HIV and hepatitis virus infection

Poles, Michael A.; Dieterich, Douglas T.

doi:10.1007/s11908-000-0078-9

Cited by 3 publications

(3 citation statements)

References 53 publications

(43 reference statements)

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“…Furthermore, in HCV patients with liver inflammation and fibrosis, elevated serum levels of IL-8, tumor necrosis factor-␣, adhesion molecules, and E-selectin have been reported (33,34). Moreover, prior data on liver specimens from patients with HCV infection indicate robust expression of IL-8, thus confirming the pathophysiological relevance of our findings (45,63). In addition to the chemotactic properties of IL-8, this chemokine is a natural antagonist of interferon (64).…”

Section: Discussionsupporting

confidence: 86%

Hepatitis C Virus and HIV Envelope Proteins Collaboratively Mediate Interleukin-8 Secretion through Activation of p38 MAP Kinase and SHP2 in Hepatocytes

Balasubramanian

Ganju

Groopman

2003

Journal of Biological Chemistry

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Hepatitis C virus (HCV) infects ϳ40% of human immunodeficiency virus (HIV) patients, and the resulting hepatic dysfunction that occurs is the primary cause of death in patients with co-infection. We hypothesized that hepatocytes exposed to HCV and HIV proteins might be susceptible to injury via an "innocent bystander" mechanism. To assess this, we studied the effects of envelope proteins, E2 of HCV and gp120 of HIV, in model HepG2 cells. Upon co-stimulation with HCV-E2 and HIV-gp120, we observed a potent proinflammatory response with the induction of IL-8. Furthermore, our studies revealed that HCV-E2 and HIV-gp120 act collaboratively to trigger a specific set of downstream signaling pathways that include activation of p38 mitogenactivated protein (MAP) kinase and the tyrosine phosphatase, SHP2. Both specific inhibitors of p38 MAP kinase and sodium vanadate, a potent protein-tyrosine phosphatase inhibitor, blocked IL-8 production in a dosedependent manner. The role of p38 MAP kinase and SHP2 was further defined by transiently overexpressing dominant negative mutants of these proteins into HepG2 cells. These studies revealed that overexpression of an inactive p38 MAP kinase or SHP2 mutant partially abrogated HCV-E2-and HIV-gp120-induced IL-8 production. Further studies revealed that IL-8 induction was not mediated through activation of the NF-B pathway. However, HCV-E2 plus HIV-gp120 was shown to increase the DNA binding activity of AP-1. These results emphasize that expression of the proinflammatory chemokine IL-8, induced by HCV-E2 and HIV-gp120, may be mediated through p38 MAP kinase and SHP2 in an NF-B-independent manner, albeit through AP-1-driven processes.

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Section: Discussionsupporting

confidence: 86%

Hepatitis C Virus and HIV Envelope Proteins Collaboratively Mediate Interleukin-8 Secretion through Activation of p38 MAP Kinase and SHP2 in Hepatocytes

Balasubramanian

Ganju

Groopman

2003

Journal of Biological Chemistry

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“…A history of risk factors, including intravenous drug abuse and male homosexual practices may alert the physician for an increased possibility of HIV infection; still, the infection rate is elevated in heterosexual patients as well. Hepatitis B (HBV) and C (HCV) viruses are common coinfections 10 . A complete history of medications may lead to possible diagnosis, given that certain antiviral drugs are recognized as causes of pancreatitis (didanosine) and kidney stones (indivar) 11,12 .…”

Section: Clinical Assessmentmentioning

confidence: 99%

Acute Abdomen and HIV Infection

Kosmidis¹,

Anthimidis²,

Vasiliadou³

2011

HIV Infection in the Era of Highly Active Antiretroviral Treatment and Some of Its Associated Complications

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“…Segundo POLES e DIETERICH (24) , metade de todos os pacientes infectados pelo HIV são co-infectados com o VHB ou com o VHC, o que causa impacto na qualidade de vida, na sobrevida e nos custos com tais pacientes.…”

Section: Introductionunclassified

Prevalência ambulatorial em um hospital geral de marcadores para hepatites B e C em pacientes com infecção pelo vírus da imunodeficiência humana

Tovo

Santos

Mattos

et al. 2006

Arq. Gastroenterol.

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RESUMO -Racional -Os vírus das hepatites B (VHB) e C (VHC) e da imunodefi ciência humana (HIV) utilizam a mesma rota de transmissão, sendo a prevalência de VHB e VHC em pacientes infectados pelo HIV maior do que aquela encontrada na população em geral. Objetivo -Determinar a prevalência de marcadores para hepatites B e C em uma população de pacientes com HIV, bem como os fatores de risco envolvidos.

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HIV and hepatitis virus infection

Cited by 3 publications

References 53 publications

Hepatitis C Virus and HIV Envelope Proteins Collaboratively Mediate Interleukin-8 Secretion through Activation of p38 MAP Kinase and SHP2 in Hepatocytes

Hepatitis C Virus and HIV Envelope Proteins Collaboratively Mediate Interleukin-8 Secretion through Activation of p38 MAP Kinase and SHP2 in Hepatocytes

Acute Abdomen and HIV Infection

Prevalência ambulatorial em um hospital geral de marcadores para hepatites B e C em pacientes com infecção pelo vírus da imunodeficiência humana

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