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Duck hepatitis A virus 1 has lymphoid tissue tropism altering the organic immune responses of mature ducks.

Duck hepatitis A virus 1 (DHAV-1) is a highly prevalent pathogen within adult ducks causing acute as well as chronic hepatitis which closely emulates the progression of human hepatitis. However, the underlying mechanisms of DHAV-1 persistence and the pathogenesis of chronic liver disease are not well defined. The association between hematopoietic reservoirs of virus and persistent infection is increasingly concerning. Here we explored the ability of lymphoid replication of DHAV-1 and the effect on immunity. We found that DHAV-1 was able to infect and replicate productively in the lymphoid organs of model ducks, persisting over 6 months. Moreover, a significant correlation of viral loads between these organs and blood was found, documenting a major contribution of lymphoid replication to DHAV-1 viremia. Along with viral replication, the mRNA of PRRs and immune-related cytokines was up-regulated in these organs during the early phase of infection, showing tissue-dependent expression patterns but all inclining toward Th2 responses due to the consistently higher level of IL-4 than IL-2 and IFN-γ. Additionally, the expression of CCL19, CCL21, MHC-I and MHC-II, which are involved in T cell homing to the periphery and priming, was dysmodulated. Our data indicate that DHAV-1 possesses lymphoid tissue tropism, contributing to persistent infection and chronic hepatitis via altering the early endogenous transcription of immune-related genes and thereby perturbing organic immunity. These results may be useful to develop novel strategies to treat chronic viral hepatitis based on stimulation of the early innate system and regulation of T cell trafficking.