By Gwyneth Astles


BRINGING YOU THE LATEST NEWS & EVENTS FROM THE SCIENCE INDUSTRY How viruses hijack mitochondria to evade the immune system


“This reveals how viruses can rewire mitochondria to evade immunity,” said Dr Chengyu Liang, Professor and co-leader of the Molecular & Cellular Oncogenesis Program at The Wistar Institute Ellen and Ronald Caplan Cancer Center and senior author of the study. “It broadens our understanding of Bcl-2 proteins and points to new therapeutic targets.”


Dr Chengyu Liang. Credit: The Wistar Institute


In a discovery poised to reshape our understanding of viral survival strategies, scientists at The Wistar Institute have uncovered a viral trick that transforms the cell’s mitochondria - its energy and signalling hubs - into accomplices. Using advanced molecular and imaging techniques, the team revealed how Kaposi’s sarcoma-associated herpesvirus (KSHV) hijacks the host’s mitochondrial architecture to silence immune alarms and ensure its own replication.


The research [1], published in Nature Microbiology, centres on a small but powerful viral protein called vBcl-2, long associated with blocking cell death. But the Wistar team found it does far more - it reprograms the cell’s mitochondria to disable the immune response machinery at its root.


Using high-resolution microscopy and structural biology tools, the team showed how vBcl-2 recruits a host enzyme, NM23-H2, and redirects it to the mitochondria. Once there, NM23-H2 powers a fragmentation process - essentially slicing up the normally connected mitochondrial network. This physical disruption dismantles a key antiviral signal hub known as MAVS before it can alert the rest of the cell to the infection.


“Instead of blocking one immune protein, the virus disrupts the whole immune signalling hub,” said Liang. “It’s like FEMA failing after a disaster - MAVS is that hub, so the cell can’t coordinate its response to the virus.”


By stopping MAVS from assembling, the virus blocks activation of Type I interferon responses - our cells’ first line of defence against viral invaders. Without these signals, the cell fails to deploy crucial antiviral proteins such as TRIM22 and MxB, which normally trap virus particles in the nucleus and prevent their release.


What makes this discovery even more compelling is its broader implication: similar Bcl-2-like proteins are encoded by other herpesviruses, including the Epstein-Barr virus. This suggests that mitochondrial sabotage may be a common tactic across the herpesvirus family.


Global study reveals gender-linked patterns in antimicrobial resistance


A landmark international study [1] led by the University of Turku, Finland, has uncovered striking differences in antibiotic resistance genes between men and women, with significant implications for tackling one of the world’s most urgent health crises.


Antibiotic resistance, which undermines the effectiveness of life-saving drugs, currently contributes to over 1.3 million deaths each year worldwide. Yet, until now, little was known about how resistance gene patterns differ between genders on a global scale.


The research team analysed DNA data from more than 14,000 human gut microbiomes spanning 32 countries, drawing on a vast international repository of public datasets. Their analysis revealed that women in high-income countries carry around 9% more antibiotic resistance genes than men, suggesting


greater exposure to antibiotics or resistant bacteria.


Conversely, in low- and middle-income countries, men tended to have higher resistance gene loads, although this difference diminished after accounting for age and living conditions.


“Our findings highlight how gender, geography, and lifestyle intersect to shape antimicrobial resistance in the human gut,” explained Professor Leo Lahti, head of the data science group leading the research.


The study also found that resistance gene diversity varied with age, peaking in infants and the elderly, and was generally higher in populations with elevated antibiotic use.


“This is the first large-scale study to reveal such complex gender-based patterns in antimicrobial resistance globally,” noted postdoctoral researcher Katariina Pärnänen.


“Understanding these differences is critical for designing targeted interventions that ensure equitable healthcare outcomes.”


More information online: ilmt.co/PL/B2o1


1. ‘Gender differences in global antimicrobial resistance’ published in npj Biofilms and Microbiomes on 19 May 2025 64985pr@reply-direct.com


EGFR inhibition alters metabolism in KRAS-mutant colon cancer


A new study [1] from the Medical University of Vienna has uncovered a surprising vulnerability in colorectal cancers driven by KRAS mutations - one of the most common and notoriously treatment-resistant alterations in cancer. Published in EMBO Molecular Medicine, the findings suggest that blocking EGFR, a receptor long thought irrelevant in KRAS-mutant tumours, could significantly impair tumour metabolism and improve patient outcomes.


The research team, led by Professor Maria Sibilia at the Center for Cancer Research, used colorectal cancer organoids - miniature tumour models grown from mouse-derived cancer cells - to show that genetic deletion of EGFR altered how the cells process nutrients. Specifically, EGFR loss shifted metabolism from glycolysis towards glutamine use, while suppressing key growth signals and triggering gene expression


changes linked to longer survival in patients.


“This contradicts the prevailing belief that EGFR has no therapeutic value in KRAS-mutated tumours,” said first author Dana Krauß. “We found that EGFR remains functionally important and creates metabolic dependencies that could be exploited.”


One gene in particular, Smoc2, was identified as a critical regulator of the tumour’s metabolic reprogramming following EGFR loss. The team also observed that EGFR-deficient tumours activated alternative developmental pathways - including stem cell signatures and Wnt signalling - suggesting a complex adaptive response with potential druggable nodes.


The results raise fresh questions about current treatment strategies that exclude patients with KRAS mutations from EGFR-targeted therapies. They also open the door to


combination treatments targeting both KRAS and EGFR.


“These findings provide a molecular rationale for re- evaluating EGFR inhibition in KRAS-mutant colorectal cancer,” said Professor Maria Sibilia, Head of the Center for Cancer Research at the Medical University of Vienna. “It’s a reminder of the value of re-examining established dogmas in cancer biology.”


More information online: ilmt.co/PL/xoJn


1. Krauß, D. et al. EGFR controls transcriptional and metabolic rewiring in KRASG12D colorectal cancer published in EMBO Molecular Medicine (2025)


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The team also identified a small-molecule inhibitor, VBNI-1, that can disrupt the vBcl-2/NM23-H2 interaction. In lab tests, this compound restored mitochondrial structure, revived immune signalling, and halted viral escape - without harming healthy cells.


“This is one of the first candidate drugs that targets the virus-mitochondria interface,” said Liang. “It gives us a potential therapeutic pathway where none existed before for KSHV - and possibly other latent viral infections.”


The breakthrough was made possible by a cross- disciplinary effort drawing on Wistar’s cutting-edge imaging, proteomics, and drug screening capabilities.


“This discovery shows the power of collaboration in science,” said Liang. “We began by studying a viral protein and uncovered a new way mitochondria regulate immunity, opening doors for new KSHV treatments.”


With no current vaccine or cure for KSHV, and rising concern over herpesvirus-driven cancers in immunocompromised patients, this research may offer a new route to protect those most at risk.


More information online: ilmt.co/PL/j9ln


1. Kaposi’s Sarcoma-Associated Herpesvirus Induces Mitochondrial Fission to Evade Host Immune Responses and Promote Viral Production published in Nature Microbiology


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