Department of Fisheries, Wildlife, and Conservation Sciences, Coastal Oregon Marine Experiment Station, Oregon State University, Hatfield Marine Science Center, Newport, OR 97365, USA.
Department of Biomedical Sciences, Carlson College of Veterinary Medicine, Oregon State University, Corvallis, OR 97331, USA.
Virus Res. 2024 Jan 2;339:199245. doi: 10.1016/j.virusres.2023.199245. Epub 2023 Oct 25.
Ostreid herpesvirus 1 (OsHV-1) is one of the most economically important pathogens of Pacific oysters. Understanding the pathogenesis of this virus is critical to developing tools to control outbreaks on shellfish farms. OsHV-1 is genetically related to vertebrate herpesviruses, which have a lytic and a latent stage, with the latent stage capable of being reactivated to the lytic stage. Here, OsHV-1 latency in Pacific oysters was investigated in experimentally and naturally infected oysters. Lytic infection in one-year-old oysters injected with the Tomales Bay strain of OsHV-1 was detectable between 1 and 4 days post-injection (dpi) but was not detectable after 5 dpi. The injected oysters shed 1 × 10 to 1 × 10 DNA copies/ml into the water during the 4-day acute phase. Lytic shedding was not detectable in two-year-old oysters injected similarly with the same strain of OsHV-1; however, the OsHV-1 genome was detectable by qPCR in the adductor muscle, gill, mantle, and hemocytes within the first 3 dpi, after which it became undetectable. No OsHV-1 was detectable in the adductor muscle, gill, or mantle from experimentally infected oysters on days 15 and 21 post-injection or from oysters sampled 9 months after surviving an OsHV-1 mortality event; however, OsHV-1 DNA could be detected in hemocytes of both experimentally infected oysters at 21 dpi and naturally infected oysters using nested PCR. In addition, lytic viral gene transcription was detectable in hemocytes of experimentally infected oysters between 1 and 21 dpi and in hemocytes of naturally infected oysters. Furthermore, OsHV-1 reactivation from latency was induced in experimentally infected oysters at 21 dpi and in naturally infected oysters 12 months after an OsHV-1 outbreak.
牡蛎疱疹病毒 1(OsHV-1)是太平洋牡蛎最重要的经济病原体之一。了解该病毒的发病机制对于开发贝类养殖场暴发控制工具至关重要。OsHV-1 与脊椎动物疱疹病毒在基因上相关,具有裂解和潜伏阶段,潜伏阶段能够被重新激活到裂解阶段。在这里,在实验和自然感染的牡蛎中研究了太平洋牡蛎的 OsHV-1 潜伏。在注射了 Tomales Bay 株 OsHV-1 的一年生牡蛎中,在注射后 1 至 4 天(dpi)之间可检测到裂解感染,但在 5 dpi 后则无法检测到。在急性 4 天期间,注射的牡蛎向水中释放了 1×10 至 1×10 的 DNA 拷贝/ml。在类似地注射了相同的 OsHV-1 株的两年生牡蛎中,未检测到裂解性脱落;然而,在注射后 1 至 3 dpi 内,可以通过 qPCR 在肌肉、鳃、套膜和血细胞中检测到 OsHV-1 基因组,此后则无法检测到。在注射后 15 和 21 天或在经历了 OsHV-1 死亡率事件 9 个月后从实验感染的牡蛎或从采样的牡蛎中,均无法在肌肉、鳃或套膜中检测到 OsHV-1;然而,在 21 dpi 的实验感染牡蛎和自然感染牡蛎的血细胞中,使用嵌套 PCR 可以检测到 OsHV-1 DNA。此外,在实验感染的牡蛎中,在 1 至 21 dpi 之间可检测到裂解病毒基因转录,并且在自然感染的牡蛎中也可检测到。此外,在 21 dpi 的实验感染牡蛎中和在 OsHV-1 暴发 12 个月后的自然感染牡蛎中,可诱导潜伏的 OsHV-1 重新激活。