La Crosse virus: replication in vertebrate and invertebrate hosts

Borucki, Monica K.; Kempf, Brian J.; Blitvich, Bradley J.; Blair, Carol D.; Beaty, Barry J.

doi:10.1016/s1286-4579(02)01547-2

Cited by 76 publications

(64 citation statements)

References 39 publications

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“…triseriatus is a known vector of LACV, which can cause serious disease in humans, and is the most common cause of pediatric arboviral encephalitis in the U.S., with 42-172 cases reported annually (1960s-1990s). Case numbers, however, are suspected to be underestimated (McJunkin et al 2001;Borucki et al 2002). Jamestown canyon virus has repeatedly been isolated from field-collected A. triseriatus in the U.S. (Andreadis et al 2008), and the mosquito has also been suggested to be a possible bridge vector for WNV following isolation of the virus from field collections (Centers for Disease Control and Prevention 2009), and demonstration of vector competence under laboratory conditions (Styler et al 2007).…”

Section: Aedes Triseriatusmentioning

confidence: 99%

A Review of the Invasive Mosquitoes in Europe: Ecology, Public Health Risks, and Control Options

Medlock¹,

Hansford²,

Schaffner

et al. 2012

Vector-Borne and Zoonotic Diseases

575

511

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There has been growing interest in Europe in recent years in the establishment and spread of invasive mosquitoes, notably the incursion of Aedes albopictus through the international trade in used tires and lucky bamboo, with onward spread within Europe through ground transport. More recently, five other non-European aedine mosquito species have been found in Europe, and in some cases populations have established locally and are spreading. Concerns have been raised about the involvement of these mosquito species in transmission cycles of pathogens of public health importance, and these concerns were borne out following the outbreak of chikungunya fever in Italy in 2007, and subsequent autochthonous cases of dengue fever in France and Croatia in 2010. This article reviews current understanding of all exotic (five introduced invasive and one intercepted) aedine species in Europe, highlighting the known import pathways, biotic and abiotic constraints for establishment, control strategies, and public health significance, and encourages Europe-wide surveillance for invasive mosquitoes.

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Section: Aedes Triseriatusmentioning

confidence: 99%

A Review of the Invasive Mosquitoes in Europe: Ecology, Public Health Risks, and Control Options

Medlock¹,

Hansford²,

Schaffner

et al. 2012

Vector-Borne and Zoonotic Diseases

575

511

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“…In the case of La Crosse virus, which belongs to the Orthobunyavirus genus and is the principal cause of pediatric encephalitis in several geographic areas of North America, apoptosis was detected after infection of both newborn mice and a neuronal cell line, whereas another neuronal cell line was resistant to apoptosis or other cytopathic effects (42). More recently, it has also been shown that La Crosse virus can induce apoptosis in BHK-21 cells but not the mosquito cell line C6/36 (3).…”

mentioning

confidence: 99%

Bunyamwera Virus Nonstructural Protein NSs Counteracts Interferon Regulatory Factor 3-Mediated Induction of Early Cell Death

Kohl

Clayton

Weber

et al. 2003

J Virol

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The genome of Bunyamwera virus (BUN; family Bunyaviridae, genus Orthobunyavirus) consists of three segments of negative-sense RNA. The smallest segment, S, encodes two proteins, the nonstructural protein NSs, which is nonessential for viral replication and transcription, and the nucleocapsid protein N. Although a precise role in the replication cycle has yet to be attributed to NSs, it has been shown that NSs inhibits the induction of alpha/beta interferon, suggesting that it plays a part in counteracting the host antiviral defense. A defense mechanism to limit viral spread is programmed cell death by apoptosis. Here we show that a recombinant BUN that does not express NSs (BUNdelNSs) induces apoptotic cell death more rapidly than wild-type virus. Screening for apoptosis pathways revealed that the proapoptotic transcription factor interferon regulatory factor 3 (IRF-3) was activated by both wild-type BUN and BUNdelNSs infection, but only wild-type BUN was able to suppress signaling downstream of IRF-3. Studies with a BUN minireplicon system showed that active replication induced an IRF-3-dependent promoter, which was suppressed by the NSs protein. In a cell line (P2.1) defective in double-stranded RNA signaling due to low levels of IRF-3, induction of apoptosis was similar for wild-type BUN and BUNdelNSs. These data suggest that the BUN NSs protein can delay cell death in the early stages of BUN infection by inhibiting IRF-3-mediated apoptosis.

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“…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.…”

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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La Crosse virus: replication in vertebrate and invertebrate hosts

Cited by 76 publications

References 39 publications

A Review of the Invasive Mosquitoes in Europe: Ecology, Public Health Risks, and Control Options

A Review of the Invasive Mosquitoes in Europe: Ecology, Public Health Risks, and Control Options

Bunyamwera Virus Nonstructural Protein NSs Counteracts Interferon Regulatory Factor 3-Mediated Induction of Early Cell Death

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

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