Human Immunodeficiency Virus Type 1 Cellular Entry and Exit in the T Lymphocytic and Monocytic Compartments

Aiamkitsumrit, Benjamas; Sullivan, Neil T.; Nonnemacher, Michael R.; Pirrone, Vanessa; Wigdahl, Brian

doi:10.1016/bs.aivir.2015.04.001

Cited by 12 publications

(6 citation statements)

References 248 publications

(365 reference statements)

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“…In a relatively short period of time, several case reports and two series of post-mortem tissue sample analysis from China have begun to shed some light on potential mechanisms of kidney injury associated with COVID-19, even though many open issues remain (Table 1 [23][24][25][26]).…”

Section: A Proposed Pathogenesis Of Kidney Injurymentioning

confidence: 99%

“…For example, endothelial tubuloreticular inclusions also called myxovirus-like particles [ 22 ] Purported virus particles in the cytoplasm of kidney tubular epithelium and podocytes could represent clathrin-coated vesicles, which are normal cell organelles involved in intracellular transport [ 23 ] Viral nephrotoxic effects SARS-CoV-2 viral load has been quantified in autopsy kidneys, together with single cell RNA sequencing of viral receptors in kidney specimens and in situ hybridization. This analysis has revealed viral RNA in microdissected portions of the same specimens, thus suggesting both viral entry and replication into kidney cells [ 29 ] Viral entry and replication do not necessarily translate into cytopathic damage, as best exemplified by other viral infections such as HIV [ 24 ] SARS-CoV, whose genome is largely similar to that of SARS-CoV-2, was shown to be capable of entering kidney cells and replicating—but did not cause apparent harm [ 25 ] There has not yet been reproducible proof of viral tropism with active infection, which would require the concurrent demonstration of kidney cell infection (i.e. viral entry) together with viral replication/cytopathy ICU intensive care unit, ARDS acute respiratory distress syndrome, ATN acute tubular necrosis, RNA ribonucleic acid, EM electron microscopy, COVID - 19 novel corona virus disease infection …”

Section: A Proposed Pathogenesis Of Kidney Injurymentioning

confidence: 99%

“…SARS-CoV, whose genome is largely similar to that of SARS-CoV-2, was shown to be capable of entering kidney cells and replicating—but did not cause apparent harm [ 25 ]…”

Section: A Proposed Pathogenesis Of Kidney Injurymentioning

confidence: 99%

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COVID-19 and the kidney: what we think we know so far and what we don’t

et al. 2020

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The novel coronavirus disease infection (COVID-19) outbreak that was declared a global pandemic in March 2020 had led to an internationally variable but concerning incidence of COVID-associated acute kidney injury (AKI), with prevalence reported as high as 46% in large cohorts of hospitalized patients. Variability in AKI may be explained by differences in traditional risk factors for AKI, heterogeneity among patient cohorts, and differences in racial and ethnic groups. Further, AKI requiring kidney replacement therapies (KRT) has been associated with increased mortality. Proposed mechanisms of kidney injury include direct viral-induced tubular or glomerular injury, sepsis-associated AKI, and thrombotic disease. Kidney pathology include acute tubular injury, glomerular fibrin thrombi, pigmented tubular casts, and collapsing focal segmental glomerulosclerosis. "Viral-like" particles have been observed in renal samples at electron microscopy and viral RNA has been identified in both glomerular and tubular compartments of kidney specimens, but the link between viral presence and injury remain unclear. Though the link between AKI and poor outcomes is clear, prevalence and outcomes of COVID-19 in patients with chronic kidney disease and end stage kidney disease has not yet been reported. In patients on immunosuppression like those with kidney transplants or glomerular disease, COVID-19 has presented a management dilemma. Herein, we review the existing literature on kidney disease in COVID-19 and discuss what remains to be learned.

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Section: A Proposed Pathogenesis Of Kidney Injurymentioning

confidence: 99%

Section: A Proposed Pathogenesis Of Kidney Injurymentioning

confidence: 99%

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COVID-19 and the kidney: what we think we know so far and what we don’t

et al. 2020

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“…For animal viruses, in general, forces of selection (fitness constraints) emanate from host immunogenic responses, and also during 270 replication and transmission between hosts. Evolutionarily fit (selected) strains develop tropism, and infect different cell types or tissues of the host, reproduce within them, and in turn give rise to a variety of new strains having diverse chronic to acute infectious characteristics [26,27]. The advent of affordable high-throughput nucleotide sequencing techniques has enabled the generation of large scale genomic data, which in turn can reveal where, when, 275 and (sometimes) how viral pathogens have responded to various forces of natural selection.…”

Section: High Rate Of Nonsynonymous Mutations In the Structural Protementioning

confidence: 99%

Trends of Mutation Accumulation Across Global SARS-CoV-2 Genomes: Implications for the Evolution of the Novel Coronavirus

Roy¹,

Mandal²,

Mondol³

et al. 2020

Preprint

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To understand SARS-CoV-2 microevolution, this study explored the genome-wide frequency, gene-wise distribution, and molecular nature of all point-mutations detected across its 71,703 RNA-genomes deposited in the GISAID repository, till 21 August 2020. Globally, nsp1/nsp2/nsp3/ nsp11 and orf7a/orf3a/S were the most mutation-ridden non-structural and structural genes respectively. Phylogeny based on 4,618 spatiotemporally-representative genomes revealed that entities belonging to the early lineages are mostly spread over Asian countries (including India, the biggest hotspot of the pandemic) whereas the recently-derived lineages are more globally distributed. Of the total 16,602 polymorphism-bearing sites in the pan-genome, 11,037 and 4,965 involved transitions and transversions, which in turn were predominated by cytidine-to-uridine and guanosine-to-uridine conversions, respectively. Positive selection of nonsynonymous mutations (dN/dS >1) in most of the structural, but not non-structural, genes indicated that SARS-CoV-2 has already harmonized its replication/transcription machineries with the host’s metabolic system, while it is still redefining virulence/transmissibility strategies at the molecular level.

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“…HIV infection is associated with a very high viral load in the body leading to a progressive depletion of immune cells, particularly CD4 + T cells [ 1 , 2 ]. The infection can be treated with highly active antiretroviral therapy (HAART) consisting of at least three drugs from at least two classes of antiretroviral agents [ 3 ].…”

Section: Introductionmentioning

confidence: 99%

PLGA-PEG Nanoparticles Coated with Anti-CD45RO and Loaded with HDAC Plus Protease Inhibitors Activate Latent HIV and Inhibit Viral Spread

et al. 2015

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Activating HIV-1 proviruses in latent reservoirs combined with inhibiting viral spread might be an effective anti-HIV therapeutic strategy. Active specific delivery of therapeutic drugs into cells harboring latent HIV, without the use of viral vectors, is a critical challenge to this objective. In this study, nanoparticles of poly(lactic-co-glycolic acid)-polyethylene glycol diblock copolymers conjugated with anti-CD45RO antibody and loaded with the histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) and/or protease inhibitor nelfinavir (Nel) were tested for activity against latent virus in vitro. Nanoparticles loaded with SAHA, Nel, and SAHA + Nel were characterized in terms of size, surface morphology, zeta potential, entrapment efficiency, drug release, and toxicity to ACH-2 cells. We show that SAHA- and SAHA + Nel-loaded nanoparticles can target latently infected CD4+ T-cells and stimulate virus production. Moreover, nanoparticles loaded with SAHA + NEL were capable of both activating latent virus and inhibiting viral spread. Taken together, these data demonstrate the potential of this novel reagent for targeting and eliminating latent HIV reservoirs.

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Human Immunodeficiency Virus Type 1 Cellular Entry and Exit in the T Lymphocytic and Monocytic Compartments

Cited by 12 publications

References 248 publications

COVID-19 and the kidney: what we think we know so far and what we don’t

COVID-19 and the kidney: what we think we know so far and what we don’t

Trends of Mutation Accumulation Across Global SARS-CoV-2 Genomes: Implications for the Evolution of the Novel Coronavirus

PLGA-PEG Nanoparticles Coated with Anti-CD45RO and Loaded with HDAC Plus Protease Inhibitors Activate Latent HIV and Inhibit Viral Spread

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