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Oxidized LDL predicts SVR after interferon-based therapy for HCV

Oxidized low-density lipoprotein accurately predicted a patient’s response to interferon-based therapy for hepatitis C virus infection, according to new study data.

“While highly effective direct-acting antivirals have become the new standard of care for patients with hepatitis C, these treatments come with a hefty price tag,” Philipp Solbach, MD, from Hannover Medical School in Niedersachsen, Germany, said in a press release. “There may still be a role for the more affordable interferon-based therapies, and with this new information, we can better assess which patients will respond to this less-expensive treatment.”

Solbach and colleagues analyzed data and samples of 379 treatment-naive patients with HCV genotype 1 who participated in the INDIV-2 trial. All of the patients previously received therapy with pegylated interferon (PEG-IFN) with ribavirin for 24 to 72 weeks, depending on baseline viral load.

To determine any correlation between oxidized low-density lipoprotein (LDL), the researchers measured oxidized LDL using a commercial enzyme-linked immunosorbent assay system and then conducted in vitro studies using full-length and subgenomic HCV genomes replicating in hepatoma cells, according to the research.

In univariate analysis, LDL and oxidized LDL serum were found to be associated with a sustained virologic response. Serum oxidized LDL levels were higher in patients who had achieved SVR from previous therapy compared with those who did not (P < .001). Multivariate analysis showed that oxidized LDL was an independent predictor of SVR, but not native LDL.

Oxidized LDL did not correlate with alanine transaminase serum or ferritin, as well as was not affected by exogenous interferon administration.

In addition, oxidized LDL did not change the sensitivity of HCV replication to interferon. However, HCV transmission from cell to cell was studied using an in vitro culture system and it was determined that oxidized LDL inhibited cell-to-cell spread. This may suggest there is a mechanism underlying the relationship between oxidized LDL and a sustained viral response to interferon therapy, according to the press release.

Decline of viral load after treatment with interferon-based therapy could be driven by the rate of infected cell loss, which is an important predictor for treatment response, according to the research.

“We provide data suggesting that [oxidized] LDL is neither a marker of inflammation nor a modulator of the interferon response, but might enhance SVR rates by limiting the rate of viral spread to uninfected cells,” the researchers concluded. “This finding may even be relevant for other forms of chronic viral disease as it suggests that entry inhibition may have a beneficial effect even in the context of already established infections.” – by Melinda Stevens

Disclosure: Solbach reports no relevant financial disclosures. Please see the study for a full list of all other authors’ relevant financial disclosures.