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Pre-exposure to infectious hypodermal and haematopoietic necrosis virus or to inactivated white spot syndrome virus (WSSV) confers protection against WSSV in Penaeus vannamei (Boone) post-larvae
Melena, J.; Bayot, B.; Betancourt, I.; Amano, Y.; Panchana, F.; Alday, V.; Calderon, J.; Stern, S.; Roch, P.; Bonami, J.R. (2006). Pre-exposure to infectious hypodermal and haematopoietic necrosis virus or to inactivated white spot syndrome virus (WSSV) confers protection against WSSV in Penaeus vannamei (Boone) post-larvae. J. Fish Dis. 29(10): 589-600. dx.doi.org/10.1111/j.1365-2761.2006.00739.x
In: Journal of Fish Diseases. Blackwell Science: Oxford; London; Edinburgh; Boston; Melbourne. ISSN 0140-7775; e-ISSN 1365-2761, more
Peer reviewed article  

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Keywords
    Penaeus vannamei Boone, 1931 [WoRMS]; White spot syndrome virus [WoRMS]
    Marine/Coastal
Author keywords
    infectious hypodermal and haematopoietic necrosis virus; Penaeusvannamei; viral co-infection; viral inactivation; viral interference;white spot syndrome virus

Authors  Top 
  • Melena, J.
  • Bayot, B.
  • Betancourt, I.
  • Amano, Y.
  • Panchana, F.
  • Alday, V.
  • Calderon, J.
  • Stern, S.
  • Roch, P.
  • Bonami, J.R.

Abstract
    Larvae and post-larvae of Penaeus vannamei (Boone) were submitted to primary challenge with infectious hypodermal and haematopoietic necrosis virus (IHHNV) or formalin-inactivated white spot syndrome virus (WSSV). Survival rate and viral load were evaluated after secondary per os challenge with WSSV at post-larval stage 45 (PL45). Only shrimp treated with inactivated WSSV at PL35 or with IHHNV infection at nauplius 5, zoea 1 and PL22 were alive (4.7% and 4%, respectively) at 10 days post-infection (p.i.). Moreover, at 9 days p.i. there was 100% mortality in all remaining treatments, while there was 94% mortality in shrimp treated with inactivated WSSV at PL35 and 95% mortality in shrimp previously treated with IHHNV at N5, Z1 and PL22. Based on viral genome copy quantification by real-time PCR, surviving shrimp previously challenged with IHHNV at PL22 contained the lowest load of WSSV (0–1 × 103 copies μg−1 of DNA). In addition, surviving shrimp previously exposed to inactivated WSSV at PL35 also contained few WSSV (0–2 × 103 copies μg−1 of DNA). Consequently, pre-exposure to either IHHNV or inactivated WSSV resulted in slower WSSV replication and delayed mortality. This evidence suggests a protective role of IHHNV as an interfering virus, while protection obtained by inactivated WSSV might result from non-specific antiviral immune response.

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