CD4+ T-lymphocytopenia in HIV-infected patients receiving interferon therapy for chronic hepatitis C

Soriano, Vincent; Bravo, R.; García-Samaniego, Javier; González, Juan; Odriozola, Pedro Martínez; Arroyo, Esteban Alexis; Vicário, José L.; Castro, Ángeles; Colmenero, M.; Carballo, E.; Pedreira, José

doi:10.1097/00002030-199411000-00016

Cited by 52 publications

(30 citation statements)

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“…In an intention-to-treat analysis, 18 (20%) of the 90 HIV-infected patients achieved a sustained virological response to therapy, determined 12 months after the end of therapy; as expected, sustained response was associated with a pretreatment CD4 cell count 1500/mm 3 (OR, 2.92). In this study IFN-a appeared to be well-tolerated, although 10 patients experienced a 150% reduction in CD4 cell count, which was irreversible for 3 patients [82,83]. Thus, on the basis of limited data, IFN-a therapy appears to be reasonably well-tolerated and may be effective for the treatment of HCV infection in HIV-infected patients.…”

Section: Secondary Prevention Of Diseasementioning

confidence: 73%

Hepatitis C Virus Infection as an Opportunistic Disease in Persons Infected with Human Immunodeficiency Virus

et al. 2000

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Hepatitis C virus (HCV) is an RNA virus of the Flaviviridae family and is a major cause of chronic hepatitis, cirrhosis, and hepatocellular carcinoma. Owing to shared routes of transmission, HCV and human immunodeficiency virus (HIV) coinfection are common, affecting approximately one-third of all HIV-infected persons in the United States. In addition, HIV coinfection is associated with higher HCV RNA level and a more rapid progression of HCV-related liver disease, which leads to an increased risk of cirrhosis. HCV infection may also impact the course and management of HIV disease, particularly by increasing the risk of antiretroviral drug-induced hepatotoxicity. Thus, chronic HCV infection acts as an opportunistic disease in HIV-infected persons, because the incidence of infection is increased and the natural history of HCV infection is accelerated in coinfected persons. Strategies to prevent primary HCV infection and to modify the progression of HCV-related liver disease are urgently needed for HIV-HCV-coinfected individuals.

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Section: Secondary Prevention Of Diseasementioning

confidence: 73%

Hepatitis C Virus Infection as an Opportunistic Disease in Persons Infected with Human Immunodeficiency Virus

et al. 2000

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“…Among these, the development of lymphopenia often limits its use, particularly in those patients who have received aggressive chemotherapy or who have T-cell depletion, such as that associated with chronic HIV infection. 9,11,12,38 On the other hand, the administration of recombinant IL-7 in several recent phase I/II trials in either cancer patients after aggressive chemotherapy or in HIV-infected patients under HAART [19][20][21] demonstrated good tolerance and high efficiency. Recombinant glycosylated simian IL-7 therapy elicited a significant and prolonged increase in circulating T-cell numbers, increased thymic output, and diversification of T-cell repertoire.…”

Section: Discussionmentioning

confidence: 99%

Interleukin-7 treatment counteracts IFN-α therapy-induced lymphopenia and stimulates SIV-specific cytotoxic T lymphocyte responses in SIV-infected rhesus macaques

Parker

Dutrieux

Beq

et al. 2010

Blood

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Interferon-␣ (IFN-␣)-based therapy ispresently the standard treatment for hepatitis C virus (HCV)-infected patients. Despite good effectiveness, this cytokine is associated with major side effects, including significant lymphopenia, that limits its use for HIV/HCV-coinfected patients. Interleukin-7 (IL-7) has recently shown therapeutic potential and safety in several clinical trials designed to demonstrate T-cell restoration in immunodeficient patients. The purpose of this study was to evaluate, in simian immunodeficiency virus-infected rhesus macaques, the relevance of IL-7 therapy as a means to overcoming IFN-␣-induced lymphopenia. We showed that low-dose IFN-␣ treatment induced strong lymphopenia in chronically infected monkeys. In contrast, high-dose IFN-␣ treatment stimulated IL-7 production, leading to increased circulating T-cell counts. Moreover, IL-7 therapy more than abrogated the lymphopenic effect of low-dose IFN-␣. Indeed, the association of both cytokines resulted in increased circulating T-cell IntroductionCoinfection with HIV and hepatitis C virus (HCV) has become an increasingly common occurrence, with an estimated 25% to 30% of HIV ϩ patients also being HCV ϩ . 1 As a consequence, since the appearance of highly active antiretroviral therapy (HAART), chronic liver disease has become one of the most common causes of morbidity and mortality in HIV patients. 2,3 Although the effectiveness of standard HCV treatment, based on interferon-␣ (IFN-␣) injections, is known to decrease the longer a patient has been infected with the virus, HCV patients are not systematically put under treatment. Rather, initiation of treatment depends on the state of the patient's liver (fibrosis markers, serum aminotransferases, HCV RNA, hepatitis B virus status) and other parameters, which in turn are used to determine whether the potential benefits of therapy outweigh the risks of treatment-related toxicity. 4 For HIV-HCV-coinfected patients, some of these parameters are: the assessment of HIV disease status, such as current and past opportunistic infections, HIV-associated malignancies, CD4 count, HIV viral load, and details of HAART therapy, with CD4 count being one of the main criteria. Unfortunately, coinfected patients are poor responders to standard treatment as a sustained viral response occurs in only 27% to 40% of these patients, approximately half the rate seen in HCV-monoinfected patients. [5][6][7] The main reason for this difference can be attributed to exhaustion of the immune system. In addition, IFN-␣ treatment causes a leukopenia, including a decrease of lymphocyte numbers and thus of CD4 count, often leading to premature treatment interruption. [8][9][10][11][12] Therefore, to enhance the efficiency of anti-HVC therapy in coinfected patients, it is critically important to develop an alternative treatment that limits the lymphopenic effect of IFN-␣ therapy.Interleukin 7 (IL-7), a cytokine that promotes precursor B-and T-cell maturation [13][14][15] and supports peripheral T-cell homeostasis, [16][17][18...

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“…Actually, in HIV-HCV-infected patients, a sustained IFN response has been associated with a pretreatment CD4 ϩ cell count. 10 Thus IFN therapy should be performed under as nearnormal immune conditions as possible.…”

Section: Responsementioning

confidence: 99%

“…Hence, interferon therapy influenced the tolerability of HAART and could affect long-term antiretroviral response. Further problems may originate from the use of combination therapy with IFN plus ribavirin because of the drug interaction (in vitro studies have demonstrated that ribavirin could affect intracellular phosphorylation of deoxynucleoside, mainly AZT, 9,10 leading to a reduced therapeutic effect) and the increase of pill burden, which reduces the adherence to HAART. In conclusion, we do not agree with Yokozaki et al and suggest that therapy for hepatitis should precede HAART, at least in patients without severe immunodeficiency, because the interferences between the 2 treatments limit the adherence and the response to both therapies.…”

mentioning

confidence: 99%

Hepatitis C virus RNA dynamics during antiretroviral therapy

Bruno

Sacchi

Filice

2001

Blood

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CD4+ T-lymphocytopenia in HIV-infected patients receiving interferon therapy for chronic hepatitis C

Cited by 52 publications

References 0 publications

Hepatitis C Virus Infection as an Opportunistic Disease in Persons Infected with Human Immunodeficiency Virus

Hepatitis C Virus Infection as an Opportunistic Disease in Persons Infected with Human Immunodeficiency Virus

Interleukin-7 treatment counteracts IFN-α therapy-induced lymphopenia and stimulates SIV-specific cytotoxic T lymphocyte responses in SIV-infected rhesus macaques

Hepatitis C virus RNA dynamics during antiretroviral therapy

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