#plos pathogens

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Persistent Problem

Although most infected adults experience few symptoms, Zika virus is a serious concern for pregnant women, as approximately 10% of children born after infection in the first three months of pregnancy suffer severe congenital defects. Infections later in pregnancy or in infants appear less devastating, but evidence of some serious conditions warrants further investigation. After infecting one-day-old mice with Zika virus, researchers found that, while most animals recovered within a week after experiencing symptoms, the virus persisted much longer. Zika virus could be found in localised spots in the brain over a year after infection, associated with signs of inflammation (pictured in a mouse cerebellum, with dying cells highlighted in green and active microglia, the brain’s immune cells, in red). Mice also displayed long-lasting symptoms, including a smaller cerebellum, impaired motor control, and hyperactivity, suggesting that infections early in life could have long-term consequences, which may require monitoring and treatment.

Written by Emmanuelle Briolat

Image from work by Derek D. C. Ireland and colleagues

US Food and Drug Administration, Office of Biotechnology Products, Silver Spring, MD, USA

Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in PLOS Pathogens, December 2020

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Features of Films

Living in a tight-knit community can provide safety and support. Bacteria find this too, and huddle together to form dense biofilms, which increase their survival and infectious potency. These films are glued together by a sugary slime called exopolysaccharides, without which the structure begins to fall apart. A new study has revealed a key factor in the production of this material in cholera biofilms (Vibrio exopolysaccharide, VPS). By adjusting the amount to which a particular enzyme attaches to and removes phosphate (dephosphorylation), the researchers changed the structural integrity of the biofilms (pictured, in several experiments). The production of VPS was directly regulated by the phosphorylation status, revealing a potential weakness that treatments could target to help prevent cholera settling in. Furthermore, these systems are similar among many bacteria that produce equivalent biofilms, meaning the insights could help tackle a wide range of diseases.

Written by Anthony Lewis

Image from work by Carmen Schwechheimer and colleagues

University of California—Santa Cruz, Santa Cruz, CA, USA

Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in PLOS Pathogens, August 2020

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Surface Trouble

Going to hospital is never good news, and it’s even more frustrating for people who pick up an extra infection while there. Pseudomonas aeruginosa is the bacteria behind one of the most common hospital-acquired infections, and is extra powerful when it attaches to a solid surface. How this anchoring makes it more virulent is unclear, so a new study used a biosensor to detect a key material produced by the bacteria. The experiments revealed that the bacteria ramp up their production and release of toxic alkyl-quinolone molecules, pictured with the sensor on a surface-attached population. When the bacteria latch on, the compounds are packaged up and secreted to harm nearby host cells. Revealing how this physical attachment dictates molecular behaviour to bolster the bacteria’s attack may point to new ways to tackle or prevent infections from P. aeruginosa and other similarly troublesome foes.

Written by Anthony Lewis

Image by Geoffrey D. Vrla and colleagues

Department of Molecular Biology, Princeton University, Princeton, NJ, USA

Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in PLOS Pathogens, September 2020

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Fuse and Conquer

Hijacking the host cytoskeleton is a popular pathogen trick, but the bacterium Burkholderia thailandensis takes this strategy even further. Once inside a host cell, B. thailandensis (in green) uses the host’s actin fibres (in red) to promote fusion with other cells, forming giant cells in which it rapidly replicates. Studying this behaviour in mouse macrophages, researchers uncovered how the immune system fights back: activated by type I interferon, molecules known as guanylate-binding proteins (GBPs) prevent the bacteria from manipulating actin, ultimately hindering cell fusion. Without GBPs, the macrophages are more likely to fuse when infected by B. thailandensis, and mice lacking GBPs are more susceptible to infection. Closely-related pathogens B. mallei and B. pseudomallei, which cause serious diseases in humans, also rely on cell fusion to spread, so unpicking this process in B. thailandensis is a useful step towards understanding their strategies.

Written by Emmanuelle Briolat

Image from work by David E. Place and colleagues, published on the cover of PLOS Pathogens

Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Department of Immunology, St. Jude Children’s Research Hospital, Memphis, TN, USA

Published in PLOS Pathogens, April 2020

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Pinpointing Persistent Pain

Nobody likes a guest who overstays their welcome. Particularly one that wasn’t invited in the first place. Chikungunya is a virus spread spread by mosquitoes that causes fever and severe muscle and joint pain that can persist for months. The cause of this lingering is unclear as researchers have struggled to track the virus during this chronic phase of the illness. To catch it in action, a new study developed a ‘reporter virus’ that permanently marked cells infected by chikungunya (red in the mouse foot pictured 28 days after infection). This molecular tell-tale revealed viral material 112 days after initial infection, and was then used to test what effect a potential treatment has on the number of infected cells and their persistence. The new approach presents a useful tool to pick out cells that harbour traces of infection and cause long term problems, which will ultimately help restrict their impact.

Written by Anthony Lewis

Image from work by Alissa R. Young and Marissa C. Locke, and colleagues

Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO, USA

Image originally published under a Creative Commons Licence (BY 4.0)

Published in PLOS Pathogens, August 2019

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Seeing Candida Differently

We’re all fundamentally the same yet can look vastly different from each other. Turn to the microbe Candida albicans and it too shows considerable differences within its species. This pathogenic yeast forms almost impenetrable sheets called biofilms when infecting humans, making treatment difficult. Research however often focuses on just one strain of C. albicans. Now researchers look at the effects of mutating four key genes needed for biofilm production in the strain most commonly studied in the lab as well as several others isolated from patients. Using confocal microscopy, they visualised the production of projections called hyphae (pictured), a key feature of C. albicans biofilms. They found the effects of each mutation (second to fourth columns) relative to the normal state (far left column) varied significantly across strains (rows, top to bottom). To get a more complete picture of how C. albicans functions, research into multiple strains is therefore needed.

Written by Lux Fatimathas

Image from work by Manning Y. Huang and colleagues

Department of Biological Sciences, Carnegie Mellon University, Pittsburgh, PA, USA

Image originally published under a Creative Commons Licence (BY 4.0)

Published in PLOS Pathogens, May 2019

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Hide and Stick

Urinary tract infections (UTIs) make life miserable for millions of people – mostly women – every year. More than half of women will have a UTI at some point in their life and although the infection can be treated with antibiotics, it often comes back. In the worst cases, UTIs become chronic and very difficult to treat effectively, although it’s not exactly clear why this happens. By studying the way that two different UTI-causing bacteria affect the cells that make up the lining of the bladder in mice (highlighted green and red), researchers think they have found an explanation. They’re discovered that the bugs responsible for chronic infections can engineer the cells in the bladder to make a cosy hiding place where the immune system can’t find them, leading to persistent UTIs that are resistant to antibiotics – an important insight that could lead to new ideas for preventing and treating chronic infections.

Written by Kat Arney

Image from work by Valerie P. O’Brien and colleagues, Washington University School of Medicine

Department of Molecular Microbiology and Center for Women’s Infectious Disease Research, Washington University School of Medicine, St. Louis, MO, USA

Originally published under a Creative Commons Licence (BY 4.0)

Published in PLOS Pathogens, December 2018

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Secrets of Secretion

Responsible for causing tuberculosis, a disease affecting millions of people worldwide, Mycobacterium tuberculosis can infect macrophages, immune cells which normally engulf and destroy pathogens. Critical to the bacterium’s success is a sophisticated secretion system, enabling it to transport useful compounds into host cells. Multiple proteins make up this system but their specific roles are difficult to disentangle, so researchers are investigating them in a closely-related pathogen, Mycobacterium marinum, causing tuberculosis in fish. They found especially intriguing results for one protein, named EspH. While bacteria lacking EspH were less effective at infecting macrophages in the lab, they were very virulent when infecting zebrafish larvae, forming aggregates inside and around zebrafish blood vessels, a phenomenon known as cording (pictured, with bacteria in red, blood vessels in green and macrophages in blue).This suggests that host factors interact with the bacterium’s own proteins, adding another layer of complexity to the processes behind tuberculosis infections.

Written by Emmanuelle Briolat

Image from work by Trang H. Phan and Lisanne M. van Leeuwen, and colleagues

Department of Medical Microbiology and Infection Control, Amsterdam University Medical Centers; and Section Molecular Microbiology, Amsterdam Institute of Molecules, Medicines & Systems, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands

Image originally published under a Creative Commons Licence (BY 4.0)

Published in PLOS Pathogens, August 2018

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