A biovar-specific signal of Rhizobium leguminosarum bv. viciae induces increased nodulation gene-inducing activity in root exudate of Vicia staiva subsp. nigra

Microbial Biotechnolog

Feline calicivirus virulent systemic disease: Clinical epidemiology, analysis of viral isolates and in vitro efficacy of novel antivirals in australian outbreaks

Feline calicivirus (FCV) causes upper respiratory tract disease (URTD) and sporadic outbreaks of virulent systemic disease (FCV-VSD). The basis for the increased pathogenicity of FCVVSD viruses is incompletely understood, and antivirals for FCV-VSD have yet to be developed. We investigated the clinicoepidemiology and viral features of three FCV-VSD outbreaks in Australia and evaluated the in vitro efficacy of nitazoxanide (NTZ), 2′-C-methylcytidine (2CMC) and NITD008 against FCV-VSD viruses. Overall mortality among 23 cases of FCV-VSD was 39%. Metagenomic sequencing identified five genetically distinct FCV lineages within the three outbreaks, all seemingly evolving in situ in Australia. Notably, no mutations that clearly distinguished FCVURTD from FCV-VSD phenotypes were identified. One FCV-URTD strain likely originated from a recombination event. Analysis of seven amino-acid residues from the hypervariable E region of the capsid in the cultured viruses did not support the contention that properties of these residues can reliably differentiate between the two pathotypes. On plaque reduction assays, dose–response inhibition of FCV-VSD was obtained with all antivirals at low micromolar concentrations; NTZ EC50, 0.4–0.6 µM, TI = 21; 2CMC EC50, 2.7–5.3 µM, TI > 18; NITD-008, 0.5 to 0.9 µM, TI > 111. Investigation of these antivirals for the treatment of FCV-VSD is warranted

Distinct lineages of feline parvovirus associated with epizootic outbreaks in Australia, New Zealand and the United Arab Emirates

Feline panleukopenia (FPL), a frequently fatal disease of cats, is caused by feline parvovirus (FPV) or canine parvovirus (CPV). We investigated simultaneous outbreaks of FPL between 2014 and 2018 in Australia, New Zealand and the United Arab Emirates (UAE) where FPL outbreaks had not been reported for several decades. Case data from 989 cats and clinical samples from additional 113 cats were obtained to determine the cause of the outbreaks and epidemiological factors involved. Most cats with FPL were shelter-housed, 9 to 10 weeks old at diagnosis, unvaccinated, had not completed a primary vaccination series or had received vaccinations noncompliant with current guidelines. Analysis of parvoviral VP2 sequence data confirmed that all FPL cases were caused by FPV and not CPV. Phylogenetic analysis revealed that each of these outbreaks was caused by a distinct FPV, with two virus lineages present in eastern Australia and virus movement between different geographical locations. Viruses from the UAE outbreak formed a lineage of unknown origin. FPV vaccine virus was detected in the New Zealand cases, highlighting the difficulty of distinguishing the co-incidental shedding of vaccine virus in vaccinated cats. Inadequate vaccination coverage in shelter-housed cats was a common factor in all outbreaks, likely precipitating the multiple re-emergence of infection events

Sitting Time and Body Mass Index in Diabetics and Pre-Diabetics Willing to Participate in a Lifestyle Intervention

This cross-sectional study examined the relationship between Body Mass Index (BMI), total sitting time and total physical activity time in a generally overweight or obese population of type 2 diabetics or pre-diabetics willing to participate in a lifestyle intervention [n = 221, 55.1% male, mean age (SD) 62.0 (9.9), mean BMI (SD) 31.4 (5.0)]. In addition, we aimed to identify demographic and psychosocial associates of the motivation to become more physically active. The measurement instrument was a self-report questionnaire. Results showed that total sitting time was more closely related to BMI than total physical activity time. Subjects with a higher weight status were more sedentary, but they were also more motivated to be physically active. On the other hand, their self-efficacy to be physically active was lower than subjects with a lower weight status. Lifestyle interventions to decrease the risk of obesity and type 2 diabetes should aim not only at increasing total physical activity time, but also at reducing the total sitting time. Despite generally high levels of motivation among these obese participants, intervention designers and intermediaries should be aware of their low level of self-efficacy towards being physically active

Ancient, independent evolution and distinct molecular features of the novel human T-lymphotropic virus type 4

<p>Abstract</p> <p>Background</p> <p>Human T-lymphotropic virus type 4 (HTLV-4) is a new deltaretrovirus recently identified in a primate hunter in Cameroon. Limited sequence analysis previously showed that HTLV-4 may be distinct from HTLV-1, HTLV-2, and HTLV-3, and their simian counterparts, STLV-1, STLV-2, and STLV-3, respectively. Analysis of full-length genomes can provide basic information on the evolutionary history and replication and pathogenic potential of new viruses.</p> <p>Results</p> <p>We report here the first complete HTLV-4 sequence obtained by PCR-based genome walking using uncultured peripheral blood lymphocyte DNA from an HTLV-4-infected person. The HTLV-4(1863LE) genome is 8791-bp long and is equidistant from HTLV-1, HTLV-2, and HTLV-3 sharing only 62–71% nucleotide identity. HTLV-4 has a prototypic genomic structure with all enzymatic, regulatory, and structural proteins preserved. Like STLV-2, STLV-3, and HTLV-3, HTLV-4 is missing a third 21-bp transcription element found in the long terminal repeats of HTLV-1 and HTLV-2 but instead contains unique c-Myb and pre B-cell leukemic transcription factor binding sites. Like HTLV-2, the PDZ motif important for cellular signal transduction and transformation in HTLV-1 and HTLV-3 is missing in the C-terminus of the HTLV-4 Tax protein. A basic leucine zipper (b-ZIP) region located in the antisense strand of HTLV-1 and believed to play a role in viral replication and oncogenesis, was also found in the complementary strand of HTLV-4. Detailed phylogenetic analysis shows that HTLV-4 is clearly a monophyletic viral group. Dating using a relaxed molecular clock inferred that the most recent common ancestor of HTLV-4 and HTLV-2/STLV-2 occurred 49,800 to 378,000 years ago making this the oldest known PTLV lineage. Interestingly, this period coincides with the emergence of <it>Homo sapiens sapiens </it>during the Middle Pleistocene suggesting that early humans may have been susceptible hosts for the ancestral HTLV-4.</p> <p>Conclusion</p> <p>The inferred ancient origin of HTLV-4 coinciding with the appearance of <it>Homo sapiens</it>, the propensity of STLVs to cross-species into humans, the fact that HTLV-1 and -2 spread globally following migrations of ancient populations, all suggest that HTLV-4 may be prevalent. Expanded surveillance and clinical studies are needed to better define the epidemiology and public health importance of HTLV-4 infection.</p

The antioxidant enzyme peroxiredoxin-2 is depleted in lymphocytes seven days after ultra-endurance exercise

Purpose: Peroxiredoxin-2 (PRDX-2) is an antioxidant and chaperone-like protein critical for cell function. This study examined whether the levels of lymphocyte PRDX-2 are altered over one month following ultra-endurance exercise. Methods: Nine middle-aged men undertook a single-stage, multi-day 233 km (145 mile) ultra-endurance running race. Blood was collected immediately before (PRE), upon completion/retirement (POST), and following the race at DAY 1, DAY 7 and DAY 28. Lymphocyte lysates were examined for PRDX-2 by reducing SDS-PAGE and western blotting. In a sub-group of men who completed the race (n = 4) PRDX-2 oligomeric state (indicative of redox status) was investigated. Results: Ultra-endurance exercise caused significant changes in lymphocyte PRDX-2 (F (4,32) 3.409, p=0.020, ?(2) =0.299): seven-days after the race, PRDX-2 levels in lymphocytes had fallen to 30% of pre-race values (p=0.013) and returned to near-normal levels at DAY 28. Non-reducing gels demonstrated that dimeric PRDX-2 (intracellular reduced PRDX-2 monomers) was increased in 3 of 4 race completers immediately post-race, indicative of an "antioxidant response". Moreover, monomeric PRDX-2 was also increased immediately post-race in 2 of 4 race-completing subjects, indicative of oxidative damage, which was not detectable by DAY 7. Conclusions: Lymphocyte PRDX-2 was decreased below normal levels 7 days after ultra-endurance exercise. Excessive accumulation of reactive oxygen species induced by ultra-endurance exercise may underlie depletion of lymphocyte PRDX-2 by triggering its turnover after oxidation. Low levels of lymphocyte PRDX-2 could influence cell function and might, in part, explain reports of dysregulated immunity following ultra-endurance exercise

Plant-inducible virulence promoter of the Agrobacterium tumefaciens Ti plasmid

Agrobacterium tumefaciens is the causative agent of crown gall, a plant tumour that can arise on most species of dicotyledonous plants. The tumour-inducing capacity of the bacterium requires the presence of a large plasmid, designated the Ti plasmid, which itself contains two regions essential for tumour formation-the T(umour)-region and the Vir(ulence)-region. The T-region is transferred to plant cells by an unknown mechanism, and becomes stably integrated into the plant genome. The Vir-region has been identified by transposon mutagenesis, but the DNA of this region has never been detected in tumour lines. However, trans-complementation of Vir mutants indicates that genes of the Vir-region are functional in the bacterium. Moreover, the Vir- and T-regions can be physically separated in A. tumefaciens without loss of tumour-inducing capacity. Seven loci, designated virA-F and virO, have been identified in the Vir-region of the octopine Ti plasmid, but their functions are unknown. As virC mutants in the octopine-type plasmid pTiB6 are invariably avirulent in tests on various plant species, this gene seems to be essential for virulence and we are studying it in detail. We report here that the promoter of virC shows no detectable activity in A. tumefaciens and Escherichia coli K-12 grown in standard medium, but that its activity is induced by a plant product.