Topical Review: La Crosse and Other Forms of California Encephalitis

Rust, Robert S.; Thompson, Wayne H.; Matthews, Charles G.; Beaty, Barry J.; Chun, Raymond W. M.

doi:10.1177/088307389901400101

Cited by 110 publications

(72 citation statements)

References 114 publications

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“…Both initially present as a summertime febrile illness with headache, nausea, vomiting, abdominal pain, and lethargy [3]. Encephalitis is characterized by fever, focal neurologic abnormalities with altered mental status that can progress to seizures and coma.…”

Section: Bunyaviridaementioning

confidence: 99%

“…Arbovirus members of the Bunyaviridae family that cause neuroinvasive disease include viruses from 2 different genera, Orthobunyavirus and Phlebovirus. The Orthobunyaviruses California encephalitis virus (CEV) and La Crosse virus (LACV) are members of the California serogroup viruses, which include 15 related arboviruses that cause neuroinvasive and non-neuroinvasive diseases [3]. Toscana virus (TOSV) and Rift Valley fever virus (RVFV) belong to the genus Phlebovirus, which is predominately transmitted by sandfly and tick.…”

Section: Introduction To Encephalitic Arbovirusesmentioning

confidence: 99%

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Encephalitic Arboviruses: Emergence, Clinical Presentation, and Neuropathogenesis

2016

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Arboviruses are arthropod-borne viruses that exhibit worldwide distribution, contributing to systemic and neurologic infections in a variety of geographical locations. Arboviruses are transmitted to vertebral hosts during blood feedings by mosquitoes, ticks, biting flies, mites, and nits. While the majority of arboviral infections do not lead to neuroinvasive forms of disease, they are among the most severe infectious risks to the health of the human central nervous system. The neurologic diseases caused by arboviruses include meningitis, encephalitis, myelitis, encephalomyelitis, neuritis, and myositis in which virus-and immune-mediated injury may lead to severe, persisting neurologic deficits or death. Here we will review the major families of emerging arboviruses that cause neurologic infections, their neuropathogenesis and host neuroimmunologic responses, and current strategies for treatment and prevention of neurologic infections they cause.

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Section: Bunyaviridaementioning

confidence: 99%

Section: Introduction To Encephalitic Arbovirusesmentioning

confidence: 99%

Encephalitic Arboviruses: Emergence, Clinical Presentation, and Neuropathogenesis

2016

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“…LACV infections are an important cause of severe encephalitis and meningitis in children and young adults in the Western United States (1)(2)(3). Around 75-100 cases per year require hospitalizations (4), and more than 10% of those patients will have long-lasting neurological deficits (1,5).…”

Section: La Crosse Virus (Lacv)mentioning

confidence: 99%

Interferon Antagonist NSs of La Crosse Virus Triggers a DNA Damage Response-like Degradation of Transcribing RNA Polymerase II

Verbruggen

Ruf

Blakqori

et al. 2011

Journal of Biological Chemistry

107

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La Crosse encephalitis virus (LACV) is a mosquito-borne member of the negative-strand RNA virus family Bunyaviridae. We have previously shown that the virulence factor NSs of LACV is an efficient inhibitor of the antiviral type I interferon system. A recombinant virus unable to express NSs (rLACVdelNSs) strongly induced interferon transcription, whereas the corresponding wt virus (rLACV) suppressed it. Here, we show that interferon induction by rLACVdelNSs mainly occurs through the signaling pathway leading from the pattern recognition receptor RIG-I to the transcription factor IRF-3. NSs expressed by rLACV, however, acts downstream of IRF-3 by specifically blocking RNA polymerase II-dependent transcription. Further investigations revealed that NSs induces proteasomal degradation of the mammalian RNA polymerase II subunit RPB1. NSs thereby selectively targets RPB1 molecules of elongating RNA polymerase II complexes, the so-called IIo form. This phenotype has similarities to the cellular DNA damage response, and NSs was indeed found to transactivate the DNA damage response gene pak6. Moreover, NSs expressed by rLACV boosted serine 139 phosphorylation of histone H2A.X, one of the earliest cellular reactions to damaged DNA. However, other DNA damage response markers such as up-regulation and serine 15 phosphorylation of p53 or serine 1524 phosphorylation of BRCA1 were not triggered by LACV infection. Collectively, our data indicate that the strong suppression of interferon induction by LACV NSs is based on a shutdown of RNA polymerase II transcription and that NSs achieves this by exploiting parts of the cellular DNA damage response pathway to degrade IIo-borne RPB1 subunits. La Crosse virus (LACV)3 is a mosquito-borne member of the family Bunyaviridae, genus Orthobunyavirus. LACV infections are an important cause of severe encephalitis and meningitis in children and young adults in the Western United States (1-3). Around 75-100 cases per year require hospitalizations (4), and more than 10% of those patients will have long-lasting neurological deficits (1, 5). Recent observations suggest that the virus is spreading to new geographic regions (6).Like other arboviruses, LACV cycles between vertebrate and invertebrate hosts, being able to replicate both in mammals and in insects. Depending on the host, however, the outcome of infection is different (7). In mammalian cells, infection is lytic and causes host cell shutoff and cell death. In insect cells infection is non-cytolytic and leads to long term viral persistence.LACV is enveloped and has a tri-segmented singlestranded RNA genome of negative-sense polarity. Transcription and replication of the genome occur in the cytoplasm, and particles bud into the Golgi apparatus before being secreted. The viral genome encodes four structural proteins, the viral polymerase (L) on the large (L) segment, two glycoproteins (Gn and Gc) on the medium (M) segment, and the viral nucleocapsid protein (N) on the smallest (S) segment. In addition, LACV expresses two nonstructural protei...

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“…Therefore, affected encephalitic patients suffer long-term neurological impairment as a result from the infection [18,28]. These symptoms include short-term or long-term memory loss, seizures, and impaired judgment [28,84,85]. A neurological exam is performed to evaluate the mental status, detect neurological problems, such as motor dysfunction and seizures, and help determine which area of the brain is affected [18].…”

Section: Pathogenesis Of Arboviral Infectionsmentioning

confidence: 99%