Viral Pathogenesis in Cyprinid Fish Species

Cyprinid fish, including goldfish, crucian carp and gibel carp, are susceptible to a range of viral pathogens that impede aquaculture productivity worldwide. Herpesviruses such as Cyprinid herpesvirus 2 (CyHV-2) and Carassius auratus herpesvirus (CaHV) are among the most devastating agents, causing rapid systemic infection, tissue necrosis and high mortality. Infection typically begins at mucosal surfaces—particularly the skin and gill epithelium—where viruses attach, enter host cells and initiate replication. Host factors such as developmental stage critically influence susceptibility and permissivity; larvae often demonstrate higher permissivity despite lower initial susceptibility, whereas adults mount stronger innate defences. Viral replication perturbs physiological homeostasis by altering host metabolism, inducing dysbiosis of the gut microbiota and triggering apoptotic or immune signalling cascades. Following acute infection, certain herpesviruses establish latency in neuronal or lymphoid tissues, reactivating under stress. Progress in molecular diagnostics has illuminated immediate-early, early and late gene expression programmes of these large double-stranded DNA viruses, revealing potential antiviral targets. Control strategies balance improved husbandry, biosecurity, rapid point-of-care diagnostics and development of vaccines or molecular adjuvants to prime mucosal immunity. A holistic understanding of pathogen–host interactions, including the role of microbial co-infections and environmental stressors, is essential to safeguard global cyprinid aquaculture and ensure sustainable fish production.

Research from Nature Portfolio

No recent Nature Portfolio content available.

Viral Pathogenesis in Cyprinid Fish Species publication trend

The graph below shows the total number of articles in viral pathogenesis in cyprinid fish species across all publications each year (not limited to Nature Index journals).

Technical terms

Pathogenesis: The sequence of events by which a virus infects a host and induces disease manifestations.

Permissivity: The ability of host cells or tissues to support viral entry, replication and assembly.

Susceptibility: The likelihood that a host or developmental stage will become infected upon exposure to a virus.

Ribonucleotide reductase: An enzyme that converts ribonucleotides into deoxyribonucleotides, enabling viral DNA synthesis.

Gut microbiota: The community of microorganisms residing in the intestinal tract, influencing nutrition, immunity and disease resistance.

References

1. Cyprinid herpesvirus 2 infection changes microbiota and metabolites in the gibel carp (Carassius auratus gibelio) midgut. Frontiers in Cellular and Infection Microbiology (2023).
2. The identification of viral ribonucleotide reductase encoded by ORF23 and ORF141 genes and effect on CyHV-2 replication. Frontiers in Microbiology (2023).
3. In Vivo Imaging Sheds Light on the Susceptibility and Permissivity of Carassius auratus to Cyprinid Herpesvirus 2 According to Developmental Stage. Viruses (2023).
4. Identification of the Immediate-Early Genes of Cyprinid Herpesvirus 2. Viruses (2020).
5. Evaluation of Cyprinid Herpesvirus 2 Latency and Reactivation in Carassius gibel. Microorganisms (2020).