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Dive into the research topics where Joanna E. Huddleston is active.

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Featured researches published by Joanna E. Huddleston.


Nature Reviews Microbiology | 2011

Cellular microbiology: Rulers and sensors in Chlamydomonas

Joanna E. Huddleston

Chlaymydomonas reinhardtii senses the absolute length of its flagella and converts this length to a phosphorylation signal.


Nature Reviews Microbiology | 2011

Symbiosis: Market economics in plant–fungus relationships

Joanna E. Huddleston

Plants and fungi can detect the most cooperative partners and reward them with more nutrients.


Nature Reviews Microbiology | 2011

Bacterial secretion: Contact killing by Pseudomonas

Joanna E. Huddleston

Tse1 and Tse3 of the Pseudomonas aeruginosa type VI secretion system degrade the peptidoglycan of other bacteria.


Nature Reviews Microbiology | 2011

HIV: HIV hides in haematopoietic stem cells.

Joanna E. Huddleston

HIV/AIDS seek to manage the disease, the ultimate aim of any therapy is complete eradication of the virus. Unfortunately, full eradication of HIV is challenging, as the virus establishes latent reservoirs in resting CD4+ T cells. Now, Carter et al. show that HIV can infect haematopoietic stem cells (HSCs); thus, the reservoir of HIV is even more persistent than previously thought. Previous reports had suggested that HSCs are resistant to infection by HIV, but known viral reservoirs cannot fully account for the disease progression of AIDS, indicating that there are other reservoirs of latent infection. A study from the authors, published in 2010, suggested that HIV can infect haemato poietic proxad genitor cells (HPCs), but the assays used could not differentiate HSCs from other cell types within the HPC population. Now, using a multixad lineage engraftment experiment (that is, the ability of haemato poietic cells engrafted into sublethally irradiated mice to form multiple blood lineages and persist for more than 4–6 weeks, which is the definitive assay for stem cell potential), Carter et al. show that HIV can indeed infect HSCs. They began the current study by investigating whether the cellular receptor that HIV uses to enter cells influences the type of HPCs that become infected. HIV enters cells through the interaction of the HIV envelope protein (Env) with the CD4 receptor and either of the chemokine coxadreceptors CXCR4 or CCR5. The authors generated replicationxad deficient, nonxadtoxic HIV in a system in which they could vary the tropism of the Env protein. In addition, they tagged the HIV genome with GFP under a constitutive promoter, allowing the use of flow cytometry to isolate infected cells. They found that HIV particles containing a CXCR4xadtropic Env protein could infect cells that have a CD34hiCD133+ phenotype, which is associated with multipotency. By contrast, using the CCR5xadtropic Env protein, the virus could only efficiently infect the more differentiated CD34lowCD133– cells. Next, the authors used colony formaxad tion assays, in which progenitor cells differentiate in vitro into colonies that are representative of the lineages that can form in vivo, to show that cells infected by CXCR4xadtropic HIV can form colonies that are derived from immature HPCs, including HSCs. By contrast, CCR5xadtropic HIVxadinfected cells formed very few colonies. To confirm that CXCR4xadtropic HIV can infect HSCs, the authors performed the multilineage engraftxad ment experiment, introducing human HPCs infected with CXCR4xadtropic HIV into irradiated mice. Humanxad derived, GFP+ lymphoid and myeloid cells were detected in the blood of the mice up to 20 weeks after transplantxad ation. This indicates that the original HIVxadinfected cells were indeed HSCs. Thus, treatments to cure HIV will need to eradicate the reservoir of latent HIV in slowxaddividing HSCs. However, as active infection with HIV causes HSCs to undergo apoptosis, it is possible that therapies to activate HSCs may be effective in reducing the HIV reservoir, in comxad bination with standard antiretroviral therapy. Joanna E. Huddleston H I V


Nature Reviews Microbiology | 2011

Plant virology: Sign turns yellow for Y-sat-infected tobacco

Joanna E. Huddleston

Two papers show how small interfering RNAs (siRNAs) that are derived from Y-satellite RNAs can cause disease symptoms in plants.


Nature Reviews Microbiology | 2011

Contact killing by Pseudomonas: Bacterial secretion

Joanna E. Huddleston

Tse1 and Tse3 of the Pseudomonas aeruginosa type VI secretion system degrade the peptidoglycan of other bacteria.


Nature Reviews Microbiology | 2011

Parasitology: Leishmania turns down the heat.

Joanna E. Huddleston

The increased virulence of Leishmania amazonsis compared with Leishmania major may result from the ability of L. amazonensis to induce the macrophage inhibitor CD200.


Nature Reviews Microbiology | 2011

Parasitology: It takes II to induce NF-κB

Joanna E. Huddleston

Some strains of Toxoplasma gondii secrete a protein into the host cells that activates the host nuclear factor-κB pathway.


Nature Reviews Microbiology | 2011

Bacterial pathogenesis: Neisseria meningitidis : hit and run

Joanna E. Huddleston

Modification of type IV pili with phosphoglycerol destabilizes these pili, allowing bacteria to separate from microcolonies and spread the infection.


Nature Reviews Microbiology | 2011

Environmental microbiology: Boring bacteria?

Joanna E. Huddleston

A new paper describes a mechanism by which some bacteria can bore through carbonate rock by locally readjusting the calcium concentration.

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