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Marcello Pinti

Researcher at University of Modena and Reggio Emilia

Publications -  185
Citations -  13448

Marcello Pinti is an academic researcher from University of Modena and Reggio Emilia. The author has contributed to research in topics: Mitochondrion & Immune system. The author has an hindex of 46, co-authored 163 publications receiving 11592 citations. Previous affiliations of Marcello Pinti include University of Milan & National Institutes of Health.

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Mitochondrial Proteases as Emerging Pharmacological Targets.

TL;DR: Six mitochondrial proteases are focused on, namely CLPP, HTRA2 and LONP1, by analysing the current knowledge about their functions, their involvement in the pathogenesis of human diseases, and the compounds currently available for inhibiting their functions.
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Novel genetic association of TNF-α-238 and PDCD1-7209 polymorphisms with long-term non-progressive HIV-1 infection

TL;DR: The novel genetic associations between allelic variants of genes TNF-α-238 and PDCD1-7209 with the LTNP condition underline the importance of host genetic factors in the progression of HIV-1 infection and in immunological preservation.
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MMP-7 promoter polymorphisms do not influence CD4+ recovery and changes in plasma viral load during antiretroviral therapy for HIV-1 infection.

TL;DR: It is found that two polymorphisms in MMP‐7 promoter could influence CD4+ recover in response to antiretroviral therapy, and found that these polymorphisms are ineffective.
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Plasma HIV load and proviral DNA decreases after two standard antiretroviral regimens in HIV-positive patients naïve to antiretrovirals.

TL;DR: In this paper, the authors compared early decrease of HIV plasma viral load after two standard combinations of highly active antiretroviral therapy (HAART) and evaluated variations of proviral HIV-DNA load on conditions of sustained pVL undetectability.
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Predictive value of intracellular HIV-1 DNA levels during CD4-guided treatment interruption in HIV+ patients.

TL;DR: Intacellular HIV-1 DNA is a predictive marker for the length of CD4-guided treatment interruption, and it is found that patients with a stable level had a lower risk to reach a CD4(+) T cell count <350 cells/microl, and thus to restart therapy, whereas this risk was significantly higher in those with a marked increase of HIV- 1 DNA.