Impact of current antiretroviral therapies on neuroAIDS

Vivithanaporn, Pornpun; Gill, M. John; Power, Christopher

doi:10.1586/eri.10.179

Cited by 24 publications

(18 citation statements)

References 44 publications

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“…The mutation and recombination rates and frequencies, the virion production rate, and a short generation time all contribute to HIV-1 exhibiting quasispecies dynamics (references 145,369,385,407,478,511,552,588,589,639,655,674,675,735,800,804,844, and 852, among numerous other studies). The interpretation of the origin of HIV-1 heterogeneity and diversification of viral sequences is complicated by the compartmentalization of the infection, the presence of viral reservoirs (and therefore replicative and nonreplicative quasispecies memory), and reactivation of latent provirus (85,110,127,176,296,390,458,488,706,835,872). Retroviral sequences integrated into cellular DNA will be subjected to the relative evolutionary stasis typical of cellular genes (except in the case of potential integration at sites undergoing cellular hypermutational events).…”

Section: Human Immunodeficiency Virus Typementioning

confidence: 99%

Viral Quasispecies Evolution

Domingo

Sheldon

Perales

2012

Microbiol Mol Biol Rev

874

880

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SUMMARY Evolution of RNA viruses occurs through disequilibria of collections of closely related mutant spectra or mutant clouds termed viral quasispecies. Here we review the origin of the quasispecies concept and some biological implications of quasispecies dynamics. Two main aspects are addressed: (i) mutant clouds as reservoirs of phenotypic variants for virus adaptability and (ii) the internal interactions that are established within mutant spectra that render a virus ensemble the unit of selection. The understanding of viruses as quasispecies has led to new antiviral designs, such as lethal mutagenesis, whose aim is to drive viruses toward low fitness values with limited chances of fitness recovery. The impact of quasispecies for three salient human pathogens, human immunodeficiency virus and the hepatitis B and C viruses, is reviewed, with emphasis on antiviral treatment strategies. Finally, extensions of quasispecies to nonviral systems are briefly mentioned to emphasize the broad applicability of quasispecies theory.

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Section: Human Immunodeficiency Virus Typementioning

confidence: 99%

Viral Quasispecies Evolution

Domingo

Sheldon

Perales

2012

Microbiol Mol Biol Rev

874

880

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“…The advent of highly active antiretroviral therapy (HAART) has not only decreased the mortality rates substantially among individuals living with AIDS [6], but has also significantly decreased the incidence of HIV-1-associated dementia (HAD) [7]. However, the incidence of HIV-1-associated neurocognitive disorders (HAND), especially the milder form, has actually increased, perhaps due to central nervous system (CNS) toxicities mediated by HAART [8, 9]. Consumption of drugs of abuse, such as alcohol, tobacco, cocaine, methamphetamine and marijuana, has also been shown to exacerbate HIV-1 pathogenesis by accelerating the incidence and progression of HAND/HAD [10].…”

Section: Introductionmentioning

confidence: 99%

Tobacco smoking effect on HIV-1 pathogenesis: role of cytochrome P450 isozymes

Ande

McArthur

Kumar

et al. 2013

Expert Opinion on Drug Metabolism & Toxicology

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Introduction Tobacco smoking is highly prevalent among the HIV-1-infected population. In addition to diminished immune response, smoking has been shown to increase HIV-1 replication and decrease response to antiretroviral therapy, perhaps through drug–drug interaction. However, the mechanism by which tobacco/nicotine increases HIV-1 replication and mediates drug–drug interaction is poorly understood. Areas covered In this review, the authors discuss the effects of smoking on HIV-1 pathogenesis. Since they propose a role for the cytochrome P450 (CYP) pathway in smoking-mediated HIV-1 pathogenesis, the authors briefly converse the role of CYP enzymes in tobacco-mediated oxidative stress and toxicity. Finally, the authors focus on the role of CYP enzymes, especially CYP2A6, in tobacco/nicotine metabolism and oxidative stress in HIV-1 model systems monocytes/macrophages, lymphocytes, astrocytes and neurons, which may be responsible for HIV-1 pathogenesis. Expert opinion Recent findings suggest that CYP-mediated oxidative stress is a novel pathway that may be involved in smoking-mediated HIV-1 pathogenesis, including HIV-1 replication and drug–drug interaction. Thus, CYP and CYP-associated oxidative stress pathways may be potential targets to develop novel pharmaceuticals for HIV-1-infected smokers. Since HIV-1/TB co-infections are common, future study involving interactions between antiretroviral and antituberculosis drugs that involve CYP pathways would also help treat HIV-1/TB co-infected smokers effectively.

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“…Despite these advances, the prevalence of HIV-associated neurocognitive disorders (HAND) has increased [8, 9]. It is important to determine the mechanisms by which HIV proteins cause neural dysfunction and how opiates potentially interact via an additive or synergistic effect.…”

Section: Introductionmentioning

confidence: 99%

Effects of Opiates and HIV Proteins on Neurons: The Role of Ferritin Heavy Chain and a Potential for Synergism

Festa

Meucci²

2012

CHR

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Human immunodeficiency virus 1 (HIV-1) and its associated proteins can have a profound impact on the central nervous system. Co-morbid abuse of opiates, such as morphine and heroin, is often associated with rapid disease progression and greater neurological dysfunction. The mechanisms by which HIV proteins and opiates cause neuronal damage on their own and together are unclear. The emergence of ferritin heavy chain (FHC) as a negative regulator of the chemokine receptor CXCR4, a co-receptor for HIV, may prove to be important in elucidating the interaction between HIV proteins and opiates. This review summarizes our current knowledge of central nervous system damage inflicted by HIV and opiates, as well as the regulation of CXCR4 by opiate-induced changes in FHC protein levels. We propose that HIV proteins and opiates exhibit an additive or synergistic effect on FHC/CXCR4, thereby decreasing neuronal signaling and function.

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Impact of current antiretroviral therapies on neuroAIDS

Cited by 24 publications

References 44 publications

Viral Quasispecies Evolution

Viral Quasispecies Evolution

Tobacco smoking effect on HIV-1 pathogenesis: role of cytochrome P450 isozymes

Effects of Opiates and HIV Proteins on Neurons: The Role of Ferritin Heavy Chain and a Potential for Synergism

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