Betanodavirus: Dissection of the viral life cycle

Abstract

Progressive research has been recently made in dissecting the molecular biology of Betanodavirus life cycle, the causative pathogen of viral encephalopathy and retinopathy in economic important marine fish species. Establishment of betanodavirus infectious clone allows the manipulation of virus genome for functional genomic study, which elucidates the biological event of the viral life cycle at molecular level. The betanodavirus strategizes its replication by expressing anti-apoptosis/antinecrotic proteins to maintain the cell viability during early infection. Subsequently utilizes and controls the biological machinery of the infected cells for viral genome replication. Towards the late phase of infection, mass production of capsid protein for virion assembly induces the activation of host apoptosis pathway. It eventually leads to the cell lysis and death, which the lysis of cell contributes to the accomplishment of viral shedding that completes a viral life cycle. The recent efforts to dissect the entire betanodavirus life cycle are currently reviewed.

Molecular biology of Macrobrachium rosenbergii nodavirus infection in giant freshwater prawn

“…Since the crystallographic data of the Mr NV are not available, the well‐characterized betanodavirus capsid protein is referred. The capsid protein of betanodavirus adopts conformations of the C‐terminus to protrude exteriorly of the viral capsid, which are known as “spikes” that interact with host cell receptors for viral binding and subsequent entry into the cells (Chen et al., ; Ito et al., ; Low et al., ; Tang et al., ). However, even though phylogenetic analysis of the Mr NV capsid affiliates Mr NV to betanodavirus (Bonami & Widada, ), but the secondary structure analysis of Mr NV capsid was found to be highly homolog with cucumber necrosis virus subunit, rather than nodaviruses (Somrit et al., ).…”

“…Although the viral infections are host species-specific, cross-species infection other than the native host has been observed in some nodaviruses: Red-spotted grouper nervous necrosis virus has been reported to infect Asian seabass, Lates calcarifer (Banerjee, Hamod, Suresh, & Karunasagar, 2014); Nile tilapia, Oreochromis niloticus (Keawcharoen et al, 2015); and Amphiprion sebae Bleeker, a marine clownfish (Binesh, Renuka, Malaichami, & Greeshma, 2013), whereas the MrNV has also been reported to infect Penaeus indicus, Penaeus monodon and P. vannamei (Ravi et al, 2009;Senapin et al, 2012). A wide range of susceptible host as observed in betanodavirus and nodavirus that infects prawns proposed a potential of low host specificity of these nodaviruses (Low, Syarul Nataqain, Chee, Rozaini, & Najiah, 2017). Nodamura virus, the type species of alphanodavirus, is able to infect mammals besides insects, causing paralysis and death of these hosts (Bailey, Newman, & Porterfield, 1975;Johnson, Price, & Ball, 2003), which evidenced the uniqueness of nodaviruses and the low host specificity (Table 1).…”

“…It is crucial to maintain the viability of the infected cell from early cell death during the course of virus infection. Thus, viruses evolve different strategies to inhibit inflammatory and apoptosis responses of the infected host (Low et al, 2017;Roulston, Marcellus, & Branton, 1999). It has been reviewed that the protein encoded by subgenomic RNA3 of betanodavirus possesses antinecrotic function, deterring cell death through the inhibition of loss of mitochondrial membrane potential (Chen, Su, & Hong, 2009;Low et al, 2017).…”

RGNNV-induced cell cycle arrest at G1/S phase enhanced viral replication via p53-dependent pathway in GS cells

“…For example, Human immunodeficiency virus (HIV)-infected T lymphocytes isolated from patients are arrested in G2 (Zimmerman et al, 2006); alphavirus M1 infection results in S phase accumulation of infected cells by downregulating p21 proteion (He et al, 2010); Hepatitis C virus (HCV) NS2 protein induces cell cycle arrest in the S-phase in mammalian cells to facilitate HCV viral replication (Yang et al, 2006). Betanodavirus infection has been shown to alter some cell signaling pathways to maintain the cell viability during early infection in previous study (Low et al, 2017). However, the effects of NNV infection on the cell cycle of host cells and the significance of cell cycle regulation in NNV replication need to be further investigated.…”

Comparative genome analysis reveals a distinct influence of nucleotide composition on virus–host species‐specific interaction of prawn‐infecting nodavirus

“…The larger segment (3.1 kb) of RNA 1 encodes the RNA‐dependent RNA polymerase (RdRp) that replicates the viral genome, whereas the RNA 2 (1.4 kb) encodes the virus capsid protein precursor (Cp). The subgenomic RNA 3 was identified to encode for protein B2 that possesses regulatory functions, which was synthesized from the 3′ terminus of RNA 1 during viral replication (Low, Syarul Nataqain, Chee, Rozaini, & Najiah, ).…”