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Background: Sindbis virus (SINV) is a mosquito-borne alphavirus found in Eurasia, Africa, and Oceania. Clinical SINV infection is characterized by febrile rash and arthritis and sometimes prolonged arthralgia and myalgia. The pathophysiological mechanisms of musculoskeletal and rheumatic disease caused by SINV are inadequately understood., Methods: We studied the muscle pathology of SINV infection ex vivo by examining a unique muscle biopsy obtained from a patient with chronic myalgia and arthralgia 6 months after acute SINV infection and assessed potential genetic predisposing factors by determining the human leukocyte antigen (HLA) and complement factor C4 genes and proteins. In addition, we performed in vitro SINV infections of primary human myoblasts and myotubes., Results: In the muscle biopsy we found evidence of muscle regeneration due to previous necrotic lesions likely caused by earlier SINV infection. We showed that human myoblasts and myotubes were susceptible in vitro for SINV infection as the cells became immunoreactive for viral antigens and cytopathic effect was observed. The patient was homozygous for HLA-B*35 alleles and heterozygous for HLA-DRB1*01 and HLA-DRB1*03 alleles and had total deficiency of C4B protein., Conclusions: This study provides new insights concerning pathological processes leading to chronic symptoms in SINV infection and demonstrates for the first time the susceptibility of human myogenic cells to SINV infection.

West Nile virus (WNV) is a mosquito-borne disease that emerged in North America where it caused in 2002 te largest arboviral meningoencephalitis outbreak ever recorded in this area. The viral variant responsible for this outbreak has been found to share 99.7% identity over the entire genome with the viral variant that caused the epizootic in Israel in 1998 and has been referred as "Isr98/NY99". It has been shown to exhibit an increased neurovirulence in humans, as well as in experimental infections in different animal models. Mouse model has allowed to demonstrate the preferential infection of neurons within the central nervous system and to point out the genetic determinism of host susceptibility to WNV. In murine neural cell cultures, the selective infection of neurons was accompanied by physiopathological changes and a cytopathic effect, showing the direct effect of infection of neurons as one of the causes of WNV neuropathogenicity.

The effect of colchicine, an inhibitor of axonal transport, on the spread of rabies virus in the central nervous system was investigated using Wistar rats. Colchicine was inoculated into the striatum at various times before and after inoculation of rabies virus into the same site. Rats were killed at various times after viral inoculation and the spread of rabies virus was monitored by rabies immunofluorescence of selected areas of brain. The most effective inhibitory effect was obtained by colchicine treatment applied two days before virus inoculation. Under these conditions, no fluorescent foci could be detected until day 3 post-infection whereas control rats exhibited infected cells as soon as two days post-infection. This inhibitory effect is reversible and the general consequence seems to be a delay in the rate of viral spread. However, five days after the virus challenge, some major brain areas were still partially preserved from infection (striatum, frontal cortex, pyriform cortex). Ten days after colchicine treatment, the microtubules have recovered their capacity to transport the virus. At the onset of paralysis, the general pattern of infection in brain sections from colchicine-treated rats was not significantly different from that of control rats. This inhibitory effect on the transport of rabies virus can be prolonged by administration of additional colchicine.