Abstract

Grass carp reovirus (GCRV) causes extensive infection and death in grass carp and black carp fingerlings, with a highly seasonal prevalence. Previous studies suggested that GCRV can become latent after primary infection. In this study, we investigated type II GCRV (GCRV-II) latency in asymptomatic grass carp with GCRV infection or exposure history. We found that during latent infection, GCRV-II was detectable only in the brain of grass carp, unlike the multi-tissue distribution observed in natural infection. GCRV-II only caused damage to the brain during latent infection, while in natural infection, brain, heart, and eye tissues had relatively higher viral loads. We also discovered viral inclusion bodies in infected fish brains. Additionally, GCRV-II distribution in grass carp was notably affected by ambient temperature, with the virus targeting the brain only during low temperatures and multi-tissue distribution during high temperatures. This study provides insights into the mechanisms of GCRV-II latent infection and reactivation and contributes to the prevention and control of GCRV pandemics.

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