Viral nervous necrosis (VNN), or viral encephalopathy and retinopathy caused by nervous necrosis virus (NNV), is an acute viral disease of fish, resulting in high mortality globally in cultured marine fish. The pathogen, Betanodavirus belonging to the family Nodaviridae, has been widely documented in both farmed and wild fish, besides in invertebrate species across the habitat barriers. However, cichlid fish, in particular Etroplus species, have a low susceptibility or resistance to this disease. The present study was undertaken to check the susceptibility of a brackishwater cichlid, orange chromide (Etroplus maculatus) through intramuscular injection and immersion challenge by NNV (RGNNV genotype). Intramuscular injection (10 μl) with NNV (10⁵ viral particles ml⁻¹) resulted in cumulative mortality of 50% at 15 days of post-infection (dpi), while immersion challenge in NNV spiked sea water (10⁵ TCID₅₀ ml⁻¹) resulting in a mortality of 25% at 19 dpi. Unlike many marine fish which showed 100% mortality within 3–5 days, E. maculatus challenged through both the routes exhibited severe clinical symptoms for 2–3 weeks followed by a recovery stage and moderate level of mortality. Reverse transcription polymerase chain reaction (RT-PCR) tests on live fish sampled during the course of the experiment and the dead fish exhibiting symptoms in both challenge groups tested NNV-positive. Histological examination of fish in challenged groups showed VNN-specific lesions characterized by vacuolations in the brain and eye with more severe lesions in the injected group than the immersion group. In survived fish, no clinical sign was observed, but NNV could be detected by RT-PCR with moderate to severe vacuolations in the brain and eyes until 30 dpi. Despite the virus entering the body and triggering typical symptoms of VNN, the fish appeared to exhibit moderate resistance with a survival of 50–75%. The results indicate that E. maculatus could serve as a brackishwater fish model to study host-pathogen interaction and development of resistance for potential application in NNV-vaccine studies.

由神经坏死病毒（NNV）引起的病毒性神经坏死（VNN）或病毒性脑病和视网膜病是鱼类的一种急性病毒病，在全球养殖海水鱼类中导致高死亡率。病原体，Betanodavirus属于家庭野田病毒科，已被广泛证明在这两个养殖和野生鱼类，除了在整个栖息地的障碍脊椎动物。但是，丽鱼科鱼，特别是Etroplus鱼，对这种疾病的敏感性或耐药性较低。本研究旨在通过肌内注射和NNV（RGNNV基因型）浸没攻击检查咸淡水丽鱼科鱼，橙色铬（Etroplus maculatus）的敏感性。肌内注射（10μl）与NNV（10 ⁵病毒颗粒ml ^-1）导致感染后15天（dpi）的累积死亡率为50％，而浸没在NNV加标海水中（10 ⁵ TCID ₅₀ ml ^-1）导致的死亡率为19％时25％ dpi。与许多海洋鱼类在3-5天内显示出100％的死亡率不同，E。maculatus通过这两种途径接受挑战的患者在2-3周内均表现出严重的临床症状，其后为恢复期和中等水平的死亡率。在实验过程中对活鱼采样的逆转录聚合酶链反应（RT-PCR）测试以及两个挑战组中死鱼均表现出症状，而NNV阳性。挑战组鱼的组织学检查显示，VNN特异性病变的特征是大脑和眼睛出现空泡，与浸入组相比，注射组的病变更为严重。在存活的鱼中，未观察到临床体征，但可通过RT-PCR检测到NNV，在大脑和眼睛中出现中度至重度空泡，直至30 dpi。尽管病毒进入人体并触发了VNN的典型症状，鱼似乎显示出中等抵抗力，存活率为50-75％。结果表明E. maculatus可以作为咸淡水鱼类模型来研究宿主-病原体相互作用和耐药性的发展，从而有可能在NNV疫苗研究中应用。