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The initial case in human outbreaks of Nipah virus has always been zoonotic [8] from exposure to contaminated secretions or tissues of infected bats or pigs. Subsequent human-to-human transmission of Nipah virus occurs via close contact with NiV-infected persons or exposure to NiV-infected body fluids (e.g., blood, urine, nasal secretions). [1]
The Nipah virus structural model, constructed at an atomic resolution, depicts a particle with a diameter of 90 nm, adorned with spikes. This model affords a glimpse into the virus's interior. The Nipah virus is known for its high mortality rate and is viewed as a potential candidate for the next pandemic.
The first site of the virus in Ipoh in 1998 and later occurrence to other places with the virus extent in blue while Hendra virus in red, both belong to the Paramyxoviridae family. The 1998–1999 Nipah virus outbreak areas in West Malaysia , blue is the origin source of the virus while the red are further affected areas.
Both viruses are contagious, highly virulent, and capable of infecting a number of mammalian species and causing potentially fatal disease. Due to the lack of either a licensed human vaccine (a Hendra virus vaccine exists for horses) or antiviral therapies, Hendra virus and Nipah virus are designated as Biosafety level (BSL) 4 agents.
Mononegavirales is an order of negative-strand RNA viruses which have nonsegmented genomes. Some members that cause human disease in this order include Ebola virus, human respiratory syncytial virus, measles virus, mumps virus, Nipah virus, and rabies virus. Important pathogens of nonhuman animals and plants are also in the group.
Nipah was first identified about 25 years ago in Malaysia and has led to outbreaks in Bangladesh, India and Singapore. The first participants in the Oxford trial received doses of the vaccine over ...
In its sixth outbreak in the country since 2001 this year, the virus, known for its 70% mortality rate, has claimed two lives out of the six who were infected in a span of few days in September ...
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