Abstract
DedicationThis review is dedicated in the memory of Dr Radha K. Maheshwari, a great mentor and colleague, whose passion for research and student training has left a lasting effect on this manuscript and many other works.Venezuelan equine encephalitis virus (VEEV) is an alphavirus in the family Togaviridae. VEEV is highly infectious in aerosol form and a known bio-warfare agent that can cause severe encephalitis in humans. Periodic outbreaks of VEEV occur predominantly in Central and South America. Increased interest in VEEV has resulted in a more thorough understanding of the pathogenesis of this disease. Inflammation plays a paradoxical role of antiviral response as well as development of lethal encephalitis through an interplay between the host and viral factors that dictate virus replication. VEEV has efficient replication machinery that adapts to overcome deleterious mutations in the viral genome or improve interactions with host factors. In the last few decades there has been ongoing development of various VEEV vaccine candidates addressing the shortcomings of the current investigational new drugs or approved vaccines. We review the current understanding of the molecular basis of VEEV pathogenesis and discuss various types of vaccine candidates.
Highlights
Venezuelan equine encephalitis virus (VEEV) is a member of genus Alphavirus in the familyTogaviridae
It is known that the inflammation contributes to the severity of the VEEV infection in the brain, and increased inflammation due to the influx of activated Natural Killer (NK)-cells could explain the enhanced encephalitis resulting in death of C3H/HeN mice following intranasal infection with TC-83 [28,31,32]
The DNA vaccine platform expressing structural genes of VEEV is attractive from the safety standpoint as it completely avoids the potential of reversal of candidate vaccine platforms to the virulent type, a cause of adverse event associated with virus replication
Summary
Venezuelan equine encephalitis virus (VEEV) is a member of genus Alphavirus in the family. VEEV is an enveloped virus which is maintained in nature in a cycle between rodents and mosquitoes with epizootic strains sporadically causing outbreaks in equines and humans (Figure 1) [2,3]. Epizootic strains are transmitted by mosquitoes to equines, causing high titer viremia mortality. VEEV primarily infects the neurons, but glia and oligodendrocytes are and enters the olfactory lobe of the brain (large insert). VEEV induced inflammation causes vascular cuffing and alteration in the BBB neurons, but glia and oligodendrocytes are targets of VEEV infection. VEEV mediated alteration of the BBB may allow inflammation causes vascular cuffing and alteration in the BBB allowing mononuclear lymphocytes the virus to enter the brain, but this route of entry is debated. Table of mutations in Venezuelan equine encephalitis virus (VEEV) strains and resulting this route1.ofDescription entry is debated. Envelope protein (E) 2 170 silent nsp codon 260 (Ser to Thr) mutationE2removing
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