The results may reflect the distinct nature of the two yeasts that have evolved in different nutritional environments. The dataset presented here would provide a promising resource for studying the characteristic nature of these differentially domesticated yeasts upon PM stresses.

Cell Membrane↗
PubMed2004

Effect of glycosylphosphatidylinositol (GPI)-phospholipase D overexpression on GPI metabolism.

GPI-PLD [glycosylphosphatidylinositol (GPI)-specific phospholipase D (PLD)] is a secreted mammalian enzyme that specifically cleaves GPI-anchored proteins. In addition, the enzyme has been shown to cleave GPI anchor intermediates in cell lysates. The biosynthesis of the GPI anchor is well characterized; however, the mechanisms by which the levels of GPI anchor intermediates are regulated are still unknown. To investigate whether GPI-PLD plays a role in this regulation, we isolated stable HeLa cells overexpressing the enzyme. GPI-PLD-HeLa (GPI-PLD-transfected HeLa) cells showed a 3-fold increase in intracellular GPI-PLD activity and drastically decreased the levels of GPI-anchored proteins when compared with untransfected HeLa controls. Intracellular cleavage of GPI-anchored proteins has been suggested to occur early in the secretory pathway and, in agreement with this proposal, GPI-PLD activity in GPI-PLD-HeLa cells was detected not only in the endoplasmic reticulum and Golgi apparatus, but also in the plasma membrane. The enzyme was also active in lipid rafts, membrane microdomains in which GPI-anchored proteins and GPI anchor intermediates are concentrated, indicating that intracellular GPI-PLD cleavage may also occur in this compartment. Pulse-chase paradigms revealed the turnover rate of the last intermediate of the GPI anchor pathway in GPI-PLD-HeLa cells to be accelerated compared with the controls. Furthermore, 1,10-phenanthroline, a GPI-PLD inhibitor, reversed this effect. Our studies demonstrated that GPI-PLD can cleave not only GPI-anchored proteins, but also GPI anchor intermediates intracellularly. This observation opens the possibility that GPI-PLD can influence the steady-state levels of GPI-anchored proteins by hydrolysing the anchor before and after its attachment to proteins.

Cell Membrane↗
PubMed2004

Current-voltage-time records of ion translocating enzymes.

Membrane currents, as non-linear functions of membrane voltage, V, and time, t, can be recorded quickly by triangular V protocols. From the differences, d I(V, t), of these relationships upon addition of a putative substrate of a charge-translocating membrane protein, the I(V, t) relationships of the transporter itself can be determined. These relationships likely comprise a steady-state component, I(a)(V), of the active transporter, and a dynamic component, p(a)(V, t), of its V- and time-dependent activity, p(a). Here, the steady-state component is modeled by a central reaction cycle, which senses a fraction delta(tr) of the total V, whereas 1-delta(tr) can be assigned to an inner and outer pore section with delta(i) and delta(o), respectively (delta(i)+delta(tr)+delta(o) = 1). For the enzymatic cycle, fast binding/debinding is assumed, plus V-sensitive and -insensitive reaction steps which may become rate limiting for charge translocation. At given substrate concentrations, I(a)(V) is defined by eight independent system parameters, including a coefficient for the barrier shape of charge translocation. In ordinary cases, the behavior of p(a)(V, t) can be described by two rate constants (for activation and inactivation) and their respective V-sensitivity coefficients. Here, the effects of the individual system parameters on I(V, t) from triangular V-clamp experiments are investigated systematically. The results are illustrated by panels of typical curve shapes for non-gated and gated transporters to enable a first classification of mechanisms. We demonstrate that all system parameters can be determined fairly well by fitting the model to "experimental" data of known origin. Applicability of the model to channels, pumps and cotransporters is discussed.

Cell Membrane↗