Newly identified HMO-2011-type phages reveal genomic diversity and biogeographic distributions of this marine viral group.

Viruses play critical roles in influencing biogeochemical cycles and adjusting host mortality, population structure, physiology, and evolution in the ocean. Marine viral communities are composed of numerous genetically distinct subfamily/genus-level viral groups. Among currently identified viral groups, the HMO-2011-type group is known to be dominant and broadly distributed. However, only four HMO-2011-type cultivated representatives that infect marine SAR116 and Roseobacter strains have been reported to date, and the genetic diversity, potential hosts, and ecology of this group remain poorly elucidated. Here, we present the genomes of seven HMO-2011-type phages that were isolated using four Roseobacter strains and one SAR11 strain, as well as additional 207 HMO-2011-type metagenomic viral genomes (MVGs) identified from various marine viromes. Phylogenomic and shared-gene analyses revealed that the HMO-2011-type group is a subfamily-level group comprising at least 10 discernible genus-level subgroups. Moreover, >2000 HMO-2011-type DNA polymerase sequences were identified, and the DNA polymerase phylogeny also revealed that the HMO-2011-type group contains diverse subgroups and is globally distributed. Metagenomic read-mapping results further showed that most HMO-2011-type phages are prevalent in global oceans and display distinct geographic distributions, with the distribution of most HMO-2011-type phages being associated with temperature. Lastly, we found that members in subgroup IX, represented by pelagiphage HTVC033P, were among the most abundant HMO-2011-type phages, which implies that SAR11 bacteria are crucial hosts for this viral group. In summary, our findings substantially expand current knowledge regarding the phylogenetic diversity, evolution, and distribution of HMO-2011-type phages, highlighting HMO-2011-type phages as major ecological agents that can infect certain key bacterial groups.

Usefulness of quantitative assessment of JunB gene expression as a marker for monitoring chronic myeloid leukemia patients undergoing imatinib therapy.

JunB is a component of the activator protein 1 transcription factors and has been identified to be important in hematopoiesis. Transgenic mice lacking JunB expression develop myeloproliferative disease resembling human chronic myeloid leukemia (CML). JunB expression was significantly decreased in CML patients. We used real-time quantitative reverse transcription-polymerase chain reaction analysis to monitor both JunB and BCR-ABL expression during imatinib therapy. Nineteen patients were evaluated every 2 to 4 weeks, and their levels of JunB expression before therapy were significantly decreased compared with those of healthy individuals. After imatinib therapy, an increase in JunB expression was found in 5 patients, all of whom achieved a complete cytogenetic response (CCR) and molecular response (MR), with a decrease in BCR-ABL expression. JunB expression decreased to a very low level in 2 patients, both of whom showed progression to blast crisis. Variable JunB expression was found in the other 12 patients, and their outcomes were mostly driven by BCR-ABL levels. The patients with an increase in JunB expression were statistically more likely to achieve a major cytogenetic response (P = .045), CCR (P = .033), and MR (P = .033) than the group with no increase in JunB expression, and a durable response was observed. This study revealed that an increase in JunB expression is a good prognostic marker for predicting clinical response in CML patients treated with imatinib when such data are combined with an evaluation of BCR-ABL expression.

Clinical manifestations and laboratory assessment in an enterovirus 71 outbreak in southern Taiwan.

An epidemic of enterovirus 71 (EV71) infection compatible with hand, foot and mouth disease and associated with high morbidity and mortality occurred in Taiwan in 1998. We recruited 90 patients (50 males, 40 females) with definite EV71 infections for clinical and laboratory analysis. The neurological signs and symptoms, all of which occurred during the febrile period, in patients with central nervous system (CNS) involvement (aseptic meningitis, encephalitis or myelitis) were myoclonic jerks (23/33), vomiting (10/33), ataxia (7/33), lethargy (6/33), seizure (4/33) and tremor (2/33). Patients with CNS involvement had longer durations of fever (4.6+/-0.2 vs. 3.1+/-0.3 d; p <0.01) and a higher white blood cell count (12,512+/-658 vs. 10,607+/-409 cells/mm3; p = 0.01) than patients without CNS involvement. The case fatality rate in patients with CNS involvement was 4/33 (12%), whereas no fatalities (0/57) occurred in patients without CNS involvement. Six of 11 patients subjected to MRI showed a high intensity T2-weighted signal in the brainstem. A nested fluorescent RT-PCR for detection of virus in throat and stool specimens showed higher sensitivity than viral culture. Viremia was detectable using RT-PCR in 20% of cases (3/15), whereas no virus was isolated from culture or detected by RT-PCR in cerebrospinal fluid.