A VLP-based vaccine provides complete protection against Nipah virus challenge following multiple-dose or single-dose vaccination schedules in a hamster model.

Nipah virus is a highly lethal zoonotic paramyxovirus that was first recognized in Malaysia during an outbreak in 1998. During this outbreak, Nipah virus infection caused a severe febrile neurological disease in humans who worked in close contact with infected pigs. The case fatality rate in humans was approximately 40%.

Mammalian Cell-Derived Respiratory Syncytial Virus-Like Particles Protect the Lower as well as the Upper Respiratory Tract.

Globally, Respiratory Syncytial Virus (RSV) is a leading cause of bronchiolitis and pneumonia in children less than one year of age and in USA alone, between 85,000 and 144,000 infants are hospitalized every year. To date, there is no licensed vaccine. We have evaluated vaccine potential of mammalian cell-derived native RSV virus-like particles (RSV VLPs) composed of the two surface glycoproteins G and F, and the matrix protein M.

Vaccine potential of Nipah virus-like particles.

Nipah virus (NiV) was first recognized in 1998 in a zoonotic disease outbreak associated with highly lethal febrile encephalitis in humans and a predominantly respiratory disease in pigs. Periodic deadly outbreaks, documentation of person-to-person transmission, and the potential of this virus as an agent of agroterror reinforce the need for effective means of therapy and prevention. In this report, we describe the vaccine potential of NiV virus-like particles (NiV VLPs) composed of three NiV proteins G, F and M.

Cis-acting elements in the antigenomic promoter of Nipah virus.

Genome synthesis in paramyxoviruses, including Nipah virus (NiV), is controlled by sequence elements that reside in the non-coding nucleotides at the 5'-trailer (3'-antigenomic) end that make up the antigenomic promoter (AGP). Using a chloramphenicol acetyl transferase-based plasmid-driven minigenome system, the terminal 96 nt of NiV AGP were first mutagenized in blocks of three hexamers to enable broad mapping of the minigenome functional regions. This was followed by further dissection of these functional regions to define the cis-acting elements contained therein.

Reverse genetics of negative-stranded RNA viruses: a global perspective.

The advent of reverse genetics technology has revolutionized the field of RNA viruses. It is now possible to manipulate even negative-stranded RNA viruses at will, and evaluate the effects of these changes on the biology and pathogenesis of these viruses. The fundamental insights gleaned from the reverse genetics-based studies over the last several years have provided a new momentum for the development of designed therapies for the control and prevention of these viral pathogens.

An internal element of the measles virus antigenome promoter modulates replication efficiency.

The cis-acting sequence elements that direct measles virus (MV) genome synthesis reside in the 109 base non-coding region at the 5' trailer (3' antigenomic) end of MV genome that makes up the antigenomic promoter (AGP). The MV-AGP nucleotides 79-96, corresponding to nucleotide hexamers 14, 15 and 16 (the C' element), show sequence similarity with the equivalent region of many paramyxoviruses and are analogous to the three nucleotide hexamers that form the second replication control element in the Sendai virus AGP. In this study, results of two independent procedures demonstrate that the MV C' element also is a replication control sequence.

Expression of a foreign gene by recombinant canine distemper virus recovered from cloned DNAs.

A canine distemper virus (CDV) genomic cDNA clone and expression plasmids required to establish a CDV rescue system were generated from a laboratory-adapted strain of the Onderstepoort vaccine virus. In addition, a CDV minireplicon was prepared and used in transient expression studies performed to identify optimal virus rescue conditions. Results from the transient expression experiments indicated that minireplicon-encoded reporter gene activity was increased when transfected cell cultures were maintained at 32 rather than 37 degrees C, and when the cellular stress response was induced by heat shock.