# Mechanisms of HAHV-1 Interaction with Hemocytes in Haliotis diversicolor supertexta: An In Vitro Study

## TL;DR

This study explores how HAHV-1 interacts with abalone cells in the lab, revealing how the virus weakens immune defenses and boosts its replication.

## Contribution

The study establishes an in vitro model to investigate HAHV-1's mechanisms of immune evasion and replication in abalone hemocytes.

## Key findings

- HAHV-1 hijacks host actin and microtubule networks to suppress immune responses early in infection.
- The virus exploits host energy and redox metabolism to increase viral loads in later stages.
- H. diversicolor supertexta hemocytes are highly susceptible to HAHV-1, with viral loads peaking at 4.0 × 10⁷ copies/ng DNA.

## Abstract

Abalone are high-priced and mobile-grazing gastropod mollusks, cultivated or fished primarily in east Asia and Australia. A devastating pandemic related to Haliotid herpesvirus 1 (HAHV-1) swept across mainland China, Taiwan, and Australia, causing severe damage and property loss to the industry. The pandemic has led to the collapse of the Haliotis diversicolor supertexta aquaculture industry in mainland China. The mechanisms of interaction between HAHV-1 and susceptible abalone remain underexplored. In this study, we establish an in vitro infection model for HAHV-1 and investigate the virus–host interaction mechanisms. The results indicated that the virus hijacks the host’s actin cytoskeletons and microtubule network, resulting in immune deficiency during the early stages of infection. Furthermore, the virus hijacks the host’s energy metabolism and redox metabolism, contributing to the rapid increase of viral loads in the later stages of infection. These findings provide valuable insights into the pathogenic mechanism of HAHV-1.

Haliotid herpesvirus 1 (HAHV-1) causes significant damage to the abalone aquaculture industry. Knowledge of HAHV-1 invasion and host defense mechanisms is limited due to the lack of stable molluscan cell lines. The present study established an in vitro infection model of HAHV-1 using the primary suspension cultures of hemocytes from Haliotis diversicolor supertexta and Haliotis discus hannai. The cytopathic effects of HAHV-1 on adherent-cultured hemocytes of both species were also investigated. The HAHV-1 DNA loads were firstly monitored by means of quantitative PCR during the development of viral infection, and subsequently the mechanism of interaction between HAHV-1 and hemocytes was explored by means of a transcriptome analysis. H. diversicolor supertexta hemocytes exhibited a high degree of susceptibility to HAHV-1, with viral loads reaching a peak of 4.0 × 10⁷ copies/ng DNA. In contrast, no significant replication was observed in H. discus hannai hemocytes. Transcriptome analysis revealed that HAHV-1 evades the host immune response in the early stages of infection, and hijacks the host’s energy and redox metabolism to promote its replication at the late stages. Consequently, this study provides a valuable reference point for the investigation of virus−host interaction between HAHV-1 and abalone in vitro.