Paradoxical Effect of Chloroquine Treatment in Enhancing Chikungunya Virus Infection.

Since 2005, Chikungunya virus (CHIKV) re-emerged and caused numerous outbreaks in the world, and finally, was introduced into the Americas in 2013. The lack of CHIKV-specific therapies has led to the use of non-specific drugs. Chloroquine, which is commonly used to treat febrile illnesses in the tropics, has been shown to inhibit CHIKV replication in vitro.

Mapping of the exchangeable and dispensable domains of the RNA 2-encoded 2A(HP) protein of arabis mosaic nepovirus.

The N-terminal domains of the RNA 2-encoded 2A(HP) proteins of the arabis mosaic (ArMV) and grapevine fanleaf (GFLV) nepoviruses were shown to be highly variable and a hotspot for intra- and inter-species recombination events. Chimeric ArMV-NW clones in which the N-terminal domain of 2A(HP) or the entire 2A(HP) of GFLV isolates replaced the corresponding domains of ArMV retained their infectivity, showing that the 2A(HP) proteins of ArMV-NW and GFLV are exchangeable. ArMN-NW clones with deletions of the N-terminal, core, or C-terminal domains of the ArMV-NW 2A(HP) were infectious in Chenopodium quinoa although viral RNA (especially RNA 2) accumulated at reduced levels.

In vitro and in vivo evidence for differences in the protease activity of two arabis mosaic nepovirus isolates and their impact on the infectivity of chimeric cDNA clones.

Regulated processing of nepovirus polyproteins allows the release of mature proteins and intermediate polyproteins. Infectious cDNA clones of the mild NW isolate of arabis mosaic virus (ArMV) and chimeric clones incorporating RNA1 segments of Lv, a severe isolate, were generated. Clones containing the Lv X2-NTB cleavage site were not infectious unless the Lv protease was present.

Chikungunya fever: epidemiology, clinical syndrome, pathogenesis and therapy.

Chikungunya virus (CHIKV) is the aetiological agent of the mosquito-borne disease chikungunya fever, a debilitating arthritic disease that, during the past 7years, has caused immeasurable morbidity and some mortality in humans, including newborn babies, following its emergence and dispersal out of Africa to the Indian Ocean islands and Asia. Since the first reports of its existence in Africa in the 1950s, more than 1500 scientific publications on the different aspects of the disease and its causative agent have been produced. Analysis of these publications shows that, following a number of studies in the 1960s and 1970s, and in the absence of autochthonous cases in developed countries, the interest of the scientific community remained low.

Chikungunya disease: infection-associated markers from the acute to the chronic phase of arbovirus-induced arthralgia.

At the end of 2005, an outbreak of fever associated with joint pain occurred in La Réunion. The causal agent, chikungunya virus (CHIKV), has been known for 50 years and could thus be readily identified. This arbovirus is present worldwide, particularly in India, but also in Europe, with new variants returning to Africa.

[Chikungunya physiopathology: Infection data from acute to chronic phase].

During the 2005-2006 austral summer, an outbreak of fever associated with joint pain hit the Reunion Island inhabitants. Chikungunya virus (CHIKV), the agent involved in this epidemic, was known since 50 years and was thus brought to general attention together with the risk of emergence or re-emergence of arboviral infections. This arbovirus rapidly spread worldwide, specifically in India with millions of cases, but also in Europe through imported cases (>2,000) and fewautochthonous cases in Italy and in France.