Assessing Seed Longevity of the Invasive Weed Navua Sedge (Cyperus aromaticus), by Artificial Ageing

Navua sedge (Cyperus aromaticus (Ridley) Mattf. & Kukenth) is a significant agricultural and environmental weed found in tropical island countries including north Queensland, Australia. It is a prolific seed producer and consequently forms a high-density seedbank, and therefore understanding the longevity and persistence of the seeds can provide critical information required for the management of this species. A laboratory-controlled artificial ageing experiment was conducted where the seeds were exposed to a temperature of 45 °C and 60% relative humidity for 125 days. Seeds were removed at various times (1, 2, 5, 9, 20, 30, 50, 75, 100 and 125 days) and their viability determined through standard germination tests. It took 20 days in the artificial ageing environment for the seeds to decline to 50% viability which indicates that Navua sedge has relatively short-lived persistent seeds. These findings will assist in developing a better understanding of the seedbank dynamics of this invasive species, allowing managers to tactically implement control strategies and prepare budgets for ongoing treatments, and have implications for the duration and success of management programs

Evaluation of Florpyrauxifenbenzyl for the control of Cyperus aromaticus (Navua sedge).

Background: Cyperus aromaticus (Navua sedge) is a creeping perennial sedge common to tropical environments, currently threatening many agroecosystems and ecosystems in Pacific Island countries and northern Queensland in Australia. Objective: A glasshouse study was conducted to evaluate the efficacy of florpyrauxifen-benzyl on C. aromaticus plants with and without established rhizomes. Methods: The plants with established rhizomes were treated at three application times being mowed, pre-flowering and flowering growth stages and plants without established rhizomes were treated at seedling, pre-flowering and flowering growth stages. At each application time, plants were treated with four rates of florpyrauxifen-benzyl: 0, 15, 30 and 60 g a.i. ha−1 and control. Results: There was no mortality in the plants with established rhizomes. Reduction in the number of tillers was observed at four weeks after treatment (WAT) in plants treated with 30 and 60 g a.i. ha−1 of herbicide, however, there was new growth from the rhizomes and the number of tillers increased at 8 WAT. Conversely, florpyrauxifen-benzyl provided above 95% control in plants without established rhizomes. Conclusions: These results indicate florpyrauxifen-benzyl can help manage a new C. aromaticus infestation prior to the establishment of rhizomes. However, it has little to no impact on C. aromaticus plants with established rhizomes, and other management options should be employed to control them

Germination Biology of Three Populations of Navua Sedge (Cyperus aromaticus)

Navua sedge [Cyperus aromaticus (Ridley) Mattf. & Kük.] is an aggressive perennial sedge native to equatorial Africa that has become problematic in many Pacific islands and wet, tropical Queensland, Australia. It has had a significant impact on the livestock-grazing industry, sugarcane (Saccharum officinarum L.) and banana (Musa acuminata Colla) plantations, and various other ecosystems. A laboratory-based research investigation was conducted to understand germination and emergence requirements under various environmental conditions of three geographically varied populations sourced from South Johnstone (SJ), Mackay (M) and Nyleta Creek (NC) in Queensland. Germination was identified to be stimulated by light, with no germination recorded under darkness. Populations SJ and NC had optimal germination at alternating temperatures of 25/15, 30/20, and 35/25 C, whereas population M had optimal germination at 25/15 and 30/20 C. All populations recorded greater than 85% germination at all pH levels tested. Seeds of population SJ were more sensitive to salinity compared with populations M and NC, with SJ showing no germination at 100 mM, whereas populations M and NC had 23% and 9% germination, respectively. An inverse relationship was observed between osmotic potential and germination, with no germination recorded at osmotic potentials below –0.8 MPa in any population, indicating moisture availability is a critical requirement for germination. Exposing seeds to 120 C radiant heat completely inhibited germination in populations M and NC, whereas 3% of population SJ germinated following a 180-s exposure at 120 C. Seedling emergence decreased as planting depth increased. Emergence was greatest for seeds on the soil surface or at 0.5-cm burial depth, consistent with germination being stimulated by light. Knowledge of these biological characteristics of C. aromaticus seed germination will assist in investigation of suitable control actions for this species, particularly in the early stage of its invasion into new areas, and will contribute to significant reduction in the soil seedbank

Mobilization of HIV Spread by Diaphanous 2 Dependent Filopodia in Infected Dendritic Cells

Paramount to the success of persistent viral infection is the ability of viruses to navigate hostile environments en route to future targets. In response to such obstacles, many viruses have developed the ability of establishing actin rich-membrane bridges to aid in future infections. Herein through dynamic imaging of HIV infected dendritic cells, we have observed how viral high-jacking of the actin/membrane network facilitates one of the most efficient forms of HIV spread. Within infected DC, viral egress is coupled to viral filopodia formation, with more than 90% of filopodia bearing immature HIV on their tips at extensions of 10 to 20 µm. Live imaging showed HIV filopodia routinely pivoting at their base, and projecting HIV virions at µm.sec−1 along repetitive arc trajectories. HIV filopodial dynamics lead to up to 800 DC to CD4 T cell contacts per hour, with selection of T cells culminating in multiple filopodia tethering and converging to envelope the CD4 T-cell membrane with budding HIV particles. Long viral filopodial formation was dependent on the formin diaphanous 2 (Diaph2), and not a dominant Arp2/3 filopodial pathway often associated with pathogenic actin polymerization. Manipulation of HIV Nef reduced HIV transfer 25-fold by reducing viral filopodia frequency, supporting the potency of DC HIV transfer was dependent on viral filopodia abundance. Thus our observations show HIV corrupts DC to CD4 T cell interactions by physically embedding at the leading edge contacts of long DC filopodial networks

Expression of DC-SIGN and DC-SIGNR on human sinusoidal endothelium: a role for capturing hepatitis C virus particles.

Hepatic sinusoidal endothelial cells are unique among endothelial cells in their ability to internalize and process a diverse range of antigens. DC-SIGNR, a type 2 C-type lectin expressed on liver sinusoids, has been shown to bind with high affinity to hepatitis C virus (HCV) E2 glycoprotein. DC-SIGN is a closely related homologue reported to be expressed only on dendritic cells and a subset of macrophages and has similar binding affinity to HCV E2 glycoprotein. These receptors function as adhesion and antigen presentation molecules. We report distinct patterns of DC-SIGNR and DC-SIGN expression in human liver tissue and show for the first time that both C-type lectins are expressed on sinusoidal endothelial cells. We confirmed that these receptors are functional by demonstrating their ability to bind HCV E2 glycoproteins. Although these lectins on primary sinusoidal cells support HCV E2 binding, they are unable to support HCV entry. These data support a model where DC-SIGN and DC-SIGNR on sinusoidal endothelium provide a mechanism for high affinity binding of circulating HCV within the liver sinusoids allowing subsequent transfer of the virus to underlying hepatocytes, in a manner analogous to DC-SIGN presentation of human immunodeficiency virus on dendritic cells

HIV research in Australia: linking basic research findings with clinical and public health outcomes

Despite a population of only 20 million and sustained low prevalence of HIV infection in Australia, Australian researchers have provided many substantial original findings to the fields of HIV pathogenesis, treatment and prevention. More recently, Australian clinicians and scientists have turned their attention to assisting other countries in developing effective responses, particularly within the Asia-Pacific region. It is therefore fitting that the 4th International AIDS Society (IAS) Conference on HIV Pathogenesis, Treatment and Prevention will be held in Sydney in July 2007. The meeting is expected to attract over 5000 participants and will have a dynamic and innovative programme within the three major themes of HIV basic science, clinical research and biomedical prevention

Patients with treated indolent lymphomas immunized with BNT162b2 have reduced anti-spike neutralizing IgG to SARS-CoV-2 variants, but preserved antigen-specific T cell responses

Patients with indolent lymphoma undertaking recurrent or continuous B cell suppression are at risk of severe COVID-19. Patients and healthy controls (HC; N = 13) received two doses of BNT162b2: follicular lymphoma (FL; N = 35) who were treatment naïve (TN; N = 11) or received immunochemotherapy (ICT; N = 23) and Waldenström's macroglobulinemia (WM; N = 37) including TN (N = 9), ICT (N = 14), or treated with Bruton's tyrosine kinase inhibitors (BTKi; N = 12). Anti-spike immunoglobulin G (IgG) was determined by a high-sensitivity flow-cytometric assay, in addition to live-virus neutralization. Antigen-specific T cells were identified by coexpression of CD69/CD137 and CD25/CD134 on T cells. A subgroup (N = 29) were assessed for third mRNA vaccine response, including omicron neutralization. One month after second BNT162b2, median anti-spike IgG mean fluorescence intensity (MFI) in FL ICT patients (9977) was 25-fold lower than TN (245 898) and HC (228 255, p =.0002 for both). Anti-spike IgG correlated with lymphocyte count (r =.63; p =.002), and time from treatment (r =.56; p =.007), on univariate analysis, but only with lymphocyte count on multivariate analysis (p =.03). In the WM cohort, median anti-spike IgG MFI in BTKi patients (39 039) was reduced compared to TN (220 645, p =.0008) and HC (p <.0001). Anti-spike IgG correlated with neutralization of the delta variant (r =.62, p <.0001). Median neutralization titer for WM BTKi (0) was lower than HC (40, p <.0001) for early-clade and delta. All cohorts had functional T cell responses. Median anti-spike IgG decreased 4-fold from second to third dose (p =.004). Only 5 of 29 poor initial responders assessed after third vaccination demonstrated seroconversion and improvement in neutralization activity, including to the omicron variant

Surfactant protein D modulates HIV infection of both T-cells and dendritic cells

Surfactant Protein D (SP-D) is an oligomerized C-type lectin molecule with immunomodulatory properties and involvement in lung surfactant homeostasis in the respiratory tract. SP-D binds to the enveloped viruses, influenza A virus and respiratory syncytial virus and inhibits their replication in vitro and in vivo. SP-D has been shown to bind to HIV via the HIV envelope protein gp120 and inhibit infectivity in vitro. Here we show that SP-D binds to different strains of HIV (BaL and IIIB) and the binding occurs at both pH 7.4 and 5.0 resembling physiological relevant pH values found in the body and the female urogenital tract, respectively. The binding of SP-D to HIV particles and gp120 was inhibited by the presence of several hexoses with mannose found to be the strongest inhibitor. Competition studies showed that soluble CD4 and CVN did not interfere with the interaction between SP-D and gp120. However, soluble recombinant DC-SIGN was shown to inhibit the binding between SP-D and gp120. SP-D agglutinated HIV and gp120 in a calcium dependent manner. SP-D inhibited the infectivity of HIV strains at both pH values of 7.4 and 5.0 in a concentration dependent manner. The inhibition of the infectivity was abolished by the presence of mannose. SP-D enhanced the binding of HIV to immature monocyte derived dendritic cells (iMDDCs) and was also found to enhance HIV capture and transfer to the T-cell like line PM1. These results suggest that SP-D can bind to and inhibit direct infection of T-cells by HIV but also enhance the transfer of infectious HIV particles from DCs to T-cells in vivo

In Situ Distribution of HIV-Binding CCR5 and C-Type Lectin Receptors in the Human Endocervical Mucosa

The endocervical mucosa is believed to be a primary site of HIV transmission. However, to date there is little known about the distribution of the HIV co-receptor CCR5 and the HIV-binding C-type lectin receptors, including Langerin, dendritic cell (DC)-specific intercellular adhesion molecule-grabbing non-integrin (DC-SIGN) and mannose receptor (MR) at this site. We therefore characterized the expression of these molecules in the endocervix of HIV seronegative women by computerized image analysis. Endocervical tissue biopsies were collected from women (n = 6) undergoing hysterectomy. All study individuals were diagnosed with benign and non-inflammatory diseases. CCR5+ CD4+ CD3+ T cells were found within or adjacent to the endocervical epithelium. The C-type lectin Langerin was expressed by intraepithelial CD1a+ CD4+ and CD11c+ CD4+ Langerhans cells, whereas DC-SIGN+ MR+ CD11c myeloid dendritic cells and MR+ CD68+ macrophages were localized in the submucosa of the endocervix. The previously defined immune effector cells including CD8+, CD56+, CD19+ and IgD+ cells were also found in the submucosa as well as occasional CD123+ BDCA-2+ plasmacytoid dendritic cells. Understanding the spatial distribution of potential HIV target cells and immune effector cells in relation to the endocervical canal forms a basis for deciphering the routes of HIV transmission events in humans as well as designing HIV-inhibiting compounds

HIV Traffics through a Specialized, Surface-Accessible Intracellular Compartment during trans-Infection of T Cells by Mature Dendritic Cells

In vitro, dendritic cells (DCs) bind and transfer intact, infectious HIV to CD4 T cells without first becoming infected, a process known as trans-infection. trans-infection is accomplished by recruitment of HIV and its receptors to the site of DC–T cell contact and transfer of virions at a structure known as the infectious synapse. In this study, we used fluorescent microscopy to track individual HIV particles trafficking in DCs during virus uptake and trans-infection. Mature DCs rapidly concentrated HIV into an apparently intracellular compartment that lacked markers characteristic of early endosomes, lysosomes, or antigen-processing vesicles. Live cell microscopy demonstrated that the HIV-containing compartment was rapidly polarized toward the infectious synapse after contact with a T cell; however, the bulk of the concentrated virus remained in the DCs after T cell engagement. Individual virions were observed emerging from the compartment and fusing with the T cell membrane at the infectious synapse. The compartmentalized HIV, although engulfed by the cytoplasm, was fully accessible to HIV envelope-specific inhibitors and other membrane-impermeable probes that were delivered to the cell surface. These results demonstrate that HIV resides in an invaginated domain within DCs that is both contiguous with the plasma membrane and distinct from endocytic vesicles. We conclude that HIV virions are routed through this specialized compartment, which allows individual particles to be delivered to T cells during trans-infection