Immunomodulatory effects of hyperthermia on resisting WSSV infection in Procambarus clarkii

Abstract

White spot disease remains a constant threat to aquaculture worldwide. Hyperthermia has been shown to reduce mortality in white spot syndrome virus (WSSV)-infected shrimps, but the mechanism still remains unclear. In this study, we sought to identify host immune factors that contribute to inhibition of WSSV infection during hyperthermia. In WSSV-infected red swamp crayfish Procambarus clarkii (Girard) cultured at 24 ± 1 °C, transcriptional levels of the heat shock protein 70 (Hsp70) gene showed a modest, 2.2-fold increase in haemocytes following 48 h post-infection (hpi). In contrast, in WSSV-infected crayfish cultured at 32 ± 1 °C, Hsp70 gene expression showed a rapid, 19.5-fold induction by 4 hpi. This suggests that Hsp70 plays a positive regulatory role in resistance to WSSV infection during hyperthermia. Furthermore, total haemocyte counts (THC) and phenoloxidase (PO) activity were both significantly increased in WSSV-infected crayfish cultured at 32 ± 1 °C by 48 hpi. Both may be critical for crayfish survival in the late stages of WSSV infection. Collectively, the up-regulation of host protein Hsp70 expression and increase in THC and PO activity suggest that hyperthermia has immunomodulatory effect that enhanced the resistance of P. clarkii to WSSV infection.

Hsp70 expression in shrimp Litopenaeus vannamei in response to IHHNV and WSSV infection

“…Hsp70 is one of the binding partners of VP28 during virus infection and its expression was enhanced by WSSV infection at the early stage of the process [24]. Crayfish Procambarus clarkii infected with WSSV during hyperthermia showed a rapid induction of Hsp70 4 h after infection, suggesting that Hsp70 plays a positive regulatory role in resistance to WSSV [23]. This work show that IHHNV and WSSV induce expression of Hsp70 and this can act as a regulatory immune system factor to combat the viral infection.…”

Proliferation dynamics of WSSV in crayfish, Procambarus clarkii, and the host responses at different temperatures

“…In addition to serving essential functions as molecular chaperones, HSPs also play participate in immunological process (Srivastava, ). Hsp70 transcriptions in WSSV‐infected hemocytes showed modest increased at 24 ± 1°C and rapid and high increased at 32 ± 1°C, which suggests that Hsp70 plays a positive regulatory role in resistance to WSSV infection during hyperthermia (Wu et al, ). And the transcriptions in hepatopancreas, gill and muscle of P. clarkii could also be induced by hyperthermia (Wu et al, ).…”

“…Hyperthermia reduces the expression of WSSV genes in Litopenaeus vannamei (Reyes, Salazar, & Granja, ). In P. clarkii , hyperthermia induced up‐regulation of Hsp70 expression and increased immune indicators such as THC and PO might contribute, in part, to the suppression of WSSV infection (Wu et al, ). It still existed a possibility that hyperthermia increases important mechanisms such as cell adhesion, encapsulation and phagocytosis, by which the crayfish innate immune system combats viral invasion (Wu et al, ).…”

“…In P. clarkii , hyperthermia induced up‐regulation of Hsp70 expression and increased immune indicators such as THC and PO might contribute, in part, to the suppression of WSSV infection (Wu et al, ). It still existed a possibility that hyperthermia increases important mechanisms such as cell adhesion, encapsulation and phagocytosis, by which the crayfish innate immune system combats viral invasion (Wu et al, ). Apoptosis might contribute to the increased survival of infected shrimp and suppressed WSSV replication in P. clarkii in hyperthermia state (Granja, Aranguren, Vidal, Aragon, & Salazar, ; Wu, Xiong, Wang, & Du, ).…”

“…White spot syndrome virus outbreak depends on the interactions among the pathogen, host and environmental (Sun et al, 2014). Previous studies reported that water temperature was one of the most critical environmental factors for outbreaks of WSSV infection (Sun et al, 2014;Wongmaneeprateep et al, 2010); high water temperature (32 ± 1°C) and low water temperature (≤16°C) could restrict WSSV replication in P. clarkii and reduced the morbidity rate (Du et al, 2008;Du, Li, Xu, & Kil, 2006;Granja, Vidal, Parra, & Salazar, 2006;Guan, Yu, & Li, 2003;Jiravanichpaisal, Soderhall, & Soderhall, 2004;Li, Luo, & Xu, 2013;Wu, Xiong, Wang, & Du, 2015;You et al, 2010). Sun et al reported that the low temperature (18°C) could delay the infection progression in shrimp (Sun et al, 2014).…”