The role of cytokines in the pathogenesis and treatment of HIV infection

Catálfamo, Marta; Saout, Cecile Le; Lane, H. Clifford

doi:10.1016/j.cytogfr.2012.05.007

Cited by 80 publications

(57 citation statements)

References 104 publications

(98 reference statements)

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“…In patients with HIV infection, following combination antiretroviral therapy (cART), the CD4 + T cell reconstitution is slow and could take many years, depending on the CD4 + T cell number prior to initiation of therapy (17)(18)(19). Together, these observations suggest that CD4 + and CD8 + T cell pools are differentially regulated and these characteristics may be exploited by HIV, contributing to the dysregulation of the T cell pools observed in these patients (16,(20)(21)(22)(23)(24).…”

Section: Introductionmentioning

confidence: 82%

IL-7–dependent STAT1 activation limits homeostatic CD4+ T cell expansion

Saout¹,

Luckey²,

Villarino³

et al. 2017

JCI Insight

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Section: Introductionmentioning

confidence: 82%

IL-7–dependent STAT1 activation limits homeostatic CD4+ T cell expansion

Saout¹,

Luckey²,

Villarino³

et al. 2017

JCI Insight

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“…Quality and concentration of isolated RNA were tested and cDNA was synthesised using QIAGEN RT 2 , TNFSF10 (TRAIL), TNFSF11, TNFSF12, TNFSF13, TNFSF13B, TNFSF14, TNFSF4 (OX40L), TNFSF8) and other cytokines (ADIPOQ, FAM3B, SPP1 (Osteopontin)). PCR reactions were carried out in a ABI 7500 Standard (Applied Biosystems, Foster City, California, USA) under given conditions: 10 min on 95°C, 40 cycles for 15 s on 95°C and 1 min on 60°C.…”

Section: Pcr Array Technology For Cytokine Gene Expression Analysismentioning

confidence: 99%

“…Infection with human immunodeficiency virus type 1 (HIV-1) is characterized by a continuous depletion of helper CD4+ T-cells and hyperactivation of the immune system [1] and [2]. The course of infection can be classified into several stages.…”

Section: Introductionmentioning

confidence: 99%

The comparison of Th1, Th2, Th9, Th17 and Th22 cytokine profiles in acute and chronic HIV-1 infection

Gorenec

Lepej

Grgic

et al. 2016

Microbial Pathogenesis

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“…Elevated levels of IL-6 (and other inflammatory biomarkers) have been reported in HIV patients and are associated with progression and prognosis of the disease (Nixon and Landay, 2010;Reuter et al, 2012;Catalfamo et al, 2012). One study investigated (four times over a 2 month period) the effect of HIV infection on the activity of various DMEs and correlated the phenotype with the genotype (Jones et al, 2010).…”

Section: Phenoconversion Of Dmes In Hiv Infectionmentioning

confidence: 99%

Inflammation-Induced Phenoconversion of Polymorphic Drug Metabolizing Enzymes: Hypothesis with Implications for Personalized Medicine

Shah¹,

2014

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Phenoconversion transiently converts genotypic extensive metabolizers (EMs) into phenotypic poor metabolizers (PMs) of drugs, potentially with corresponding changes in clinical response. This phenomenon, typically resulting from coadministration of medications that inhibit certain drug metabolizing enzymes (DMEs), is especially well documented for enzymes of the cytochrome P450 family. Nonclinical evidence gathered over the last two decades also strongly implicates elevated levels of some proinflammatory cytokines, released during inflammation, in down-regulation of drug metabolism, especially by certain DMEs of the P450 family, thereby potentially causing transient phenoconversion. Clinically, phenoconversion of NAT2, CYP2C19, and CYP2D6 has been documented in inflammatory conditions associated with elevated cytokines, such as human immunodeficiency virus infection, cancer, and liver disease. The potential of other inflammatory conditions to cause phenoconversion has not been studied but experimental and anecdotal clinical evidence supports infectioninduced down-regulation of CYP1A2, CYP3A4, and CYP2C9 as well. Collectively, the evidence supports a hypothesis that certain inflammatory conditions associated with elevated proinflammatory cytokines may cause phenoconversion of certain DMEs. Since inflammatory conditions associated with elevated levels of proinflammatory cytokines are highly prevalent, phenoconversion of genotypic EM patients into transient phenotypic PMs may be more frequent than appreciated. Since drug pharmacokinetics, and therefore the clinical response, is influenced by DME phenotype rather than genotype per se, phenoconversion (whatever its cause) can have a significant impact on the analysis and interpretation of genotype-focused clinical outcome association studies. There is a risk that focusing on genotype alone may miss important associations between clinical outcomes and DME phenotypes, thus compromising future prospects of personalized medicine.

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The role of cytokines in the pathogenesis and treatment of HIV infection

Cited by 80 publications

References 104 publications

IL-7–dependent STAT1 activation limits homeostatic CD4+ T cell expansion

IL-7–dependent STAT1 activation limits homeostatic CD4+ T cell expansion

The comparison of Th1, Th2, Th9, Th17 and Th22 cytokine profiles in acute and chronic HIV-1 infection

Inflammation-Induced Phenoconversion of Polymorphic Drug Metabolizing Enzymes: Hypothesis with Implications for Personalized Medicine

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