Virus

Event Date: 
Wednesday, July 29, 2015 - 18:15 - 18:30
Institution: 
Australian Institute of Marine Sciences
Title: 

Coral Reefs Go Viral: Unveiling the viruses associated with corals in a changing climate.

Abstract: 

Viruses are the most common biological agents in the global oceans, with numbers typically averaging ten billion per litre. The ability of viruses to infect all organisms indicates they most likely play a central role in marine ecosystems and have important consequences for the entire marine food web. Marine viruses influence many biogeochemical and ecological processes, including energy and nutrient cycling, host distribution and abundance, and horizontal gene transfer events. Research into viruses associated with coral reefs is a newly emerging field. Corals form an obligate symbiotic relationship with the dinoflagellate genus Symbiodinium, upon which the coral relies heavily for nutrition and calcification. Disruption of this symbiosis can lead to loss of the symbiotic algae from their host, resulting in coral bleaching and, if the symbiosis cannot re-establish, death of the coral colony. While a number of factors, including elevated reactive oxygen species production by Symbiodinium have been linked to coral bleaching, viral infection has not been methodically examined as a possible cause. Viruses that potentially target the algal symbiont, Symbiodinium sp., have been reported previously; therefore, we examined whether Symbiodinium in culture is host to a virus that switches to a lytic infection under stress, such as UV exposure or elevated temperature. Analysis of algal cultures, using techniques including flow cytometry and transmission electron microscopy, revealed prevalent viral activity, regardless of experimental conditions. This talk will present recent results and results allow for the development of molecular diagnostic probes for rapid detection of viruses in field samples, and will help monitor and assess the role of viruses in coral bleaching and holobiont functioning.

Event Date: 
Wednesday, July 29, 2015 - 18:00 - 18:15
Institution: 
University of New South Wales
Title: 

Host-virus Interactions in a Frigid, Hypersaline Antarctic Lake Revealed by Metaproteomics

Abstract: 

Deep Lake is a marine derived, hypersaline system in Antarctica that remains perennially ice-free with water temperatures dropping to -20°C. These harsh environmental conditions have led to a low complexity microbial community, completely dominated by members of the haloarchaea, including four isolated species (tADL, DL31, Hrr. lacusprofundi and DL1) that account for ~72% of the lakes cellular population. Genomic sequencing and analysis of the four isolated species combined with metagenomics have revealed an unprecedented level of inter-genera exchange of long (up to 35 kb) stretches of identical DNA. However, despite the rampant, promiscuous exchange of DNA, distinct haloarchaeal lineages appear to prevail in the lake by virtue of their unique capacities for niche adaptation (1, 2). With no apparent metazoan grazers present in the lake, viruses are hypothesised to play a dominant role in shaping the microbial community of Deep Lake. In this present study we applied metaproteomics for the first time on a hypersaline environment and combined it with in-depth genomic and metagenomic analysis of Deep Lake CRISPR (Clustered Regularly Interspaced Short Palindromic Repeat) and BREX (Bacteriophage Exclusion) (3) systems to elucidate host-virus interactions.
Shotgun metaproteomics was performed on Deep Lake biomass from 5 distinct depths, captured by sequential filtration through 3 µm, 0.8 µm and 0.1 µm filters during the Antarctic summer of 2008/2009. All identified proteins were manually annotated and grouped into taxonomic and functional categories. We characterized CRISPR systems of the four genomes and the Deep Lake metagenome and used CRISPR spacer and repeat sequences to identify sources of invading DNA.
The Deep Lake metaproteome comprised around 1100 detected proteins. A striking feature was the identification of multiple, highly abundant cell surface proteins with a high degree of sequence variation compared to the genomes of the isolate species (“variants”). E.g. we identified 6 distinct proteins all matching the main S-layer component of tADL. Furthermore we detected variants for archaella (archaeal flagella), pili and other cell surface proteins. Multiple viral proteins were detected with sequence similarity to other, mainly haloarchaeal viruses. Functional CRISPR loci could be identified in the genomes of all four isolated species and CRISPR-associated (Cas) proteins were detected for two of them. CRISPR spacers could be linked to different sources of invading DNA, with most, but not all spacers targeting viruses. We detected one BREX protein (PglX) for Hrr. lacusprofundi. Some detected proteins, including cell surface proteins, were encoded on metagenome contigs together with putative viral genes.
The detection of multiple protein variants for cell surface structures like S-layer and archaella is indicative of phylotypes that are present in the lake. Introducing variation in cell surface structures likely provides the haloarchaeal populations with a way of evading viral infection. Consistent with this is the presence of a diverse viral population in Deep Lake. We detected proteins from at least eight distinct haloarchaeal viruses (eight major capsid proteins), with some proteins confirming active viral life cycles (e.g. prohead protease). Furthermore, the CRISPR spacer analysis revealed that some viruses infect multiple species (broad host range). In addition to the acquired cell surface variation, haloarchaeal host cells have employed active CRISPR and BREX systems as defense against viral infection.                             The presence of cell surface genes on metagenomic contigs together with putative viral genes, and the high degree of sequence variation observed in many cell surface proteins, suggests that viruses are involved in the acquisition, mutation and distribution of cell surface variants within the haloarchaeal populations. Overall, we were able to identify and describe a complex network of virus-host interactions, revealing a pivotal role of viruses in shaping the microbial community in Deep Lake (4). 
 

Event Date: 
Wednesday, March 25, 2015 - 19:00 - 19:45
Institution: 
University of Sydney
Title: 

Poxviruses: Man’s Best Friend. (Or How I Learned to Stop Worrying and Love the Virus)

Abstract: 

 

Poxviruses and humans have had a chequered past. Once the scourge known as smallpox routinely devastated human populations, some estimates are as high as 200 million mortalities last century. However the discovery of a tame version of the virus led to Edward Jenner to demonstrate the practise we now know as vaccination, which has gone some way to repairing the reputation of this virus. My research is built on the premise the these viruses still have much to teach us about many aspects of virology and host cell biology. And one of the most novel and exciting applications may be just around the corner.

 

Event Date: 
Wednesday, January 28, 2015 - 18:15 - 18:30
Institution: 
University of New South Wales
Title: 

Virus-host interactions in extreme environments, hot versus cold

Event Date: 
Wednesday, September 25, 2013 - 06:00 - 06:15
Institution: 
UNSW
Title: 

Viral infections of Ecklonia radiata

Abstract: 

 
Ecklonia radiata the dominant habitat-forming seaweed in temperate Australia has experienced high rates of mortality in the last decades. Disappearance of this kelp forest would have serious consequences for the marine ecosystem. The causes of mortality are not yet understood but we hypothesise a combination of environmental stress and viral infection. We could demonstrate that disease symptoms such as discolouration and bleaching are widespread but patchy distributed around Australia, which does not correlate simply with latitudinal variation in water temperatures. Focussing on the Kelp populations along the highly urbanised coast of Sydney we observed a highly site-specific pattern in the frequency of disease symptoms in E. radiata populations. Photosynthetic activity of discoloured thalli was significantly reduced compared to co-occurring, healthy (dark brown) thalli. Moreover, we were able to demonstrate that discoloured tissue from Ecklonia radiata from multiple sites around Sydney were infected with a viral pathogen. Inoculation experiments in the laboratory with the extracted viruses of sick tissue resulted in infection of healthy tissue of Ecklonia radiata. The frequency of putative disease morphotypes, and the relative abundance of viruses in Ecklonia radiata around Sydney appear to be higher at sites that are impacted by untreated wastewater discharge.  

Event Date: 
Wednesday, July 31, 2013 - 19:00 - 19:45
Institution: 
Australian National University
Title: 

Understanding Secondary Metabolite Biosynthesis as the Key to Unlock New Chemical Diversity in Fungi – from Viridicatumtoxin to the Immunosuppressive Neosartoricin

Abstract: 

The advancement of DNA sequencing technology has unlocked an unprecedented amount of microbial genomic information. These genome sequences also revealed a large number of secondary metabolite (SM) genes in both bacteria and fungi. For filamentous fungi in particular, the number of SM gene clusters encoded in the genome are often beyond the number of compounds that are reported for individual species. This is likely attributed to the tight regulation of the SM genes by the eukaryotic fungi compared to their prokaryotic counterparts, where some SM genes are only expressed in the presence of appropriate environmental signals. Research is currently going on to uncover new methods to activate these "silent" gene clusters. However, at the same time, continuously expanding our understanding of the relationship between SM compounds, the biosynthetic genes and microbial ecology will assists us in navigating the exponentially expanding seas of genomic information in the search for new bioactive compounds. The past four years, I have been involved in the elucidation of the SM pathways for viridicatumtoxin, griseofulvin, tryptoquialanine, cytochalasins, lovastatins, echinocandin, fumagilin and azaphilones. A specific example is given here on how the investigation into the genes and enzymes involved in the biosynthesis of an interesting molecule, viridicatumtoxin, eventually leads to the discovery of a new immunosuppressive compound, neosartoricin, from the human pathogens Aspergillus fumigatus and Neosartorya fischeri.

Event Date: 
Wednesday, March 6, 2013 (All day) - Thursday, March 7, 2013 (All day)

The Molecular Microbiology Meeting for 2013 has been booked for March 6th and 7th at Waterview in Bicentenial Park, Sydney, NSW. Please put the date in your diaries.

Note that the venue has changed and we are planning a meeting over 2 days. For those travelling interstate there is accommodation nearby at the Novotel and Ibis Hotels. You can book accommodation on the registration page.

Holding the meeting over 2 days has allowed us to invite more speakers and make more space for oral presentations selected from abstracts so please plan your abstract and register for the meeting so that we can include you in the program. Closing date for oral presentations will be October 26th.

The program will include:
Professor David Livermore - Drug resistance (Keynote) University of East Anglia (UEA) and Health Protection Agency, London UK

A/Professor Leo Poon - Emerging viruses (Keynote) University of Hong Kong

Professor Tom Riley -    C.difficile (Keynote) University of Western Australia

Despite miserable weather conditions, a sizeable crowd gathered at the Australian museum for the first JAMS meeting of 2012.

Dean Procter from the University of Sydney kicked off with our first virology talk of the year at JAMS. He introduced us to the live virus vaccine used to eradicate smallpox, Vaccinia virus. It encodes three BTB-Kelch protein orthologues in the Ubiquitin-Proteasome System, where host cell proteins are selectively degraded. This mechanism can prevent the establishment of an antiviral immune response enabling it to become a viral production factory enhancing viral spread. The identification of the substrates may indicate new mechanisms by which these viruses overcome cellular defenses to cause infection.

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