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Dear Editor, I read the report by Cmet and colleagues with real interest [1]. Taking a gain-of-function observation from cell culture and testing it in 192 untreated patients with chronic hepatitis delta (CHD) is not easy work, and the association between LGP2 Q425R carriage and a lower prevalence of cirrhosis is an appealing one. I would like to raise a few points, less as criticism than as questions whose answers would help readers apply the result.
To the Editor, We read with interest the study by Cmet et al. associating the LGP2 Q425R variant with lower cirrhosis prevalence in European patients with chronic hepatitis delta [1]. By extending experimental findings on enhanced antiviral innate immunity into a clinical cohort [2], this work provides valuable evidence concerning host genetic contributions to disease severity. Long-term hepatitis delta cohorts have separately documented progression to cirrhosis and subsequent decompensation [3].
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