In situ hybridization and histopathological observations during ostreid herpesvirus-1-associated mortalities in Pacific oysters Crassostrea gigas

Bueno, Rudolfo; Perrott, Matthew R.; Dunowska, Magdalena; Brosnahan, Cara L.; Johnston, Colin

doi:10.3354/dao03062

Cited by 11 publications

(6 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…To visualize bacteria that had infiltrated the tissues, tissue sections were stained using Giemsa, which coloured the different tissues and cells in shades of pink to purple and most bacteria in deep blue (performed by Histalim Company, France). The presence of OsHV-1 in tissue sections was detected by in situ hybridization following a previously published protocol 64 . The slides were hybridized with 5 ng µl −1 of OsHV-1-specific digoxigenin-labelled (DIG) antisense probes designed based on the C2-C6 fragment of the ORF4 of the OsHV-1 reference genome (GenBank: NC_005881.2), which is also present in the OsHV-1 µVar sequence.…”

Section: Methodsmentioning

confidence: 99%

Immune-suppression by OsHV-1 viral infection causes fatal bacteraemia in Pacific oysters

et al. 2018

View full text Add to dashboard Cite

Infectious diseases are mostly explored using reductionist approaches despite repeated evidence showing them to be strongly influenced by numerous interacting host and environmental factors. Many diseases with a complex aetiology therefore remain misunderstood. By developing a holistic approach to tackle the complexity of interactions, we decipher the complex intra-host interactions underlying Pacific oyster mortality syndrome affecting juveniles of Crassostrea gigas, the main oyster species exploited worldwide. Using experimental infections reproducing the natural route of infection and combining thorough molecular analyses of oyster families with contrasted susceptibilities, we demonstrate that the disease is caused by multiple infection with an initial and necessary step of infection of oyster haemocytes by the Ostreid herpesvirus OsHV-1 µVar. Viral replication leads to the host entering an immune-compromised state, evolving towards subsequent bacteraemia by opportunistic bacteria. We propose the application of our integrative approach to decipher other multifactorial diseases that affect non-model species worldwide.

show abstract

Section: Methodsmentioning

confidence: 99%

Immune-suppression by OsHV-1 viral infection causes fatal bacteraemia in Pacific oysters

et al. 2018

View full text Add to dashboard Cite

show abstract

“…2 ). During lytic infection in Pacific oysters, OsHV-1 predominately infects hemocytes, which undergo degeneration and death ( Bueno et al., 2016 ; de Lorgeril et al., 2018 ; Delisle et al., 2022 ; Friedman et al., 2005 ). OsHV-1 has also been detected in epithelial cells of Pacific oysters in some studies ( Arzul et al., 2002 ; Martenot et al., 2016 ; Prado-Alvarez et al., 2016 ) but not in others ( Bueno et al., 2016 ; Corbeil et al., 2015 ; Lipart and Renault, 2002 ), suggesting that epithelial cells are not the primary sites of replication during lytic infection by OsHV-1.…”

Section: Discussionmentioning

confidence: 99%

“…During lytic infection in Pacific oysters, OsHV-1 predominately infects hemocytes, which undergo degeneration and death ( Bueno et al., 2016 ; de Lorgeril et al., 2018 ; Delisle et al., 2022 ; Friedman et al., 2005 ). OsHV-1 has also been detected in epithelial cells of Pacific oysters in some studies ( Arzul et al., 2002 ; Martenot et al., 2016 ; Prado-Alvarez et al., 2016 ) but not in others ( Bueno et al., 2016 ; Corbeil et al., 2015 ; Lipart and Renault, 2002 ), suggesting that epithelial cells are not the primary sites of replication during lytic infection by OsHV-1. It is unusual for hemocytes to be the primary sites of replication during lytic infection by herpesviruses, since epithelial cells are primary sites of replication during lytic infection for most vertebrate herpesviruses and most fish alloherpesviruses ( Aurelian, 1990 ; Cohen, 2020 ; Hanson et al., 2011 ).…”

Section: Discussionmentioning

confidence: 99%

Ostreid herpesvirus 1 latent infection and reactivation in adult Pacific oysters, Crassostrea gigas

Divilov,

Wang,

Swisher

et al. 2024

Virus Research

View full text Add to dashboard Cite

“…Nevertheless, OsHV-1 was detected in tissues and hemocytes of two-year old oysters on 1, 2, and 3 dpi, with higher levels of OsHV-1 in the hemocytes (Figure 2). During lytic infection in Pacific oysters, OsHV-1 predominately infects hemocytes, which undergo degeneration and death [23][24][25][26]. OsHV-1 has been detected in epithelial cells of Pacific oysters in some studies [27][28][29] but not in others [23,30,31], suggesting that epithelial cells are not the primary sites of replication during lytic infection by OsHV-1.…”

Section: Discussionmentioning

confidence: 99%

Persistent Infections of Ostreid Herpesvirus 1 in Adult Pacific Oysters, <em>Crassostrea gigas</em>

Divilov¹,

Wang²,

Fleener³

et al. 2023

Preprint

View full text Add to dashboard Cite

Ostreid herpesvirus 1 (OsHV-1) is one of the most economically important pathogens of Pacific oysters. Understanding the pathogenesis of this virus is critical to developing tools to control outbreaks on shellfish farms. OsHV-1 is genetically related to vertebrate herpesviruses, which have a lytic and a latent stage, with the latent stage capable of being reactivated to the lytic stage. Here, OsHV-1 latency in Pacific oysters was investigated in experimentally and naturally infected oysters. Lytic infection in one-year-old oysters injected with the Tomales Bay strain of OsHV-1 was detectable between 1 and 4 days post-infection (dpi) but was not detectable after 5 dpi. The infected oysters shed 1102 to 1104 DNA copies/ml during the 4-day acute phase. At 21 dpi, the recovered oysters were temperature and chemically stressed and were found to shed 1104 to 1105 DNA copies/ml over a period of 48 h. Lytic shedding was not detectable in two-year-old oysters injected similarly with the same strain of OsHV-1; however, the OsHV-1 genome was detectable by qPCR in the adductor muscle, gill, mantle, and hemocytes within the first 3 dpi, after which it became undetectable. No OsHV-1 was detectable in the adductor muscle, gill, or mantle from experimentally infected oysters on days 15 and 21 post-infection or from oysters sampled 9 months after surviving an OsHV-1 mortality event; however, OsHV-1 DNA could be detected in hemocytes of both experimentally infected oysters at 21 dpi and naturally infected oysters. In addition, lytic viral gene transcription was detectable in hemocytes of experimentally infected oysters between 1 and 21 dpi and in hemocytes of naturally infected oysters.

show abstract

In situ hybridization and histopathological observations during ostreid herpesvirus-1-associated mortalities in Pacific oysters Crassostrea gigas

Cited by 11 publications

References 51 publications

Immune-suppression by OsHV-1 viral infection causes fatal bacteraemia in Pacific oysters

Immune-suppression by OsHV-1 viral infection causes fatal bacteraemia in Pacific oysters

Ostreid herpesvirus 1 latent infection and reactivation in adult Pacific oysters, Crassostrea gigas

Persistent Infections of Ostreid Herpesvirus 1 in Adult Pacific Oysters, <em>Crassostrea gigas</em>

Contact Info

Product

Resources

About