New Drug Targets for HIV and Hepatitis C Virus Coinfection

Tedaldi, Ellen

doi:10.1086/429505

Cited by 6 publications

(5 citation statements)

References 24 publications

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“…Several new drugs for treating HCV are under various stages of development [70] . These include improved IFN molecules (albumin fused with IFN-a, Ω IFN, sequential treatment with IFN-a and IFN-g), improved RBV molecules (Viramidine with a lower potential for hemolysis, and Levovirin), immunomodulators (histamine dihydrochloride, thymosin a, and isatoribine), and directly acting anti-HCV agents (HCV protease inhibitors, HCV entry inhibitors, ribozymes, and antisense nucleotides) [70] . The anti-fibrotic effect of IFN, with the potential of reducing fibrosis and HCC, is the basis for its use as a maintenance therapy.…”

Section: Management Of Non-responders and Relapsersmentioning

confidence: 99%

Management of hepatitis C virus infection in HIV/HCV co-infected patients: Clinical review

Singal¹,

Anand²

2009

WJG

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N e a r l y o n e fo u r t h o f i n d i v i d u a l s w i t h h u m a n immunodeficiency virus (HIV) infection have hepatitis C virus (HCV) infection in the US and Western Europe. With the availability of highly active antiretroviral therapy and the consequent reduction in opportunistic infections, resulting in the prolongation of the life span of HIV-infected patients, HCV co-infection has emerged as a significant factor influencing the survival of HIV patients. Patients with HIV/HCV co-infection have a faster rate of fibrosis progression resulting in more frequent occurrences of cirrhosis, end-stage liver disease, and hepatocellular carcinoma. However, the mechanism of interaction between the two viruses is not completely understood. The treatment for HCV in co-infected patients is similar to that of HCV monoinfection; i.e., a combination of pegylated interferon and ribavirin. The presence of any barriers to anti-HCV therapy should be identified and eliminated in order to recruit all eligible patients. The response to treatment in co-infected patients is inferior compared to the response in patients with HCV mono-infection. The sustained virologic response rate is only 38% for genotype-1 and 75% for genotype-2 and -3 infections. Liver transplantation is no longer considered a contraindication for end-stage liver disease in coinfected patients. However, the 5 year survival rate is lower in co-infected patients compared to patients with HCV mono-infection (33% vs 72%, P = 0.07). A better understanding of liver disease in co-infected patients is needed to derive new strategies for improving outcome and survival.

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Section: Management Of Non-responders and Relapsersmentioning

confidence: 99%

Management of hepatitis C virus infection in HIV/HCV co-infected patients: Clinical review

Singal¹,

Anand²

2009

WJG

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“…Finally, Bean [38] and Tedaldi [39] provided up-to-date information on new pharmacotherapeutic entities that are in various stages of development and on aspects of the viruses that new antiretroviral drugs could target. Bean [38] noted that, in recent years, progress had been seen in the treatment of HIV-related illness with HAART, resulting in improvements in prognosis and diminished opportunistic infections.…”

Section: Presentationsmentioning

confidence: 99%

“…Therefore, targeting the fusion peptide presents an attractive new method of inhibiting HIV infection and a novel addendum to the current range of drugs. In the case of HCV infection, Tedaldi [39] argued that current IFN-based therapy for HCV infection in coinfected patients is limited by incomplete virological response, poor adherence, and lack of tolerability. Thus, newer therapies for HCV infection might target viral replication (e.g., HCV serine protease inhibitors, helicase inhibitors, RNA interference, or HCV polymerase inhibitors).…”

Section: Presentationsmentioning

confidence: 99%

“…At least 2 approaches with a monoclonal antibody or HCV immunoglobulin are being evaluated in clinical trials. Tedaldi [39] suggested that researchers should encourage strategic treatment trials that address the sequencing of HCV and HIV therapies with current and future therapeutic agents and combination therapy and that orthotopic liver transplantation might be a viable option for patients with decompensation.…”

Section: Presentationsmentioning

confidence: 99%

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Medical Management of HIV—Hepatitis C Virus Coinfection in Injection Drug Users

Khalsa

Kresina

Sherman

et al. 2005

Clinical Infectious Diseases

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Several million people inject drugs of abuse and, as a result, are coinfected with human immunodeficiency virus (HIV) and hepatitis C virus (HCV). The treatment of this coinfected drug-abusing population is fraught with many problems such that clinicians and other health care providers have to determine whether patients should be treated first for drug addiction, for HIV/AIDS, or for HCV infection or simultaneously treated. These proceedings present the incidence and prevalence of coinfections with HIV and HCV in high-risk populations and discuss the underlying pathophysiology of coinfections and the problems and strategies of managing the treatment of coinfections among people who also inject illicit drugs. In addition, the expert panel recommended further research to determine the best possible treatment regimens applicable to injection drug users coinfected with HIV and HCV.

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“…[1][2][3] A number of recent studies have documented the antiviral effects of small molecule inhibitors on viral or host NTPase/helicase. These inhibitors include amino-thiazolyphenyl [4] and thiazole amide derivatives, [5] inhibitors of the HSV helicase-primase; ribavirin, a nucleoside analogue inhibitor of IMPDH and also of HCV helicase; [6] and murabutide, a synthetic immunomodulator that was shown recently to suppress HIV-1 replication in macrophages and T cells by inhibiting the activity of host RNA helicase RH116. [7] Unlike HSV and HCV viruses, HIV-1 does not encode any RNA helicase, [8] and the host RNA helicase A was recently found to serve as a GTP Depletion Induced Translocation of DHX-9 705 viral helicase to regulate the reverse transcription and transport of HIV-l viral mRNA.…”

Section: Introductionmentioning

confidence: 99%

Guanine Nucleotide Depletion Mediates Translocation of Nucleolar Proteins, Including RNA Helicase A (DHX-9)

Huang

Mitchell

2008

Nucleosides, Nucleotides and Nucleic Acids

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DHX-9, a member of the DEXH family of RNA helicases, unwinds dsRNA/dsDNA by ATP or GTP-dependent hydrolysis. We asked whether DHX-9 played a role in the GTP depletion-induced inhibition of rRNA synthesis and/or nucleolar disruption. MPA, a specific inhibitor of inosine monophosphate dehydrogenase (IMPDH), induced a rapid translocation of DHX-9 from the nucleolus to the nucleus. EGFP-tagged DHX-9 mutated at the GTP binding site also localized to the nucleus. However, knockdown of DHX-9 by siRNA did not inhibit the rRNA synthesis or cause the nucleolar disruption. Thus, DHX-9 translocation found with IMPDH inhibition does not mediate the inhibition of rRNA synthesis.

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New Drug Targets for HIV and Hepatitis C Virus Coinfection

Cited by 6 publications

References 24 publications

Management of hepatitis C virus infection in HIV/HCV co-infected patients: Clinical review

Management of hepatitis C virus infection in HIV/HCV co-infected patients: Clinical review

Medical Management of HIV—Hepatitis C Virus Coinfection in Injection Drug Users

Guanine Nucleotide Depletion Mediates Translocation of Nucleolar Proteins, Including RNA Helicase A (DHX-9)

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