Toscana Virus Epidemiology: From Italy to Beyond

Cusi, Maria

doi:10.2174/1874357901004010022

Cited by 37 publications

(56 citation statements)

References 50 publications

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“…We focused on TOSV, a phlebovirus transmitted to humans by the same insect vector as Leishmania parasites (42). Mimicking the likely biological route of concomitant infection, TOSV was inoculated together with Lgy parasites s.c. into the footpad.…”

Section: Resultsmentioning

confidence: 99%

Type I interferons induced by endogenous or exogenous viral infections promote metastasis and relapse of leishmaniasis

Rossi

Castiglioni

Hartley

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

103

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The presence of the endogenous Leishmania RNA virus 1 (LRV1) replicating stably within some parasite species has been associated with the development of more severe forms of leishmaniasis and relapses after drug treatment in humans. Here, we show that the disease-exacerbatory role of LRV1 relies on type I IFN (type I IFNs) production by macrophages and signaling in vivo. Moreover, infecting mice with the LRV1-cured Leishmania guyanensis (LgyLRV1 − ) strain of parasites followed by type I IFN treatment increased lesion size and parasite burden, quantitatively reproducing the LRV1-bearing (LgyLRV1 + ) infection phenotype. This finding suggested the possibility that exogenous viral infections could likewise increase pathogenicity, which was tested by coinfecting mice with L. guyanensis and lymphocytic choriomeningitis virus (LCMV), or the sand fly-transmitted arbovirus Toscana virus (TOSV). The type I IFN antiviral response increased the pathology of L. guyanensis infection, accompanied by down-regulation of the IFN-γ receptor normally required for antileishmanial control. Further, LCMV coinfection of IFN-γ-deficient mice promoted parasite dissemination to secondary sites, reproducing the LgyLRV1 + metastatic phenotype. Remarkably, LCMV coinfection of mice that had healed from L. guyanensis infection induced reactivation of disease pathology, overriding the protective adaptive immune response. Our findings establish that type I IFN-dependent responses, arising from endogenous viral elements (dsRNA/LRV1), or exogenous coinfection with IFN-inducing viruses, are able to synergize with New World Leishmania parasites in both primary and relapse infections. Thus, viral infections likely represent a significant risk factor along with parasite and host factors, thereby contributing to the pathological spectrum of human leishmaniasis.Leishmania RNA virus 1 | Totiviridae | arboviruses | trypanosomatid protozoan parasite | Leishmania subgenus Viannia

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Section: Resultsmentioning

confidence: 99%

Type I interferons induced by endogenous or exogenous viral infections promote metastasis and relapse of leishmaniasis

Rossi

Castiglioni

Hartley

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

103

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“…RVFV is spread via mosquitoes or through extensive contact with blood, milk, and body tissues from infected livestock [37]. TOSV is transmitted by sandflies and causes 100 to 200 cases of meningoencephalitis each summer in Europe and North Africa [38]. Although the natural reservoirs for TOSV remain unidentified, canines have been identified as potential candidates [39].…”

Section: Epidemiology Of Encephalitic Arbovirusesmentioning

confidence: 99%

“…Similar to other members of the Bunyaviridae, TOSV infection is generally asymptomatic or causes a flu-like, febrile illness with headache and myalgia, mostly in younger people [38]. This newly emerging pathogen causes outbreaks of meningitis and meningoencephalitis mostly in older individuals.…”

Section: Bunyaviridaementioning

confidence: 99%

“…This newly emerging pathogen causes outbreaks of meningitis and meningoencephalitis mostly in older individuals. There have also been reports of severe cases complicated by hydrocephalus, deafness, and ischemic events [38]. Neuropathologic studies have been performed in a single lethal case of meningoencephalitis and showed extensive perivascular and parenchymal infiltration of CD8 T cells with microglial activation in a variety of CNS regions, including the neocortex, basal ganglia, hypothalamus, thalamus, limbic areas and brain stem, and infiltration of immune cells within the meninges [80].…”

Section: Bunyaviridaementioning

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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“…The second pathogen within the Phlebovirus genus that has been linked with bats is the Toscana virus, a serotype of Sand fly fever distributed in the Mediterranean region (Fig. 3.1b) (Charrel et al 2005;Cusi et al 2010). In 1971, the Toscana virus was isolated for the first time from the sand fly Phlebotomus perniciosus in Monte Argentario, Toscana (Braito et al 1997;Cusi et al 2010;Valassina et al 2003;WHO 2004).…”

Section: Bunyaviridaementioning

confidence: 99%