Liquidating the Foreign Personal Holding Company: Alternative Considerations

Prior to 1937, it was common for United states taxpayers to utilize offshore corporate entities, structured in the form of a foreign personal holding company ( FPHC ) to avoid United States taxation. As indi- cated by the House Committee Notes accompanying enactment of the Revenue Act of 1937, [t]he evidence presented to the joint committee has shown that foreign personal holding companies have afforded one of the most flagrant loopholes for tax avoidance. \u27 The primary problem faced by the lawmakers in 1937 was the fact that the United States was unable to acquire direct taxing jurisdiction over such companies due to the fact that such corporate entities were not located within the taxing jurisdiction of the United States.2 As a result, Congress adopted an alter- native approach which in the opinion of the lawmakers was justifiable on constitutional grounds;3 that is, to provide for a method of taxation that will reach the shareholders who own stock in such companies and over whom the United States has direct taxing authority.4 As a result, the FPHC provisions provided an alternative method of taxation which deemed the income of the FPHC to be distributed to the shareholders and required such shareholders to report as their income, the undistrib- uted net income of such FPHC.\u27 Although there are certain similarities that exist between the FPHC provisions6 and the domestic PHC provisions,7 it is not the purpose of this work to address such differences. Rather, this Article will: (1) Dis- cuss and analyze the operative provisions of the FPHC provisions;8 (2) Analyze the methods by which shareholders subject to the United States taxing jurisdiction may minimize the tax impact of liquidating a FPHC and repatriating its earnings to the United States taxing jurisdic- tion;9 and (3) Discuss miscellaneous considerations applicable in the con- text of such alternative liquidation techniques

Liquidating the Foreign Personal Holding Company: Alternative Considerations

Prior to 1937, it was common for United states taxpayers to utilize offshore corporate entities, structured in the form of a foreign personal holding company ( FPHC ) to avoid United States taxation. As indi- cated by the House Committee Notes accompanying enactment of the Revenue Act of 1937, [t]he evidence presented to the joint committee has shown that foreign personal holding companies have afforded one of the most flagrant loopholes for tax avoidance. \u27 The primary problem faced by the lawmakers in 1937 was the fact that the United States was unable to acquire direct taxing jurisdiction over such companies due to the fact that such corporate entities were not located within the taxing jurisdiction of the United States.2 As a result, Congress adopted an alter- native approach which in the opinion of the lawmakers was justifiable on constitutional grounds;3 that is, to provide for a method of taxation that will reach the shareholders who own stock in such companies and over whom the United States has direct taxing authority.4 As a result, the FPHC provisions provided an alternative method of taxation which deemed the income of the FPHC to be distributed to the shareholders and required such shareholders to report as their income, the undistrib- uted net income of such FPHC.\u27 Although there are certain similarities that exist between the FPHC provisions6 and the domestic PHC provisions,7 it is not the purpose of this work to address such differences. Rather, this Article will: (1) Dis- cuss and analyze the operative provisions of the FPHC provisions;8 (2) Analyze the methods by which shareholders subject to the United States taxing jurisdiction may minimize the tax impact of liquidating a FPHC and repatriating its earnings to the United States taxing jurisdic- tion;9 and (3) Discuss miscellaneous considerations applicable in the con- text of such alternative liquidation techniques

Assessing the Limited Liability Company

The limited liability company is one of the newest forms of business organization. This form combines the limited liability of a corporation with the tax benefits normally associated with a partnership. The authors examine various implications and ramifications of this organizational form

Revisiting HIV-1 uncoating

HIV uncoating is defined as the loss of viral capsid that occurs within the cytoplasm of infected cells before entry of the viral genome into the nucleus. It is an obligatory step of HIV-1 early infection and accompanies the transition between reverse transcription complexes (RTCs), in which reverse transcription occurs, and pre-integration complexes (PICs), which are competent to integrate into the host genome. The study of the nature and timing of HIV-1 uncoating has been paved with difficulties, particularly as a result of the vulnerability of the capsid assembly to experimental manipulation. Nevertheless, recent studies of capsid structure, retroviral restriction and mechanisms of nuclear import, as well as the recent expansion of technical advances in genome-wide studies and cell imagery approaches, have substantially changed our understanding of HIV uncoating. Although early work suggested that uncoating occurs immediately following viral entry in the cell, thus attributing a trivial role for the capsid in infected cells, recent data suggest that uncoating occurs several hours later and that capsid has an all-important role in the cell that it infects: for transport towards the nucleus, reverse transcription and nuclear import. Knowing that uncoating occurs at a later stage suggests that the viral capsid interacts extensively with the cytoskeleton and other cytoplasmic components during its transport to the nucleus, which leads to a considerable reassessment of our efforts to identify potential therapeutic targets for HIV therapy. This review discusses our current understanding of HIV uncoating, the functional interplay between infectivity and timely uncoating, as well as exposing the appropriate methods to study uncoating and addressing the many questions that remain unanswered

Plasma Membrane Is the Site of Productive HIV-1 Particle Assembly

Recently proposed models that have gained wide acceptance posit that HIV-1 virion morphogenesis is initiated by targeting the major structural protein (Gag) to late endosomal membranes. Thereafter, late endosome-based secretory pathways are thought to deliver Gag or assembled virions to the plasma membrane (PM) and extracellular milieu. We present several findings that are inconsistent with this model. Specifically, we demonstrate that HIV-1 Gag is delivered to the PM, and virions are efficiently released into the extracellular medium, when late endosome motility is abolished. Furthermore, we show that HIV-1 virions are efficiently released when assembly is rationally targeted to the PM, but not when targeted to late endosomes. Recently synthesized Gag first accumulates and assembles at the PM, but a proportion is subsequently internalized via endocytosis or phagocytosis, thus accounting for observations of endosomal localization. We conclude that HIV-1 assembly is initiated and completed at the PM, and not at endosomal membranes

Polarity Changes in the Transmembrane Domain Core of HIV-1 Vpu Inhibits Its Anti-Tetherin Activity

Tetherin (BST-2/CD317) is an interferon-inducible antiviral protein that restricts the release of enveloped viruses from infected cells. The HIV-1 accessory protein Vpu can efficiently antagonize this restriction. In this study, we analyzed mutations of the transmembrane (TM) domain of Vpu, including deletions and substitutions, to delineate amino acids important for HIV-1 viral particle release and in interactions with tetherin. The mutants had similar subcellular localization patterns with that of wild-type Vpu and were functional with respect to CD4 downregulation. We showed that the hydrophobic binding surface for tetherin lies in the core of the Vpu TM domain. Three consecutive hydrophobic isoleucine residues in the middle region of the Vpu TM domain, I15, I16 and I17, were important for stabilizing the tetherin binding interface and determining its sensitivity to tetherin. Changing the polarity of the amino acids at these positions resulted in severe impairment of Vpu-induced tetherin targeting and antagonism. Taken together, these data reveal a model of specific hydrophobic interactions between Vpu and tetherin, which can be potentially targeted in the development of novel anti-HIV-1 drugs

Immunoelectron Microscopic Evidence for Tetherin/BST2 as the Physical Bridge between HIV-1 Virions and the Plasma Membrane

Tetherin/BST2 was identified in 2008 as the cellular factor responsible for restricting HIV-1 replication at a very late stage in the lifecycle. Tetherin acts to retain virion particles on the plasma membrane after budding has been completed. Infected cells that express large amounts of tetherin display large strings of HIV virions that remain attached to the plasma membrane. Vpu is an HIV-1 accessory protein that specifically counteracts the restriction to virus release contributed by tetherin. Tetherin is an unusual Type II transmembrane protein that contains a GPI anchor at its C-terminus and is found in lipid rafts. The leading model for the mechanism of action of tetherin is that it functions as a direct physical tether bridging virions and the plasma membrane. However, evidence that tetherin functions as a physical tether has thus far been indirect. Here we demonstrate by biochemical and immunoelectron microscopic methods that endogenous tetherin is present on the viral particle and forms a bridge between virion particles and the plasma membrane. Endogenous tetherin was found on HIV particles that were released by partial proteolytic digestion. Immunoelectron microscopy performed on HIV-infected T cells demonstrated that tetherin forms an apparent physical link between virions and connects patches of virions to the plasma membrane. Linear filamentous strands that were highly enriched in tetherin bridged the space between some virions. We conclude that tetherin is the physical tether linking HIV-1 virions and the plasma membrane. The presence of filaments with which multiple molecules of tetherin interact in connecting virion particles is strongly suggested by the morphologic evidence

TRIM5 Suppresses Cross-Species Transmission of a Primate Immunodeficiency Virus and Selects for Emergence of Resistant Variants in the New Species

Cross-species transmission of simian immunodeficiency virus from sooty mangabeys (SIVsm) into rhesus macaques, and subsequent emergence of pathogenic SIVmac, required adaptation to overcome restriction encoded by the macaque TRIM5 gene

Rab7A Is Required for Efficient Production of Infectious HIV-1

Retroviruses take advantage of cellular trafficking machineries to assemble and release new infectious particles. Rab proteins regulate specific steps in intracellular membrane trafficking by recruiting tethering, docking and fusion factors, as well as the actin- and microtubule-based motor proteins that facilitate vesicle traffic. Using virological tests and RNA interference targeting Rab proteins, we demonstrate that the late endosome-associated Rab7A is required for HIV-1 propagation. Analysis of the late steps of the HIV infection cycle shows that Rab7A regulates Env processing, the incorporation of mature Env glycoproteins into viral particles and HIV-1 infectivity. We also show that siRNA-mediated Rab7A depletion induces a BST2/Tetherin phenotype on HIV-1 release. BST2/Tetherin is a restriction factor that impedes HIV-1 release by tethering mature virus particles to the plasma membrane. Our results suggest that Rab7A contributes to the mechanism by which Vpu counteracts the restriction factor BST2/Tetherin and rescues HIV-1 release. Altogether, our results highlight new roles for a major regulator of the late endocytic pathway, Rab7A, in the late stages of the HIV-1 replication cycle