Among over 40 mammal species threatened by the filling of a hydroelectric dam reservoir in French Guiana, three species of primates have been translocated, comprising 124 red howler monkeys, six white-faced sakis, and 95 golden-handed tamarins. Health status of the animals was evaluated by direct physical examination and by hematological, biochemical, virological, and parasitological surveys of collected blood. The physical condition of the howlers was slightly worse toward the end of the capture period, but that of sakis and tamarins remained satisfactory. Several ectoparasites (ticks, larvae of dipterous insects, fleas, and lice) were collected, and various wounds, apparently nondebilitating, were recorded in howlers. Hematological and biochemical profiles determined for the three species revealed a slight anemia in howlers. Entamoeba, Strongyloides, and Trypanoxyurus were common in fecal samples of howlers. A survey of blood smears from the three species revealed infection by several types of microfilaria, Trypanosoma rangeli-like and Plasmodium brasilianum in all three, and Trypanosoma cruzi-like in howlers. These infections had no significant impact on the health status or the hematological profiles. Serologic investigations revealed occasional reactions against Toxoplasma gondii, a strong anti-Plasmodium response in the two Cebidae species, and a weaker one in tamarins. Attempts to isolate arbovirus failed, but antibody responses to Mayaro and yellow fever viruses were strong, especially in the howlers. A strong correlation between age and serological status led to a better understanding of the epidemic cycles. Our survey indicates French Guianan primates are reservoirs for several anthropozoonoses, including malaria, Chagas disease, and arboviruses.

Here, we report that freshly isolated unstimulated adult T-cell leukemia (ATL) cells present high telomerase activity compared to asymptomatic carriers or normal donors. In spite of this high telomerase activity, ATL cells retained shorter telomeres compared to those of uninfected cells isolated from the same patients. Because the safeguarding of telomere length is critical to the unlimited proliferation of tumor cells, we investigated the underlying mechanism for short telomere maintenance in ATL cells. Transcriptional and posttranscriptional expression of telomere-binding proteins TRF1, TRF2, TIN2 and POT1, known to regulate telomere homeostasis and protection, were evaluated. We found that TRF1 and TRF2 are overexpressed in in vivo patient's samples from ATL but not asymptomatic carriers, while levels of POT1 expression did not specifically increase in ATL. To gain insights into the regulation of TRF genes in HTLV-I infected cells, we investigated the expression of TIN2, a regulator of these genes, and found an increase in TIN2 expression in ATL patients. Together our results underscore the importance of telomerase and telomere length regulating factors as novel markers for ATL disease progression and as potential therapeutic targets for the treatment of HTLV-I-associated malignancies. ' 2006 Wiley-Liss, Inc.Key words: HTLV-I; ATL; telomerase; telomere; TRF1; leukemia Human T-cell leukemia virus type 1 (HTLV-I) is the etiological agent of adult T-cell leukemia/lymphoma (ATL), an aggressive and fatal lymphoproliferative disorder.1,2 The poor prognosis of ATL patients is associated with the resistance of neoplastic cells to the conventional combination of high-dose chemotherapy and radiotherapy. 3 The mechanism by which HTLV-I engenders ATL is not clear, but the long latency period of several decades, preceding the disease, suggests that it relies upon long term survival and proliferation of virus-infected cells. [4][5][6] In fact, previous studies have shown that proliferation of ATL cells occurs mainly by replication of infected cells, leading to oligoclonal or monoclonal expansion.4-6 HTLV-I has evolved regulatory mechanisms to usurp cell cycle checkpoints 7-12 and apoptosis regulators, [13][14][15][16][17] and infected cells may escape from immune defenses, using a combinatorial effect of the regulatory proteins p30 and p12 that reduce viral expression and downregulate major histocompatibility complex expression, respectively. 18,19The DNA polymerase is unable to replicate telomeric structures, and thus each cellular division results in a progressive shortening of the telomere length. While telomere shortening may be associated with increased chromosomal instability and may facilitate carcinogenesis, it can also lead to irreversible senescence. Although in most cancer cells avoidance of telomere shortening beyond a critical size requires reactivation of telomerase expression, the sole expression of telomerase may not be sufficient for telomere elongation because of the ''open or closed'' nature of the telo...

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We evaluated the presence of human herpesvirus 8 (HHV-8) infection among groups of Amerindians in French Guiana. The overall prevalence of antibodies against lytic HHV-8 antigens was 23.0% (180/781), increasing from 18.4% in children <6 years old to approximately 30% in older persons (>45 years). Seroprevalence was higher in Amerindians living in remote localities than it was in those living in the coastal region. Analysis of a 725-base pair fragment of the K1 gene amplified from DNA from a Wayampi Amerindian showed that the virus belonged to molecular subtype E, which has hitherto been found in only a few Amerindians in Brazil and Ecuador.

The Ile du Grand Connétable nature reserve is a rocky island off the Northern Atlantic coast of South America that hosts a unique population of Magnificent Frigatebirds (Fregata magnificens, Pelecaniformes). A high chick mortality, associated with nodular proliferative lesions, involving featherless areas, such as legs, neck, eyelids, and beak, was recorded during a consecutive 2 yr and affected almost half of the generation. Investigations were, therefore, conducted to determine the cause of these epidemics. Although histopathologic investigations suggested that malnutrition, because of fewer resources in the Frigates' fishing area, could be the cause of the epidemic, a novel alphaherpesvirus, tentatively called Fregata magnificens herpesvirus, was detected in cutaneous crusts on the diseased birds. Although in this study, we do not prove the causal link of this new virus to the symptoms observed, it can nevertheless be suggested that in debilitated hosts, a productive herpesvirus infection might accelerate, and/or be accelerated by, population declines. These results emphasize the need to take into consideration the possible role of herpesviruses in weakened populations of wild birds in conservation management plans.