Abstract

The California serogroup (CSG) comprises 18 serologically and genetically related mosquito-borne orthobunyaviruses. Of these viruses, at least seven have been shown to cause neurological disease in humans, including the leading cause of pediatric arboviral encephalitis in the USA, La Crosse virus. Despite the disease burden from these viruses, much is still unknown about the CSG viruses. This review summarizes our current knowledge of the CSG viruses, including human disease and the mechanisms of neuropathogenesis.

Highlights

  • The California serogroup (CSG) is a closely related group of orthobunyaviruses in the familyPeribunyaviridae of the order Bunyavirales

  • Eleven CSG viruses were detected in the USA, including La Crosse virus (LACV), Snowshoe hare virus (SSHV), Jamestown Canyon virus (JCV), Keystone virus (KEYV), Trivittatus virus (TVTV), California encephalitis virus (CEV), South River virus (SORV), Morro Bay virus (MBV), Jerry Slough virus (JSV), San Angelo virus (SAV), and Infirmatus virus (INFV)

  • Most monkeys developed high neutralizing antibody titers, indicating they were productively infected [125,165,168]. These results suggest that CSG virus infection in monkeys may be akin to human infections, where infection and NAb responses happen readily, but neuroinvasive disease is a rare event

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Summary

Introduction

The California serogroup (CSG) is a closely related group of orthobunyaviruses in the family. All members of the CSG are presumed arboviruses, as all have been isolated from mosquitoes [3,4,5,6,7,8,9,10,11,12,13,14,15]. Their vector, host ranges, geographic distribution, and ability to cause disease in humans differ, including their ability to cause neuroinvasive disease. This review will summarize our current knowledge of the members of the CSG and their ability to cause neuroinvasive disease in humans

Relationships of the CSG Viruses
Geographic Distribution
Vector and Host Range
Replication
Human Infection and Disease
Neuropathogenesis – Experimental Infections of Animals
Neuropathogenesis – Molecular Mechanisms
Findings
Conclusions and Future Perspectives

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