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Les arboviroses sont des maladies virales transmises par des piqures d’arthropodes, principalement de moustiques. Elles représentent une cause majeure de morbidité et parfois de mortalité. Leur expansion est constante et liée notamment aux modifications climatiques et la globalisation. Essentiellement tropicale, les arboviroses sont parfois à l’origine d’épidémie en Europe. Récemment, le chikungunya et le Zika ont été responsables de grandes épidémies en touchant des populations n’ayant jamais été en contact avec ces virus. Il n’existe à ce jour aucun traitement antiviral ou vaccin efficace contre ces virus. Les manifestations oculaires en rapport avec ces infections sont ainsi plus fréquentes et de mieux en mieux décrites. Elles se compliquent parfois, comme le Zika, d’une atteinte oculaire congénitale. L’objet de cette revue est de décrire les manifestations ophtalmologiques de la dengue, du chikungunya, de l’infection à virus Zika, de la fièvre du Nil occidental et de la fièvre jaune.

Arboviruses are viral diseases transmitted by mosquitoes and tick bites. They are a major cause of morbidity and sometimes mortality. Their expansion is constant and due in part to climate change and globalization. Mostly found in tropical regions, arboviruses are sometimes the source of epidemics in Europe. Recently, the Chikungunya virus and the Zika virus were responsible for very large epidemics impacting populations that had never been in contact with those viruses. There are currently no effective antiviral treatments or vaccines. Ocular manifestations due to those infections are thus more frequent and increasingly better described. They are sometimes, as with Zika, complicated by a congenital ocular syndrome. The goal of this review is to describe the ophthalmological manifestations of Dengue fever, Chikungunya virus, Zika virus, West Nile virus, and yellow fever.

Human T-cell leukemia virus type 1 (HTLV-1) basic-leucine zipper (bZIP) factor (HBZ) is a key player in proliferation and transformation of HTLV-1-infected cells, thus contributing to adult T-cell leukemia (ATL) development. HBZ deregulates gene expression within the host cell by interacting with several cellular partners. Through its C-terminal ZIP domain, HBZ is able to contact and activate JunD, a transcription factor of the AP-1 family. JunDmRNA is intronless but can generate two protein isoforms by alternative translation initiation: JunD full-length and Δ JunD, an N-terminal truncated form unresponsive to the tumor suppressor menin. Using various cell lines and primary T-lymphocytes, we show that after serum deprivation HBZ induces the expression of Δ JunD isoform. We demonstrate that, unlike JunD, Δ JunD induces proliferation and transformation of cells. To decipher the mechanisms for Δ JunD production, we looked into the translational machinery and observed that HBZ induces nuclear retention of RPS25mRNA and loss of RPS25 protein expression, a component of the small ribosomal subunit. Therefore, HBZ bypasses translational control of JunD uORF and favors the expression of Δ JunD. In conclusion, we provide strong evidences that HBZ induces Δ JunD expression through alteration of the cellular translational machinery and that the truncated isoform Δ JunD has a central role in the oncogenic process leading to ATL.

The human retrovirus HTLV-I is responsible for the chronic progressive myelopathy, TSP/HAM, characterized by the presence of infiltrated T lymphocytes, cytokines, and matrix metalloproteinases (MMPs) within spinal cord lesions. MMPs have been associated with several neurological diseases, and we previously reported the specific presence of the extracellular matrix-degrading protease, MMP-9, in the cerebrospinal fluid of TSP/HAM patients. Nevertheless, previous studies have not yet shown whether the expression of MMP-9 is associated with HTLV-I infection per se, or with neurological symptoms following infection. In the present work, the presence of tissue inhibitors of metalloproteinases 1 and 3 (TIMP-1 and TIMP-3) and of MMP-9 in the CSF of HTLV-I-infected individuals was compared in TSP/HAM patients versus HTLV-I carriers without neurological symptoms. TIM P-3, a regulator of MMP activity and cell survival, was detected with a significantly higher frequency in the TSP/HAM group and paralleled the increased levels of MMP-9 and neopterin, a sensitive indicator of cellular immune activation. These data may reflect the intense cell remodeling that occurs intrathecally in inflamed tissue. Changes in MMP, TIMP, and neopterin expression were not related to age at onset of disease, grade of motor disability, progressor status, or duration of disease, presumably indicating that TSP/HAM patients are continuously subjected to viral and immunological pressure. All these observations suggest that TIMPs and MMPs may contribute to the pathogenesis of TSP/HAM, and hence a new therapeutic strategy targeting the MMP/TIMP balance is needed. These observations also suggest that MMP-9 and TIMP-3 in CSF may be useful markers in the follow-up of the efficacy of therapeutic trials in TSP/HAM patients.

GB virus C/hepatitis G virus (GBV‐C/HGV) RNA was detected by reverse transcription‐polymer‐ ase chain reaction with primers derived from the nonstructural region 3 (NS3) in 9 (4.1%) of 221 blood donors and 2 of 20 (10%) hemophilia patients in Martinique, French West Indies. Anti‐E2 antibodies were found in sera from 33 (14.9%) of the blood donors and 5 (25%) of the hemophiliacs. None of the subjects was positive for both GBV‐C/HGV RNA and anti‐E2. Among the 20 hemophiliacs, 12 (60%) had anti‐HCV antibodies and 7 (35%) were positive for HCV RNA by PCR. All patients positive for HCV markers belonged to the group of 13 patients exposed previously to blood factor concentrates that were not activated virally. Nucleotide sequences of the 5′‐untranslated region (5′UTR) of the GBV‐C/HGV genome were obtained for the 10 NS3 PCR positive samples. Phylogenetic comparison of these isolates with reference isolates published previously showed a strong homology with European and American GBV‐C/HGV strains, 8 isolates belonging to the genotype 2a and 1 isolate to the type 2b. The isolate from 1 blood donor was identified as subtype 1a , indicating the presence of West African type strains. J. Med. Virol. 59:160–163, 1999. © 1999 Wiley‐Liss, Inc.

Background and Objectives: Posttransfusion hepatitis still occurs at an incidence of about 1 in 118,000 for HBV and 1 in 220,000 for HCV. This collaborative study aimed to determine the prevalence of a novel flavivirus, GBVC/HGV, even though its role in transfusion-associated hepatitis is uncertain. Materials and Methods: GBVC/HGV RNA was detected by PCR using either the Boehringer detection kit or by primers previously described. HGV antibodies were detected by a serological assay from Boehringer. Results: The observed GBVC/HGV RNA frequency was 3.4%. HGV antibodies occurred in 9.5% of donors. Conclusion: In our study, 12.9% of the donors had been in contact with the GBVC/HGV virus.