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  • The “Criminal Gene”: Is there a Genetic Link to Aggression?

    by Noluntu Buyana

    Have you ever wondered why some people seem naturally more are aggressive than others? Or how two people who are raised in similar environments have completely different reactions to stress or conflict? No?…..well I have so buckle up!

    Violence and aggression are complex behaviours shaped by an intricate interplay of environmental, psychological and biological factors. While upbringing and social context plays a major role, researchers have increasingly turned their attention to the brain and genetics with monoamine oxidase A gene (MAOA) drawing considerable interest. The interest blossomed in 1993 when Brunner et al. reported repeated explicit aggressive and violent behaviours among males across several generations in a Dutch family. They carried X-linked missense mutation in the MAOA gene causing abnormally low MAOA enzyme activity, a condition later termed Brunner syndrome.

    Loacted on the X-chromosome, the MAOA gene encodes for monoamine oxidase A enzyme, which is involved in the catabolism of neurotransmitters including dopamine, norepinephrine and serotonin in the brain. These neurotransmitters are vital to mood regulation, emotional response and stress management. Two main gene variations exist: Low-activity (MAOA-L) and high activity (MAOA-H) variants. The MAOA-L results in lower levels of MAOA enzyme, leading to the build-up of neurotransmitters. It has been associated with heightened impulsivity, antisocial traits, and increased aggressive responses, particularly in males. The MAOA-H variant, by contrast, leads to faster neurotransmitter breakdown. Some studies have suggested possible links to aggression in females, though findings remain inconsistent and not solid.

    The MAOA-L variant, nicknamed the “warrior gene”, has been associated with increased aggression following challenges in observational and survey-based studies, especially when combined with adverse childhood experiences. Noting the importance of childhood adversity and environmental contingences in behavioural outcomes, more studies started focusing on gene-by-environment interactions in MAOA-L individuals. McDermott et al. conducted an experiment aimed at observing how MAOA gene influence aggressive behaviour under varying levels of provocation, using the “host sauce” paradigm. They hypothesised that individuals MAOA-L will react more aggressively with high levels or provocation compared to the MAOA-H group, and not react aggressively with low provocation (i.e., gene by environment interaction).

    METHODS

    DNA samples were collected from 78 college male participants, and they were grouped as either MAOH-H or MAOA-L carriers. Each participant was told they were paired with an anonymous partner in a different lab (it was actually a computer). They performed a task and awarded money upon the completion. Afterwards, each participant was told their “partner” had either 0%, 20% (low take) or 80%(high take) of their earnings.

    Each participant was given 10 small doses of hot sauce. To punish their partner, the participants could give their partner varying amounts spicy hot sauce knowing the other person dislikes it. Alternately, they could trade the hot sauce for money. The amount of hot sauce given was used as a measure of behavioural aggression.

    KEY FINDINGS
    With high level provocation (i.e. when 80% was taken), participants in both groups responded more frequently and more aggressively than when 20% was taken (low provocation). Additionally, emotional survey administered after each round showed that those that lost more money reported feeling “mad” and “angry”.

    Comparing different variants, they found no difference between the 2 groups when 20% was taken. They found more MAOA-L participants(75%) were significantly more aggressive than MAOA-H participants (62%) when 80% was taken. Ignoring the amount taken, MAOA-L types had higher levels of aggression overall.

    Lastly, comparing proportions of observations administered the maximal amount of hot sauce punishment allowed, 44% of MAOA-L participants administered maximal hot sauce when 80% was taken compared to the 19% of MAOA-H. Additionally, 12% of participants administered maximal amount when 20% was taken compared to the 6% of MAOA-H.

    CONCLUSION AND DISCUSSION
    This study provided compelling evidence of gene-by-environment interaction in human behaviour. Specifically, individuals with MAOA-L variant displayed increased aggression but only when significantly provoked; that the gene does not cause aggression in isolation and context matters. This supports the idea that genetic predispositions interact with environmental triggers to cause behaviour, and MAOA gene may amplify the behavioural responses to stress or unfairness. Future work should explore the underlying psychological phenomena at work, how and why individual genetic differences cause different behavioural outcomes.

    I believe referring to the MAOA-L as the “warrior gene” is an oversimplification and ignores the complexity of behaviour. It risks creating deterministic views and such labels risks dimmish personal responsibility for behaviour, especially in criminal justice context. Although some research has explored pharmaceutical interventions targeting this gene, such interventions are risky due to MAOA’s broad role in brain chemistry. Rather than reducing people to their genes, I believe more attention should be directed towards early psychological support and social interventions. Genes may load the gun, but the environment pulls the trigger…and sometimes, therapy helps keep the safety on.

    References
    McDermott, R., Tingley, D., Cowden, J., Frazzetto, G. and Johnson, D.D.P., 2009. Monoamine oxidase A gene (MAOA) predicts behavioral aggression following provocation. Proceedings of the National Academy of Sciences, 106(7), pp.2118–2123. https://doi.org/10.1073/pnas.0808376106
    Mentis, A.-F.A., Dardiotis, E., Katsouni, E. & Chrousos, G.P., 2021. From warrior genes to translational solutions: novel insights into monoamine oxidases (MAOs) and aggression. Translational Psychiatry, 11(1), article 130. doi:10.1038/s41398-021-01257-2
    Moon, D., 2025. MAO-A and MAO-B: Neurotransmitter levels, genetics, and warrior gene studies. GeneticLifehacks, 10 July [online]. Available at: https://www.geneticlifehacks.com/maoa/

  • The Metabolic Battle Against TB

    by Tony Noveld

  • Hidden Saboteur: How Tuberculosis Outsmarts Our Immune System

    by Tony Noveld

    In this study, researchers from the University of Cape Town, the Ragon Institute, and the Francis Crick Institute set out to answer a vital question: Why does Mycobacterium tuberculosis remain the world’s deadliest bacterial pathogen despite decades of research and treatment efforts? This 2025 review synthesizes over three decades of molecular, cellular, animal, and clinical studies to build a comprehensive understanding of how the tuberculosis bacterium evades and manipulates the human host to survive and spread.

    How Did the Researchers Approach This?

    Rather than generating new experimental data, the authors performed a narrative synthesis. They systematically reviewed hundreds of peer-reviewed articles spanning microbiology, immunology, pathology, and epidemiology. This integrative approach allowed them to connect diverse findings from genetic profiling studies, experimental infection models in mice and non-human primates, detailed analyses of human tissue samples, and comprehensive TB epidemiological data. The review bridges laboratory discoveries with clinical observations to clarify how bacterial biology translates into disease dynamics in real-world human populations.

    Key Findings: A Master of Cellular Sabotage

    The review reveals that the tuberculosis bacterium is not a passive survivor—it actively reprograms the very immune cells meant to destroy it. When inhaled, tuberculosis bacteria are engulfed by macrophages, immune cells designed to digest pathogens inside acidic compartments called phagosomes. However, the bacterium employs sophisticated countermeasures: it blocks phagosomal acidification and disrupts phagosome-lysosome fusion, effectively stalling its own degradation The bacterium also hijacks host nutrient pathways, redirecting cellular resources for its survival. Remarkably, some tuberculosis bacteria can escape into the cytosol—the cell’s interior—gaining additional freedom to manipulate host processes.

    The tuberculosis bacterium demonstrates metabolic flexibility rarely observed in other bacteria. It can shift between multiple energy sources and slow its growth to enter dormancy states lasting years. This remarkable adaptability underpins latent TB infection, where individuals carry live bacteria without symptoms, creating a hidden reservoir for future disease and transmission.

    The Granuloma: Fortress or Safe Haven?

    The battle primarily occurs within granulomas—organized clusters of immune cells designed to contain the tuberculosis bacterium. Rather than static fortresses, granulomas represent complex, dynamic ecosystems where the bacterium manipulates oxygen levels and programs immune cell death pathways to create favourable microenvironments. This constant interplay between bacterial survival strategies and host containment attempts explains why granulomas sometimes fail, resulting in active disease and destructive tissue damage.

    A Silent Epidemic: Asymptomatic TB and Transmission

    Perhaps most concerning is the “silent reservoir” of asymptomatic infections (see figure 3) highlighted by the review. Large-scale prevalence surveys reveal approximately half of TB-positive individuals lack classical symptoms like persistent cough or fever. Despite appearing healthy, many remain capable of transmission, severely complicating global identification and treatment efforts.

    Strengths and Limitations

    The narrative synthesis effectively bridges research silos, connecting molecular insights with clinical and epidemiological realities. However, limitations exist: much mechanistic data derives from animal models that don’t perfectly mirror human TB (at no fault of the authors), human tissue studies face accessibility constraints, and critical gaps remain regarding reactivation triggers—being key unknowns for prevention strategies.

    Personal Interpretation and Implications

    This synthesis reaffirms the tuberculosis bacterium’s extraordinary adaptability, evolved through millennia of human co-evolution into a master of immune evasion rather than aggressive virulence. The bacterium’s ability to manipulate macrophages, survive within granulomas, remain dormant for years, and persist asymptomatically explains TB’s resistance to eradication despite available drugs and vaccines.

    As someone studying infectious diseases, and an upcoming clinician-scientist, this review fundamentally reshapes my understanding of TB latency. It’s not a binary state but a nuanced spectrum involving complex host-pathogen dialogues. It highlights a critical public health challenge: focusing solely on symptomatic cases misses much of the infectious reservoir. Future interventions must integrate improved diagnostics for silent infections, host-directed therapies targeting immune manipulation, and social interventions addressing environmental factors.

    The review underscores that TB research cannot occur in isolation. Breaking the transmission cycle demands integrating laboratory discoveries with clinical observations and epidemiological data—a true “bench to bedside to community” approach that may finally outsmart the bacterium’s sophisticated defences.

    Conclusion: An Ongoing Arms Race

    Nearly 150 years after TB’s discovery, Mycobacterium tuberculosis remains humanity’s most formidable bacterial adversary not through aggressive virulence, but via intricate, highly evolved immune system interactions. This 2025 review emphasizes that defeating TB requires understanding this complex biological dance in all its dimensions. Only with such comprehensive insight can we develop the innovative diagnostics, treatments, and preventive measures needed to finally tip the scales in humanity’s favour.

    Blog based on: “Mycobacterium tuberculosis biology, pathogenicity and interaction with the host,” 2025 review.

    References

    Warner, D.F., Barczak, A.K., Gutierrez, M.G. et al. (2025). Mycobacterium tuberculosis biology, pathogenicity and interaction with the host. Nature Reviews Microbiology. https://doi.org/10.1038/s41579-025-01201-x

  • My greatest takeaway: Feedback!

    By Angela Mutugi


    I am going to say something a little crazy but very true, so brace yourself. I only applied to one university for honours. Shocking, I know! UCT, you were my one and only… truly! It was my greatest risk, my biggest gamble, but it worked out. Yes, I have been critiqued on my decision, and no, I have not tested my luck at the lottery… yet. For the first couple of weeks, I couldn’t believe it panned out. I am living in Cape Town and attending the top-ranked university in Africa. Sorry, not sorry for the humble brag.

    Reflecting on why I applied, I remember my toughest lecturer from my undergrad. She was also the most inspiring for me. She was never shy with her commentary and encouraged risk-taking, within reason.

    But let’s focus back on the present situation. I’m here, halfway through honours, and honestly, it’s a good thing I am an adrenaline junkie cause this year’s rollercoaster of emotions has been intense. I have learnt new and re-learnt old things about myself and how to manage in this environment. It has grown me in my independence and intellect. So now that I am reflecting, if there is one piece of advice I would say everyone should take, it’s feedback. Whether it is from your friends, family, but especially if it’s from your supervisors, take it and apply it. You can question it, see it through different lenses, love it, hate it, but you should accept it.

    In this faculty, I believe we are all looking forward to understanding, creating and sustaining something much bigger than ourselves. We have all walked different paths to get here, and after we may walk different paths to get to where we are going, but in this moment where all our paths have converged, let us learn from each other and encourage one another. Sometimes the best lessons are the ones learnt outside of a classroom. Being surrounded by people striving for their best and wanting the best for those around them means that their words should not just be critical but encouraging.

    So I ask you, please take the feedback. Really understand and apply it. Give some feedback as well. Your words could shift entire perspectives and be exactly what someone needs to hear.

    Please take my advice, but if you find me unreliable because of my ‘risk-taking’ history, take this guy’s advice:
    “Feedback is the compass for greatness; it tells you what to avoid, what to learn, and where to excel.” – Henrik Ceder.

  • Blame it on your genes: why you may work better at night

    By Angela Mutugi
    Genetic testing is more often viewed as a device to trace your family’s ancestry to know where you came from or if you are secretly a royal, but your genes can help you understand why you’re ready to go to bed at 9 pm, why you sleep in and why you lie awake at night. Your genes guard the code to your ideal sleep-wake cycle, and this could greatly impact your day-to-day productivity and your health in the long term.

    A chronotype is your body’s natural preference in the sleep-wake cycle. It governs whether we are more ‘morning larks’ or ‘night owls’, and this is driven by an internal master clock, the suprachiasmatic nucleus of the brain, stitched together by our genetic code. Though it is important to note that external factors like age, lifestyle, and light exposure can still affect our sleep-wake cycle.

    In this study, three major genome-wide association studies (GWAS) were conducted using data from 23andMe and the UK Biobank. The aim was to review and synthesise findings in this genetic data that investigated the genetic underpinnings of human chronotypes. Our chronotype is a polygenic trait, influenced predominantly by the PER1, PER2, PER3, CRY1, CRY2, CLOCK and BMAL1 genes. These genes regulate the circadian rhythms of nearly every cell, managing sleep timing, hormone release and metabolism, through feedback loops all controlled and synchronised by the suprachiasmatic nucleus.

    The results affirmed the known genes of circadian rhythm and identified novel loci. Nine key genes were further confirmed and associated with specific chronotypes. Variations amongst these genes were noted to affect the longevity of sleep, the onset of melatonin and the length of your circadian rhythm.

    Furthering these studies would benefit the understanding of common and rare genetic variations affecting one’s chronotype and provide greater insight into the foundation of our circadian system. Individual sleep profiles could lead to personalised sleep recommendations, greatly impact the treatment of sleep disorders and optimise work scheduling. There is still more to uncover in this field as studies with conflicting findings regarding gene-specific polymorphism have yielded inconsistent results, suggesting that this complexity will require broader genetic approaches.

  • Charging Up On Electrolytes

    By Angela Mutugi

  • The Enemy of Your Enemy is Your Friend – Using Oncolytic Viruses to Stimulate Immune-Mediated Tumour Destruction

    By Mrittika Islam

    Cancer remains as one of the most notoriously unyielding diseases mankind has ever had to face, accounting for nearly 10 million deaths in 2022 [1]. Its precise pathological profile is still a topic of rigorous debate; it is becoming increasingly clear that what we do not know about cancer is definitively more than what we do know, and the more headway we make to dismantle this disease, the more obstacles seem to appear.

    Cancer treatment is no exception. The arsenal of tools used to treat cancer include the augmentation of the body’s own anti-tumour immune response, i.e., the ability to recognize and eliminate cancer cells, referred to as cancer immunotherapeutics. One such therapy offers a unique approach to tumour elimination; the use of naturally occurring and/or genetically modified Oncolytic Viruses (OVs). Infecting and replicating inside tumour cells, OVs induce cell lysis which releases tumour molecular markers that prime immune cells, such as T cells, and activate a new and enhanced adaptive immune response against the tumour. This immunotherapy pioneers the use of viral mechanisms to target tumours, i.e., the induction of cellular lysis after sufficient viral replication – a promising strategy using an unconventional instrument.

    The appeal of OVs primarily come from their selectivity; Oncolytic Viruses are genetically engineered to have high selectivity for malignant cells, often exploiting characteristic defects in the tumour’s anti-viral defence system. This therapy therefore minimizes toxicity to normal cells, lowering side effects, while maintaining high tumour lethality – a particularly attractive factor due to the escalation of harmful side effects in the landscape of cancer drugs. In addition to this, OVs can be used to deliver therapeutic payloads to the tumour microenvironment (TME), opening the door to novel mechanisms to supplement or suppress molecular targets to amplify immune infiltration.

    Despite the elegance of this therapy, only a handful of oncolytic viruses have been approved for commercial use, often due to shortfalls in clinical progression. One of the main limitations of viral oncotherapy is the inefficacy against immunologically ‘cold’ tumours, i.e., tumours that have established robust immunosuppression by altering the TME to prevent immune recognition, infiltration and function. As the success of OVs rely on immune efficacy, these immune resistant tumours tend to bypass oncolytic destruction. The popular attempt to overcome this by supplementing the OV-mediated immune response – for example, by delivering immune stimulatory payloads – has proven to be inadequate due to the sturdy and, rather unfortunately, ambiguous mechanisms of immune resistance. There is, therefore, much to uncover regarding this delicate immune manipulation sustaining cold tumours and impeding OV treatment.

    To this extent, Greg Delgoffe, Ph.D., and his team at the University of Pittsburgh School of Medicine took a new approach to investigating this limitation of viral oncotherapy: focusing on determining and alleviating the mechanisms of immune suppression rather than enhancing the existing immune potency [2]. Briefly, they developed genetically identical pairs of mouse head and neck tumours (MEER) that were either sensitive or resistant/unresponsive to an unmodified form of Oncolytic Vaccinia Virus (VV), and compared the composition of the immune infiltrates in each tumour model. In doing so, they discovered that resistant tumours were characterized by a persistent stability of immunosuppressive T regulatory cells (Treg) in the tumour microenvironment, which was absent in the OV sensitive forms. This was further deduced to be caused by elevated levels of a potent immune inhibitory signalling molecule, Transforming Growth Factor β (TGFβ), in the TME, suggesting that TGFβ plays a direct role in OV resistance. This highlighted an important mechanism of OV resistance – the oncogenic elevation of specific immunoregulatory components to maintain an immunosuppressive TME thereby diminishing the OV mediated immune enhancement.

    This discovery provided a new therapeutic target for combating OV resistance: TGFβ. To investigate this, they then genetically engineered the VV to deliver a powerful TGFβ inhibitor. This was met with encouraging results: upon OV treatment, TGFβ inhibition led to significant reduction in the MEER tumours that were initially resistant to the therapy, thus restoring susceptibility to OV. Importantly, oncoviral TGFβ inhibition did not appear to affect non-malignant TGFβ that functions in normal cells. This strategy therefore not only targets oncogenic TGFβ to relieve tumour mediated immunosuppression, but also does so with no notable effect on normal TGFβ functioning.

    This study provides new insights into the immunoregulatory mechanism used by cancer cells to curate OV resistance, uncovering a fundamental component – TGFβ – driving this oncogenic phenomenon. Dr Delgoffe and his team further demonstrated the profound effects of TGFβ inhibition in mitigating oncogenic immune suppression and improving OV efficacy. This new take on a familiar battle in the development of cancer therapeutics – i.e., resistance – provides exciting opportunities to deliver therapeutic payloads to dismantle the components sustaining resistance, thus strengthening treatment potency. TGFβ may very well be one amongst a plethora of immunosuppressive components contributing to OV resistance and this study provides a promising vehicle and strategy for their effective neutralisation.

    It is worth noting once again that the use of viruses to treat cancer serves as an interesting scientific unorthodox. Even so, with the recent advancements in modern biotechnology and our understanding of cancer biology and virology, the potential of viral oncotherapy seems indefinite. Research on oncolytic viruses as an immunotherapy has come impressively far but still has further to go. This is just the beginning.

    References

    1. Cancer (IARC), The International Agency for Research on Cancer. Global Cancer Observatory. https://gco.iarc.fr/ (2022)
    2. DePeaux, Kristin et al. “An oncolytic virus-delivered TGFβ inhibitor overcomes the immunosuppressive tumour microenvironment.” The Journal of Experimental Medicine vol. 220,10 (2023).

  • The Enemy of your Enemy is your friend!

    By Mrittika Islam

  • EMBRACING THE NEW

    By Moleboheng Moipatli
    Newness! I am one individual who gravitates towards change. It brims with so much hope and possibility. Change invites us into the unknown, and while it may bring some challenges, I’ve found that those challenges often become the breeding ground for growth and greatness. So, when I began this year at a new institution, in a new environment, with new opportunities to learn, I was filled with excitement. I could not wait for the classes to begin, and when we finally received an email announcing the eventual commencement of classes, I thought to myself: “Finally! The new has begun.”
    The first term was a period of discovery. I especially enjoyed the General Techniques course; every class felt like an opportunity to sharpen my skills and expand my knowledge (I really like learning new things, especially in biological sciences). But having to navigate through everything wasn’t a walk in the park. For example, making friends was not as straightforward, but because I’ve always been a bit of a loner, at first it didn’t bother me. Yet as the term progressed, the fast-paced teaching and the generalization that we all came from similar undergraduate backgrounds made me feel out of place. That was my first encounter with imposter syndrome. Strangely, what helped was realizing I wasn’t
    alone (we are never really alone). Conversations with my classmates who shared my background reminded me that many of us were experiencing the same insecurities. That realization was liberating. It also taught me to speak out more and not hide my struggles (there’s no shame in struggling).
    I found the second term both epic and demanding. Looking back, I see how much I have grown as a young scientist. I have especially gained more confidence and acquired valuable knowledge and experience through the four module cycles our stream offered. Knowledge truly is power! I believe the cycles helped me discover my voice as a scientist.
    I connected with very interesting and intelligent people…there’s hope for the future. I also noticed the support from the staff as another factor that contributed to my positive experience in my studies. One of the highlights was learning about the biology of cancer. The disease’s complexity fascinated me, but it also left me quite frustrated. After seeing the challenges researchers face, I can honestly say that cancer research and I are not a perfect match; in other words, I AM BEEFING WITH CANCER. Maybe I will join the fight in the near future, but for now, I will keep cheering for those who continue to battle that disease.
    As I now reflect, I can see that even new things come with mountains that we must surmount. However, I have come to learn that embracing the community around you and accepting the help that is offered is imperative to overcoming even the toughest challenges (two is better than one, three is even better!). My advice? Don’t wing it alone; there really is beauty and power in community, and getting to the top requires stepping out of your comfort zone while working with others. Moreover, I have learnt that blessings also come with sacrifices and hard choices. If I were to repeat my Honours year, I would only wish to undo the mistakes I made. But I am learning to be kind to myself, after all, I have not walked this path before, and mistakes are part of the journey. This Honours year taught me that growth is rarely comfortable, but it is always worthwhile. And as I move forward, not sure what my future holds, I do so with gratitude and a renewed sense of purpose for the next chapter of my career.

  • Your scalp is a whole ecosystem!

    By Moleboheng Moipatli

    We are all aware that a plethora of microorganisms reside in our stomachs. That is what is referred to as the gut microbiome. Well, if you are like me and you’ve never thought to question the origin of some of the skin-related disorders or diseases, then you are in for quite a surprise!

    Have you ever wondered what causes the buildup of dandruff, an itchy and inflamed scalp? Well, it turns out we have bacteria and fungi naturally living on our scalps too! According to previous research, the human scalp accommodates diverse bacteria and fungi that influence both healthy and diseased scalps. Fungi have been reported to cause dandruff by activating specific proteins that break down oil produced by the scalp, and certain bacteria play a role in consuming the oil (fatty acids) to avoid accumulation that can eventually lead to irritation and inflammation, which are symptoms of seborrhoeic dermatitis.

    Although the regular microbial communities there are complicated, little was known about the bacteria that reside on the human scalp. So, the researchers from Soochow University and other universities in China set out to test a theory that stated that skin problems might be caused by the collapse of a healthy microbiome, for example a drop in the variety of microbes and too much growth of some microbes. In the quest to test the hypothesis/claim, the researchers asked themselves two questions: i) Is there any difference between people with diseased scalps and normal scalps when looking at the structure and diversity of their microbial community? And ii) Is the bacterial and fungal harmony (network) disrupted?

    To help answer these questions, the researchers combined different scientific methods that included taking samples from volunteers who were categorized into two groups: those with normal scalps and those with diseased scalps (subclassed to dandruff and seborrheic dermatitis). The samples were studied using a sophisticated DNA sequencing technique known as Illumina MiSeq Sequencing and other bioinformatics tools to investigate the bacterial and fungal microbial communities on scalps associated with D/SD and the relationship and differences between the scalp microbiomes in normal and diseased groups.

    Their results showed that an increase in the diseased group (with dandruff and seborrhoeic dermatitis), the abundance of Staphylococcus was high as compared to the abundance/presence of other bacteria, such as Propionibacterium. They also showed that a type of fungi called Malassezia restrica was more abundant as compared to a different type of the Malassezia species, suggesting that these differences in the relative abundance of the microbial population may contribute to disease symptoms.