Infectious diseases showcased at research symposium

Every year the School of Biological Sciences (SBS) holds a symposium to highlight the School’s exciting discovery and translational research, celebrate its many achievements, provide new engagement opportunities for early-career researchers, and help foster a supportive community with collaboration at its heart.  

The years symposium included talks from research staff across SBS's four strategic research themes:

• Fundamental Principles and Architecture of Life 
• Life’s Resilience in our Changing World 
• Bioscience for Disease Prevention & Health 
• Sustainable & Circular Bioeconomy Powered by Nature

A large component of this research surrounds infectious diseases with a number of researchers talking on the topic throughout the day.

This article provides a summary of that research.

Professor Liz Bayne's lab in the Institute for Cell Biology aims to understand the diverse mechanisms and functions of RNA interference (RANi) pathways in fungal genome regulation.

RNAi is a mechanism of genome regulation conserved in nearly all eukaryotes. Eukaryotes are organisms whose cells contain a nucleus and other organelles. 

In her talk, Professor Bayne discussed how the human fungal pathogen Cryptococcus uses RNAi, a natural system that uses tiny RNA molecules to switch off genes and control harmful mobile DNA. This matters because Cryptococcus can cause serious lung infections and life-threatening meningitis, killing around 100,000 people each year.

Bayne’s team is investigating how this RNAi system works and how it may help the fungus adapt. They found that key RNAi proteins, including Dicer, Argonaute and HEN1, help shape these small RNA signals, with some effects strongest around transposons — mobile genetic elements that can disrupt the genome.

The work reveals a distinctive RNA-silencing pathway in Cryptococcus, offering new clues into how this dangerous pathogen controls its genome and evolves.

Dr Nisha Philip's group in the Institute of Immunology and Infection Research explore how signalling pathways regulate key life-cycle transitions in the malaria parasite. In particular, the group is interested in how protein phosphorylation and ubiquitination are critical to these life-cycle transitions. 

At the Research Symposium, Dr Philip explored how malaria parasites prepare for transmission from humans to mosquitoes. 

This stage is difficult to target because the parasite forms dormant-like gametocytes, which can survive before being taken up by a mosquito.

Her group focuses on ubiquitination, a cellular “tagging” system that controls proteins. 

In the talk, Dr Philips explained how the group found that one parasite enzyme, USP7, is essential for male gamete formation. Without USP7, Plasmodium falciparum cannot properly copy its genome, produce male gametes, or transmit to mosquitoes.

Because parasite USP7 is very different from the human version, it could offer a promising target for future drugs aimed at stopping malaria spread.

Dr Jenny Regan's team in the Institute of Immunology and Infection Research investigate why males and females have different responses to infection, why the sexes age differently, and how immunity and ageing interact.

The team want to find ways to target the immune system to promote healthy ageing in both sexes.

In her talk, Dr Regan's discussed how immune responses often differ between males and females. For example, females are more prone to autoimmune disease, while males are often more vulnerable to infections and severe outcomes — a pattern seen across many species.

Dr Regan highlighted that her group uses fruit flies as a model. In fruit flies, females survive infection better because their macrophages are more “primed” to attack bacteria, with higher phagocytosis and stronger antimicrobial activity. Male macrophages, by contrast, show more anti-inflammatory features.

These findings suggest that sex differences may be built into immune cells themselves, helping explain why infection risk and immune-related disease can vary between males and females.

Dr Takanobu Tagawa's group in the Institute of Quantitative Biology, Biochemistry and Biotechnology aims to define functions and mechanisms of non-coding RNAs in virus-host interactions.

The team are among the first to identify virus infection-induced circular RNAs.

In the talk, Dr Tagawa discussed how cancer-linked herpesviruses, including Epstein-Barr virus and Kaposi sarcoma herpesvirus, use unusual RNA molecules called circular RNAs. These viruses can hide in cells for long periods, making them hard to target.

Circular RNAs are stable loops of RNA that can interact with other RNAs and proteins while attracting little immune attention. Tagawa’s work shows that host circular RNAs change during herpesvirus infection, helping keep viral activity low during latency and suppressing full viral activation. Some herpesviruses also make their own circular RNAs.

These findings highlight circular RNAs as important players in how herpesviruses persist, manipulate host cells, and contribute to disease.