WWW.WA S .ORG • WORLD AQUACULTURE • SEP TEMBER 2022 31 shrimp challenged with WSSV showed a reduction in IHHNV load (2.7 × 107 and 9.7 × 107 copies/µg DNA) compared to shrimp inoculated only with IHHNV (2.5 × 108 – 2.6 × 109 copies/µg DNA) at 30 and 40 d, respectively. The IHHNV virus load influenced the delay in mortality due to WSSV infection in a direct manner. A significant delay in mortality occurred when IHHNV load was higher than 108 copies/µg DNA at the time of WSSV challenge (Bonnichon et al. 2006). The interference between IHHNV and WSSV was evaluated in batches of juvenile P. monodon pre-infected with IHHNV and another batch of IHHNV-negative shrimp. Both groups were challenged with WSSV by cohabitation with WSSV-infected shrimp. There were significant differences in time of mortality between the two groups: 10.3 ± 2.7 d in the IHHNV-negative group and 14.7 ± 4.9 d in the IHHNV-infected group. WSSV load was significantly different between the two groups: 1.74 × 107 ± 1.78 × 107 copies/µg DNA in the IHHNV-negative group and 2.74 × 106 ± 2.41 × 106 copies/µg DNA in the IHHNV-infected group (Molthatong et al. 2013). The interference mechanism between IHHNV and WSSV was evaluated in an in vitro assay using a competitive ELISA with L. vannamei gill cell cultures. Digoxigenin-labeled WSSV and unlabeled IHHNV were used. Gill cell membranes added with unlabeled IHHNV interfered with digoxigenin-labeled WSSV, indicating an interfering effect of IHHNV with WSSV by competition for binding to cellular membranes. An inverse assay using labeled IHHNV and unlabeled WSSV on gill cell membranes also showed that unlabeled WSSV interfered with attachment of labeled IHHNV to cell membranes to an even higher degree. This suggests that WSSV also competes with IHHNV for binding sites on the cell membrane (Yan et al. 2016). ( C O N T I N U E D O N P A G E 3 2 ) Interference between IHHNVandWSSV The first and most-recorded virus interference phenomenon in shrimp is that between IHHNV and WSSV (Tang et al. 2003, Fig. 6). Survival ofuvenile P. stylirostris was greater when preexposed to IHHNV and then challenged through the mouth (per os) with WSSV-infected tissues. Mortality occurred 48 h after WSSV challenge. Control shrimp not exposed to IHHNV died within five days of inoculation (dpi); whereas survival of IHHNV-preinfected shrimp was 31 percent and 44 percent at 5 dpi. In a second experiment, survival of P. stylirostris heavily infected with IHHNV and then orally inoculated with WSSV was 91 percent (21 out of 23 shrimp) 19 days after WSSV inoculation. Some surviving shrimp (n=10) were challenged again with WSSV-infected tissues, and six were still alive three weeks later. In a third experiment, 28 percent of IHHNV pre-infected P. stylirostris survived 22 days after exposure to WSSV. Quantitative PCR analysis demonstrated that surviving shrimp had high levels of IHHNV DNA (109 copies/µg) and low levels of WSSV DNA (50-400 copies/µg). Melena et al. (2006) evaluated the interference of IHHNV against WSSV in L. vannamei postlarvae. Shrimp treated with IHHNV at nauplius V or zoea I stages showed a delay in shrimp mortality from day 4 until the end of the experiment, indicating an interfering effect of such treatments. Nonetheless, shrimp treated with IHHNV had 4 percent survival ten days after WSSV challenge. Surviving shrimp had similar virus loads between IHHNV and WSSV (9.0 × 101 – 1.2 × 102), whereas moribund shrimp had a higher WSSV load (1.5 × 104 – 2.3 × 104) The interference between IHHNV and WSSV in juvenile L. vannamei inoculated per os was evaluated between 0 and 50 d after IHHNV inoculation. Shrimp inoculated only with WSSV died at 3 dpi, whereas shrimp treated with IHHNV between 30 and 50 d before WSSV challenge died at 5 dpi. The virus load of IHHNV in shrimp increased during the 50 d, peaking at 40 d with an average IHHNV virus load of 2.6 × 109 copies/mg DNA. IHHNV-treated FIGURE 6.Virus interference between Penstylhamaparvovirus-1 (formerly known as IHHNV) and white spot syndrome virus (WSSV). Shrimp preinfected with IHHNV may become more resistant to WSSV infection, showing higher survival and lower WSSV DNA load. A possible interfering mechanism may be virus competition for binding to cellular membranes. FIGURE 7.Virus interference between Taura syndrome virus (TSV) and yellow head virus (YHV). Shrimp pre-infected with TSV and in chronic phase were challenged 27 d after TSV inoculation with YHV and showed the highest survival against YHV. Tissue distribution of these viruses was different. TSV was only found in lymphoid organ since shrimp were at the chronic stage; whereas YHV was found in integument, connective tissues and adjacent areas of lymphoid organ tubules. TSV-treated shrimp did not show severe necrosis by YHV.
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