The emergence of Nipah virus (NiV) infection into the pig population and subsequently into the human population is believed to be due to changes in ecological conditions. In Malaysia, A major NiV outbreak occurred in pigs and humans from September 1998 to April 1999 that resulted in infection of 265 and death of 105 persons. About 1.1 million pigs had to be destroyed to control the outbreak. The disease was recorded in the form of a major outbreak in India in 2001 and then a small incidence in 2007, both the outbreaks in West Bengal only in humans without any involvement of pigs. There were series of human Nipah incidences in Bangladesh from 2001 till 2013 almost every year with mortality exceeding 70 %. The disease transmission from pigs acting as an intermediate host during Malaysian and Singapore outbreaks has changed in NIV outbreaks in India and Bangladesh, transmitting the disease directly from bats to human followed by human to human. The drinking of raw date palm sap contaminated with fruit bat urine or saliva containing NiV is the only known cause of outbreak of the disease in Bangladesh outbreaks. The virus is now known to exist in various fruit bats of Pteropus as well as bats of other genera in a wider belt from Asia to Africa.
Macrobrachium rosenbergii is the most important cultured freshwater prawn in the world and it is now farmed on a large scale in many countries. Generally, freshwater prawn is considered to be tolerant to diseases but a disease of viral origin is responsible for severe mortalities in larval, post-larval and juvenile stages of prawn. This viral infection namely white tail disease (WTD) was reported in the island of Guadeloupe in 1995 and later in Martinique (FrenchWest Indies) in Taiwan, the People's Republic of China, India, Thailand, Australia and Malaysia. Two viruses, Macrobrachium rosenbergii nodavirus (MrNV) and extra small virus-like particle (XSV) have been identified as causative agents of WTD. MrNV is a small icosahedral non-enveloped particle, 26-27 nm in diameter, identified in the cytoplasm of connective cells. XSV is also an icosahedral virus and 15 nm in diameter. Clinical signs observed in the infected animals include lethargy, opaqueness of the abdominal muscle, degeneration of the telson and uropods, and up to 100 % within 4 days. The available diagnostic methods to detect WTD include RT-PCR, dot-blot hybridization, in situ hybridization and ELISA. In experimental infection, these viruses caused 100 % mortality in post-larvae but failed to cause mortality in adult prawns. The reported hosts for these viruses include marine shrimp, Artemia and aquatic insects. Experiments were carried out to determine the possibility of vertical transmission of MrNV and XSV in M. rosenbergii. The results indicate that WTD may be transferred from infected brooders to their offspring during spawning. Replication of MrNV and XSV was investigated in apparently healthy C6/36 Aedes albopictus and SSN-1 cell lines. The results revealed that C6/36 and SSN-1cells were susceptible to these viruses. No work has been carried out on control and prevention of WTD and dsRNA against protein B2 produced RNAi that was able to functionally prevent and reduce mortality in WTD-infected redclaw crayfish.